Page 1

The Clinical ADVISOR • october 2013



■■CVD polypill ■■Knee arthritis and exercise ■■Flu shot during pregnancy

advisor forum

■■Reactivation of HPV ■■Acute adult pharyngitis ■■Punch out a pilar cyst

| octo b er 2 013 |

common causes of female

hair loss

Androgenic alopecia (shown) is the most common form of hair loss in women.

legal advisor

Clinician charged with battery after complying with police

✶ free cE courses!

n CE Feature

vulvovaginal atrophy page 58

Volume 16, Number 10

n Dermatologic Look-Alikes

enlarging white patches page 89

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Editor Joe Kopcha, Managing editor Marina Galanakis Senior editor Delicia Yard Web editor Nicole Blazek Contributing editors Bruce D. Askey, MSN, CRNP; Rebecca H. Bryan, APRN, CNP; Eileen F. Campbell, MSN, CRNP; Philip R. Cohen, MD; Deborah L. Cross, MPH, CRNP, ANP-BC; Sharon Dudley-Brown, PhD, FNP-BC; Maria Kidner, DNP, FNP-C; Joan W. Kiely, MSN, CRNP; Debra August King, PhD, PA; Ann W. Latner, JD; Claire B. O’Connell, MPH, PA-C; Kathy Pereira, MSN, FNP-BC; Sherril Sego, FNP, DNP; Julee B. Waldrop, MS, PNP; Kim Zuber, PA-C Art director Andrew Bass Group art director, Haymarket Medical Jennifer Dvoretz Production director Kathleen Millea Circulation manager Paul Silver Audience development director John Crewe National accounts manager Alison McCauley, 646.638.6098 alison.mccauley @ Group publisher Thomas P. Hennessy, 646.638.6085 tom.hennessy @ Editorial director Jeff Forster Vice president, medical magazines and digital products Jim Burke CEO, Haymarket Media, Inc. Lee Maniscalco All correspondence to: The Clinical Advisor 114 West 26th Street, 4th Floor, New York, NY 10001 For advertising sales, call 646.638.6085. For reprints, contact Wright’s Reprints at 877.652.5295. Persons appearing in photographs in “Newsline,” “The Legal Advisor,” and “Clinical Challenge” are not the actual individuals ­mentioned in the articles.They appear for illustrative purposes only. The Clinical Advisor® (USPS 017-546, ISSN 1524-7317), Volume 16, Number 10, is published 12 times a year, monthly, for $75.00 per year in the United States; $85.00 in Canada; $110.00 for all other foreign, in U.S. dollars, by Haymarket Media, Inc., 114 West 26th Street, 4th Floor, New York, NY 10001. Single copy: $20 U.S.; $30 foreign. To order or update your paid subscription, call 800.436.9269. Periodicals postage rate paid at New York, NY, and additional mailing offices. POSTMASTER: Send address change to DMD Data Inc. 10255 W. Higgins Rd, Suite 280, Rosemont, IL 60018. Call 800.430.5450 to change your address or make other subscription inquiries. Requests for subscriptions from outside the United States must be accompanied by payment. All rights reserved. Reproduction in whole or in part without permission is prohibited. Copyright © 2013.

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2 the clinical advisor • october 2013 •

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Allergic Reactions Local Allergyďż˝"TXJUIBOZJOTVMJOUIFSBQZ QBUJFOUTUBLJOH)VNBMPHNBZFYQFSJFODFSFEOFTT  swelling, or itching at the site of the injection. These minor reactions usually resolve in a few days to a few weeks, but in some occasions, may require discontinuation of Humalog. In some instances, these reactions may be related to factors other than insulin, such as irritants in a skin cleansing agent or poor injection technique. Systemic Allergy—4FWFSF  MJGFUISFBUFOJOH  HFOFSBMJ[FE BMMFSHZ  JODMVEJOH BOBQIZMBYJT  NBZ occur with any insulin, including Humalog. Generalized allergy to insulin may cause whole body rash (including pruritus), dyspnea, wheezing, hypotension, tachycardia, or diaphoresis. In controlled clinical trials, pruritus (with or without rash) was seen in 17 patients receiving SFHVMBSIVNBOJOTVMJO O BOEQBUJFOUTSFDFJWJOH)VNBMPH O  Localized reactions and generalized myalgias have been reported with injected metacresol, XIJDIJTBOFYDJQJFOUJO)VNBMPH (see Contraindications). Antibody Production *OMBSHFDMJOJDBMUSJBMTXJUIQBUJFOUTXJUIUZQF O BOEUZQF O EJBCFUFTNFMMJUVT  anti-insulin antibody (insulin lispro-specific antibodies, insulin-specific antibodies, cross-reactive antibodies) formation was evaluated in patients receiving both regular human insulin and Humalog JODMVEJOHQBUJFOUTQSFWJPVTMZUSFBUFEXJUIIVNBOJOTVMJOBOEOBJWFQBUJFOUT "TFYQFDUFE UIF largest increase in the antibody levels occurred in patients new to insulin therapy. The antibody levels peaked by 12 months and declined over the remaining years of the study. These antibodies do not appear to cause deterioration in glycemic control or necessitate an increase in insulin dose. There was no statistically significant relationship between the change in the total daily insulin dose and the change in percent antibody binding for any of the antibody types. USE IN SPECIFIC POPULATIONS Pregnancy—Pregnancy Category B. All pregnancies have a background risk of birth defects, MPTT PSPUIFSBEWFSTFPVUDPNFSFHBSEMFTTPGESVHFYQPTVSF5IJTCBDLHSPVOESJTLJTJODSFBTFEJO pregnancies complicated by hyperglycemia and may be decreased with good metabolic control. It is essential for patients with diabetes or history of gestational diabetes to maintain good metabolic control before conception and throughout pregnancy. In patients with diabetes or gestational diabetes insulin requirements may decrease during the first trimester, generally increase during the second and third trimesters, and rapidly decline after delivery. Careful monitoring of glucose control is essential in these patients. Therefore, female patients should be advised to tell their physicians if they intend to become, or if they become pregnant while taking Humalog. Although there are limited clinical studies of the use of Humalog in pregnancy, published studies with human insulins suggest that optimizing overall glycemic control, including postprandial control, before conception and during pregnancy improves fetal outcome.

“I’m sorry. Am I reading too brightly?�

Nursing Mothers�*U JT VOLOPXO XIFUIFS JOTVMJO MJTQSP JT FYDSFUFE JO IVNBO NJML 6TF PG Humalog is compatible with breastfeeding, but women with diabetes who are lactating may require adjustments of their insulin doses. Pediatric Use—Humalog is approved for use in children for subcutaneous daily injections and GPSTVCDVUBOFPVTDPOUJOVPVTJOGVTJPOCZFYUFSOBMJOTVMJOQVNQ)VNBMPHIBTOPUCFFOTUVEJFEJO pediatric patients younger than 3 years of age. Humalog has not been studied in pediatric patients with type 2 diabetes.

OVERDOSAGE &YDFTTJOTVMJOBENJOJTUSBUJPONBZDBVTFIZQPHMZDFNJBBOEIZQPLBMFNJB.JMEFQJTPEFTPG hypoglycemia usually can be treated with oral glucose. Adjustments in drug dosage, meal patterns, PSFYFSDJTFNBZCFOFFEFE.PSFTFWFSFFQJTPEFTXJUIDPNB TFJ[VSF PSOFVSPMPHJDJNQBJSNFOU may be treated with glucagon or concentrated intravenous glucose. Sustained carbohydrate intake and observation may be necessary because hypoglycemia may recur after apparent clinical recovery. Hypokalemia must be corrected appropriately.

“If only we had a system of currency other than throwing feces?�

STORAGE %POPUVTFBGUFSUIFFYQJSBUJPOEBUF 6OPQFOFE)VNBMPHTIPVMECFTUPSFEJOBSFGSJHFSBUPS ÂĄUPÂĄ'<ÂĄUPÂĄ$> CVUOPUJOUIF GSFF[FS%POPUVTF)VNBMPHJGJUIBTCFFOGSP[FO*OVTF)VNBMPHWJBMT DBSUSJEHFT QFOT BOE Humalog KwikPenâ&#x201E;˘TIPVMECFTUPSFEBUSPPNUFNQFSBUVSF CFMPXÂĄ' ÂĄ$ BOENVTUCFVTFE within 28Â days or be discarded, even if they still contain Humalog. Protect from direct heat and light. PATIENT COUNSELING INFORMATION: See FDA-approved patient labeling and Patient Counseling Information section of the Full Prescribing Information. HumalogÂŽ and HumalogÂŽ KwikPenâ&#x201E;˘ are registered trademarks of Eli Lilly and Company.

Marketed by: Lilly USA, LLC, Indianapolis, IN 46285, USA

â&#x20AC;&#x153;Find a patch of sunlight, my boy. Find a patch of sunlight and bask in it.â&#x20AC;?

Š The New Yorker Collection 2013 from All Rights Reserved.

Geriatric Useâ&#x20AC;&#x201D;Of the total number of subjects (n=2834) in eight clinical studies of Humalog, UXFMWFQFSDFOU O XFSFZFBSTPGBHFPSPWFS5IFNBKPSJUZPGUIFTFIBEUZQFEJBCFUFT HbA1c values and hypoglycemia rates did not differ by age. Pharmacokinetic/pharmacodynamic studies to assess the effect of age on the onset of Humalog action have not been performed.

$PQZSJHIUÂŞ  &MJ-JMMZBOE$PNQBOZ"MMSJHIUTSFTFSWFE Additional information can be found at HI HCP BS 28MAR2013 PV5535

011206_elhut2_HI86002_kp_ad_A_size_fa.indd 4 CA1013_Invokana.Cartoon.indd 4

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Editor Joe Kopcha, Managing editor Marina Galanakis Senior editor Delicia Yard Web editor Nicole Blazek Contributing editors Bruce D. Askey, MSN, CRNP; Rebecca H. Bryan, APRN, CNP; Eileen F. Campbell, MSN, CRNP; Philip R. Cohen, MD; Deborah L. Cross, MPH, CRNP, ANP-BC; Sharon Dudley-Brown, PhD, FNP-BC; Maria Kidner, DNP, FNP-C; Joan W. Kiely, MSN, CRNP; Debra August King, PhD, PA; Ann W. Latner, JD; Claire B. O’Connell, MPH, PA-C; Kathy Pereira, MSN, FNP-BC; Sherril Sego, FNP, DNP; Julee B. Waldrop, MS, PNP; Kim Zuber, PA-C Art director Andrew Bass Group art director, Haymarket Medical Jennifer Dvoretz Production director Kathleen Millea Circulation manager Paul Silver Audience development director John Crewe National accounts manager Alison McCauley, 646.638.6098 alison.mccauley @ Group publisher Thomas P. Hennessy, 646.638.6085 tom.hennessy @ Editorial director Jeff Forster Vice president, medical magazines and digital products Jim Burke CEO, Haymarket Media, Inc. Lee Maniscalco All correspondence to: The Clinical Advisor 114 West 26th Street, 4th Floor, New York, NY 10001 For advertising sales, call 646.638.6085. For reprints, contact Wright’s Reprints at 877.652.5295. Persons appearing in photographs in “Newsline,” “The Legal Advisor,” and “Clinical Challenge” are not the actual individuals ­mentioned in the articles.They appear for illustrative purposes only. The Clinical Advisor® (USPS 017-546, ISSN 1524-7317), Volume 16, Number 10, is published 12 times a year, monthly, for $75.00 per year in the United States; $85.00 in Canada; $110.00 for all other foreign, in U.S. dollars, by Haymarket Media, Inc., 114 West 26th Street, 4th Floor, New York, NY 10001. Single copy: $20 U.S.; $30 foreign. To order or update your paid subscription, call 800.436.9269. Periodicals postage rate paid at New York, NY, and additional mailing offices. POSTMASTER: Send address change to DMD Data Inc. 10255 W. Higgins Rd, Suite 280, Rosemont, IL 60018. Call 800.430.5450 to change your address or make other subscription inquiries. Requests for subscriptions from outside the United States must be accompanied by payment. All rights reserved. Reproduction in whole or in part without permission is prohibited. Copyright © 2013.

THE PEER NETWORK Join The Peer Network! What is it? The Peer Network is a social rewards system in which you earn points and badges for doing the things you love on our site, all while sharing your clinical knowledge with other users. How do I join? If you already have an account with, just log in. Otherwise, click on “Join now” to register for free and become a part of The Peer Network. How does it work? You start earning points right away. For example, you’ll receive 25 points just for reading an article.You can get even more points by leaving a comment. Each time you earn points, a notification will appear at the bottom of your screen. With each action, you’ll work your way toward unlocking a new level and earn badges to keep track of your accomplishments.You might start out as just a Scholar, but one day you could be the Dean!

What are you waiting for? Sign up now, and stay tuned for the exciting rewards we have planned for our top earners.





8 • the clinical advisor • october 2013 5

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contents october 2013

News and comment


22 Newsline ■■Single pill for CVD improves adherence ■■Exercise will not cause knee arthritis ■■Be alert for signs of Munchausen by proxy ■■Two-drug regimen for OAB ■■Probiotic won’t stop Crohn disease ■■Flu shot adds no pregnancy complications ■■Fluoroquinolones linked with dysglycemia ■■Ischemic stroke a growing risk for the young

76 Derm Dx Read the clinical descriptions, view the images, and make your diagnosis at 77 Legal Advisor A young clinician performs a routine procedure against the patient’s express wishes and winds up in court. Moderate activity won’t lead to knee arthritis 24

83 CME/CE Dermatology Clinic n Nonpainful and nonpruritic white papules developed on the face of a young boy who did not perspire and had sparse and brittle hair.

94 Commentary

features 35 The most common causes of hair loss among women When treating an adult female patient with the chief complaint of alopecia, the clinician should pay particular attention to the pattern of hair loss.

n An elderly woman with a history of

What causes hair loss in women? 35

45 Options for pelvic congestion syndrome This challenging diagnosis presents as a dull, throbbing, and achy pain in the vulvar region and may require referral to an interventional radiologist. 58 CME/CE Postmenopausal vulvovaginal atrophy: communication and care The primary-care clinician must be able to identify and treat this chronic and highly prevalent condition.

making contact

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Follow us on Twitter @ClinicalAdvisor

79 Stat Consult Find out the most recent information on diagosing, testing, and treating acute sinusitis in adults.

multiple actinic keratoses complained of a painful but stable and nonbleeding lesion on the helix of her right ear.

Continues on page 8

Sued for battery after helping the police 77

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Visit us on the web

Go mobile with us

9/27/13 12:35 PM

contents 87 Alternative Meds Update Categorized as an adaptogen, rhodiola is sought after for its purported ability to decrease cellular sensitivity to stress. 89 CME/CE Dermatologic Look-Alikes Two patients present with enlarging white patches—one an adolescent whose lesion began around the mouth, and the other a woman with atrophic plaques on her shoulder and hip. 93 CME/CE Posttest

Rhodiola rosea, or roseroot, has been used to treat fatigue and depression 87

advisor forum 70 Consultations ■■Testosterone and belly fat in women ■■Cast vs. splint for a child with a buckle fracture ■■Reactivation of HPV ■■Acute pharyngitis in an adult 72 Clinical Pearls ■■A cocktail for uncomplicated urinary tract infection ■■Punch out a pilar cyst ■■When to lance a skin abscess Asymptomatic white patches around a boy’s mouth and eyes 89

how to contact us

To contact an editor: • • Call 646.638.6077



■ CVD polypill ■ Knee arthritis and exercise ■ Flu shot during pregnancy advIsor forum

■ reactivation of hPV ■ acute adult pharyngitis ■ Punch out a pilar cyst

hair loss

androgenic alopecia (shown) is the most common form of hair loss in women.

Clinician charged with battery after complying with police

✶ free ce courses!

■ ce feature

VulVoVaginal aTroPhy page 58

■ dermatologic look-alikes

enlarging whiTe PaTChes page 89

CA1013_Cover.indd 1

CA1013_TOC.indd 8

| O C TO b E R 2 013 |

common causes of female

legal advIsor

Volume 16, number 10

To submit an article: • • Fax it to 646.638.6117

To submit a clinical question for publication: • w Forum • Send it by e-mail to • Fax it to 646.638.6117 • Mail it to The Clinical Advisor, 114 W. 26th St., 4th Floor, New York, NY 10001

The CliniCal aDVisor • oCTober 2013

To subscribe: •

9/26/13 2:36 PM

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exclusive to the web at Web Exclusives


CDC ranks antibiotic-resistant infections Overuse and misuse are the leading factors that contribute to antibiotic resistance.

Immunizing against vaccine-­preventable diseases Even though most U.S. infants and ­toddlers have received all recommended vaccines by age 2 years, many remain under-immunized, leaving potential for outbreaks. Review these once-common vaccine-preventable diseases, and be sure to immunize patients according to the CDC’s Routine Immunization Schedules.

Kids’ food allergies cost U.S. billions Childhood food allergies disproportionately burden family finances. U.S. cancer diagnoses to top 1.6 million Cancer projected to surpass heart disease as leading cause of U.S. death. Health insurance lags among kids with gay parents Disparities diminish when children live in states that protect legal relationship to both parents.

Derm Dx Interact with your peers by viewing the images and offering your diagnosis and comments.

The Waiting Room Official Blog of The Clinical Advisor

Robyn Carlisle, MSN, CNM, WHNP Finding strength in the patient-provider bond Many in the medical profession say that it isn’t professional to become attached to patients. I disagree. Jim Anderson, MPAS, PA-C, ATC Is it time to leave the AAPA? A growing disconnect between membership and leadership on ­several issues is prompting many physician assistants to question their support. Sharon M. O’Brien, MPAS, PA-C Facial cues signal sleep deprivation In a recent study, sleep-deprived individuals looked sadder than after normal sleep, and sadness was related to looking fatigued.

Jaw osteomas and a family history of colon cancer A woman complains of lumps on her jaw that are causing an asymmetric appearance.

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Robyn Carlisle, MSN, CNM, WHNP Vaccinating moms with Tdap protects babies, too Newborns that contract whooping cough most often catch it from other family members.

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Knee arthritis is not caused by moderate activity page 24

o c t o b e r 2 0 13

Inluenza vaccine is safe during pregnancy page 26

Risk of stroke on the rise among the young page 29

© thnikstock

Single pill for CVD improves adherence

The polypill inhibits platelet function and lowers BP and LDL levels.

Heart disease among near-elderly Americans In 2010, more than 10 million Americans aged 50-64 years had been diagnosed with heart disease. Source: Center for Financing, Access, and Cost Trends, AHRQ, Household Component of the Medical Expenditure Panel Survey

■ Men ■ Women 23.7%

25 20


Use of a fixed-dose combination (FDC) pill containing a BP drug, a statin, and aspirin significantly improved medication adherence compared with usual care in persons with, or at high risk for, cardiovascular disease (CVD). Because most patients with CVD do not take recommended medications long-term, investigators in the UMPIRE trial sought to evaluate adherence to medication (defined as self-reported use of antiplatelet, statin, and at least two BP-lowering agents), as well as changes in systolic BP and lowdensity lipoprotein cholesterol (LDL-C) from baseline. The 2,004 participants each had established CVD or were at high risk for it. Half were randomized to an FDC-based strategy and half to usual cardiovascular medications (usual care). The FDC patients received a polypill containing aspirin 75

50 FDC users (5%) and 35 usualcare patients (3.5%). “The results show that access to FDCs in patients with CVD or similarly high risk improved adherence, BP, and cholesterol levels,” wrote the authors ( JAMA. 2013;310:918-929). In another related JAMA study, Stephen J. Nicholls, MBBS, PhD, and colleagues discovered that the use of the renin inhibitor aliskiren (Tekturna) compared with placebo did not improve coronary atherosclerosis or slow its progression in persons who also had prehypertension (available at /article.aspx?articleid=1734674; accessed September 15, 2013). There was, however, some indication that renin inhibition could be of benefit to patients who have coronary artery disease and BP levels treated to goal.

mg, simvastatin (Zocor) 40 mg, lisinopril (Prinivil, Zestril) 10 mg, plus either atenolol (Tenormin) 50 mg or hydrochlorothiazide (Microzide, Oretic) 12.5 mg. Median follow-up was 15 months. At baseline, mean BP was 137/78 mm Hg and LDL-C was 91.5 mg/dL. Among all participants, 1,233 (61.5%) reported using an antiplatelet, a statin, and two or more BP-lowering medications. By the end of the study, adherence was 86.3% in the FDC group and 64.7% in the usual-care group. Systolic BP and LDL-C levels were modestly but statistically significantly lower among the polypill users. Patients with lower adherence at baseline appeared to benefit most from polypill use. Serious adverse events and cardiovascular events did not differ significantly between the FDC and usual-care groups, affecting


17.9% 12.6%

19.7% 16.9%


10 5 0





22 the clinical advisor • october 2013 •

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Newsline Clinicians can reassure their middle-aged and older patients that moderate activity does not lead to osteoarthritis of the knee, according to new findings reported in Arthritis & Rheumatism. To test the association between meeting physical activity guidelines of at least 150 minutes per week and incident knee outcomes among 1,522 adults aged 45 years and older, a team led by Joanne M. Jordan, MD, MPH, examined data from the Johnston County [N.C.] Osteoarthritis Project. Median follow-up time was 6.5 years. Incident knee radiographic osteoarthritis (ROA) was defined as the development of a KellgrenLawrence grade of 2 or higher in a knee at follow-up. Incident knee symptomatic ROA (sROA) was defined as the development

of ROA and symptoms in at least one knee at follow-up. Meeting the physical activity guidelines was not significantly associated with the development of ROA or sROA. Although adults at the highest level of physical activity (at least 300 minutes per week) had a greater risk of developing knee ROA and sROA than did adults engaging in physical activity for less than 10 minutes per week, these associations were not statistically significant. “Engaging in physical activity at these levels is not going to put you at a greater risk of knee OA,” affirmed Dr. Jordan. “This held true no matter what a person’s race, sex, or body weight is.” The American Academy of Orthopaedic Surgeons advises against needle lavage for long-term

© science source / james cavallini

Exercise will not cause knee arthritis

Narrowing of the space in the knee joint indicates loss of cartilage.

relief of knee OA, glucosamine and chondroitin to treat symptomatic knee OA, and lateral wedge insoles to treat symptomatic medial compartment knee OA (available at wp-content/uploads/2013/09/ AAOS-5things-List.pdf, accessed September 15, 2013).

Providers should have a high index of suspicion for caregiverfabricated illness, widely known as Munchausen syndrome by proxy, when seeing children with a persistent or recurrent condition that cannot be explained and that results in multiple medical procedures, or upon noticing discrepancies among the history, physical examination, and health of a child. Caregiver-fabricated illness is a relatively rare but serious form of child maltreatment, according to a clinical report from the American Academy of Pediatrics Committee on Child Abuse and

Dehydration and celiac disease may indicate fabricated illness.

Neglect (Pediatrics 2013;132:590597). The paper updates the committee’s 2007 report (Pediatrics. 2007;119:1026-1030). In caregiver-fabricated illness, a caregiver falsifies and/or induces a child’s illness, leading to unnecessary and potentially harmful medical investigations and/or treatment. Although there is no typical presentation, some forms of fabricated illness noted over the past several years are hypernatremic dehydration, immunodeficiency, and celiac disease. A review of calls made to the National Poison Data System for

pharmaceutical exposures from 2000 to 2008 revealed an average of 160 cases per year were coded as “malicious” and related to events involving children younger than age 7 years. Ethanol, laxatives, and benzodiazepines were the most common drug categories. The proper diagnosis of fabricated disease involves thorough evaluation of medical records, clear communication among professionals, and, often, a multidisciplinary approach. Clinicians should consult a specialist if unsatisfied by the response of the child protective services system.

© thinkstock

Be alert for signs of Munchausen by proxy

24 the clinical advisor • october 2013 •

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Combining high-dosage antimuscarinic agents is a more successful treatment for overactive bladder (OAB) than is antimuscarinic monotherapy with dose increase for people aged 65 years and older, indicates a recent study. Many elderly patients with OAB demonstrate insufficient treatment results under antimuscarinic monotherapy with dose increase, wrote investigators in UroToday International Journal (2013;6:47). To reduce OAB symptoms and to evaluate safety and tolerability of a different noninvasive approach, researchers launched a study of 81 persons aged 65 to 79 years who had previously received doubledose antimuscarinic monotherapy with trospium (Sanctura). After at least six months of such treatment with no or short-lived symptom improvement, patients were divided into three groups and treated with two antimuscarinics: Each set of patients continued to receive double-dose tropsium, with the addition of oxybutynin (Ditropan), tolterodine (Detrol), or solifenacin (Vesicare). Significant improvements were seen after six weeks in all three groups, with average number of daily incontinence events declining, average maximum bladder capacity increasing, average reflex volume rising, and average detrusor compliance improving. Side effects were comparable to that of normal-dosed antimuscarinics.

Probiotic won’t stop Crohn Although evidence suggests that the probiotic yeast Saccharomyces boulardii could be useful in the treatment of patients with Crohn disease (CD), the agent appeared to have no beneficial effects for persons whose CD was in remission following steroid or salicylate therapies. In a prospective study, 165 persons in CD remission after treatment with steroids or aminosalicylates were randomized to receive either S. boulardii (1 g/day) or placebo for 52 weeks. The median time to CD relapse did not differ significantly between the two groups, at 40.7 weeks for the S. boulardii patients and 39.0 weeks for the placebo users. The difference in relapse rate also was nonsignificant, at 47.5% in the S. boulardii group and 53.2% in the placebo group. In addition, the two sets of patients had similar mean CD activity index scores, erythrocyte sedimentation rates, and median levels of C-reactive protein.

Sleeping well may be a useful approach to avoiding CD relapse.

Nonsmokers given S. boulardii might have been less likely to experience a CD relapse than were nonsmokers given placebo, but investigators noted that this finding requires confirmation (Clin Gastroenterol Hepatol. 2013; 11:982-987). A more effective option may be on the horizon for CD patients: The investigational drug vedolizumab was more likely than placebo to result in remission at week 6 of treatment (N Engl J Med. 2013;369:711-721). Study participants who continued to receive vedolizumab rather than switch to placebo were more likely to be in remission at week 52. Sleeping well may eventually prove to be a useful nondrug approach to avoiding CD relapse: An analysis of 1,291 persons in CD remission at baseline showed that those with impaired sleep had a twofold increase in risk of active disease at six months (Clin Gastroenterol Hepatol. 2013;11:965-971).

Flu shot adds no pregnancy complications Influenza vaccination during pregnancy does not appear to increase a woman’s risk for various adverse obstetric events requiring medical attention (Obstet Gynecol. 2013;122:659-667). Investigators compared 13 outcomes in 74,292 pregnant women who received trivalent inactivated flu vaccine between 2002 and 2009 and 144,597 unvaccinated females. The women had been matched on age, site, and pregnancy start date.

No increased risks were observed for hyperemesis, chronic hypertension, gestational hypertension, gestational diabetes, proteinuria, or urinary tract infection (UTI) within 42 days of vaccination. From vaccination through end of pregnancy, no increased risks were observed for proteinuria, UTI, gestational hypertension, preeclampsia or eclampsia, chorioamnionitis, puerperal infection, venous complications, pulmonary embolism, or peripartum cardiomyopathy.

© science source / david m. martin, m.d.

Two-drug regimen for OAB

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Newsline Oral fluoroquinolone antibacterial drugs, particularly moxifloxacin (Avelox), can cause severe hyperglycemia or hypoglycemia in persons with diabetes. Although such reactions occurred in no more than one of 100 patients evaluated, clinicians should consider the heightened risk when prescribing fluoroquinolones to patients with diabetes, according to the Infectious Diseases Society of America (IDSA). The population-based inception cohort study yielding these findings was described in the IDSA journal Clinical Infectious Diseases (2013;57:971-980). The investigators drew on data from 78,433 persons in Taiwan with diabetes, identifying outpatients who, from January 2006 to November 2007, became new users of the

following antibiotics: (1) the fluoroquinolones ciprofloxacin (Cipro, Proquin), levofloxacin (Levaquin), and moxifloxacin; (2) second-generation cephalosporins (cefuroxime [Ceftin], cefaclor, or cefprozil); and (3) macrolides (azithromycin [Zithromax, Zmax] and clarithromycin [Biaxin]). The absolute risk of hyperglycemia per 1,000 persons was 6.9 for moxifloxacin, 4.0 for ciprofloxacin, 3.9 for levofloxacin, 2.1 for cephalosporins, and 1.6 for macrolides. The absolute risk of hypoglycemia was 10.0 for moxifloxacin, 9.3 for levofloxacin, 7.9 for ciprofloxacin, 3.7 for macrolides, and 3.2 for cephalosporins. Hypoglycemia risk was also significantly increased in patients using moxifloxacin concomitantly with insulin.

© science source / BSip

Fluoroquinolones linked with dysglycemia

The risk of hyperglycemia was highest for moxifloxacin.

As previously reported at, f luoroquinolone use can also lead to peripheral neuropathy. The FDA recently required manufacturers to update the drug labels and medication guides for all fluoroquinolones to better describe this serious side effect.

Approximately 15% of all ischemic strokes occur in adolescents and young adults, yet early diagnosis remains a challenge due to lack of awareness and relative infrequency of stroke compared with conditions that mimic it, according to members of an expert panel convened by the American Academy of Neurology. Aneesh B. Singhal, MD, and fellow panel members have now developed a consensus document on the recognition, evaluation, and management of ischemic stroke in this population, presented in the journal Neurology

The causes of ischemic stroke in the young can be uncommon.

(2013;81:1089-1097). The authors pointed out that the causes of ischemic stroke in the young are heterogeneous and can be relatively uncommon, resulting in uncertainties about diagnostic evaluation and cause-specif ic management. However, “Emerging data have raised public health concerns about the increasing prevalence of traditional vascular risk factors in young individuals, and their potential role in increasing the risk of [ischemic stroke], stroke recurrence, and poststroke mortality,” wrote Singhal and

colleagues. “These issues make it important to formulate and enact strategies to increase both awareness and access to resources for young stroke patients, their caregivers and families, and [healthcare] professionals.” According to information provided by the Loyola University Health System in Chicago, U.S. hospital discharges for stroke among persons aged 15 to 44 years increased 23% to 53% between the periods of 1995– 1996 and 2007–2008, depending on the age and gender of specific patient groups. n

© science source / medical body scans

Ischemic stroke a growing risk for the young • the clinical advisor • october 2013 29

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feature: Abby A. Jacobson, MS, PA-C

The most common causes of hair loss among women When treating an adult female patient with the chief complaint of alopecia, the clinician should pay particular attention to the pattern of hair loss.


he real or perceived symptom of increased hair loss can be psychologically devastating for female patients. This article is intended as a brief review of the most common causes of adult female alopecia and a thorough introduction to the evaluation of this complaint in the primary-care setting. Bear in mind that many women who experience hair loss will still require referral to a dermatology practice. Hair follicles constantly cycle through three phases: (1) anagen—the growth phase; (2) catagen—the phase transitioning between growth and resting; and (3) telogen—the resting phase. It is normal to lose as many as 100 hairs per day. Women who present with excessive hair loss must undergo a detailed and extensive history and thorough examination of the hair, with the clinician paying special attention to the pattern of loss and how easily the hair pulls out. The clinician also must order blood tests and examine the scalp. In some cases, pathologic analysis of a scalp biopsy may be necessary.

The initial examination

© cmsp

The following information should be obtained as part of the patient history of a woman who is experiencing hair loss: FIGURE 1. Androgenic alopecia features circular involvement of the scalp (shown).

• Duration and pattern of hair loss • Whether the lost hair is broken or intact • Current diet and any change in weight within the past six months Continues on page 36 • the clinical advisor • october 2013 35

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female hair loss

To avoid unnecessary panic, the terms androgenic alopecia and female pattern hair loss may be preferable to female pattern baldness. • Any surgeries in the past six months • All medications (current and taken within the past six months) • Any illnesses or infections within the past six months • Any other symptoms (a full review of systems) • Whether she has ever experienced similar hair loss before • A family history of hair loss and other medical conditions (e.g., metabolic disorders) • Date of most recent menstrual period • Normal hair and beauty routine. A thorough physical examination should discern the pattern and distribution of hair loss. Assess all areas of body hair, including eyebrows, eyelashes, arm hair, and pubic hair. The scalp should be assessed for erythema, flaking, or scaring. Firmly grasp approximately 60 hairs and pull. If fewer than six hairs come out, this is considered normal shedding (or a negative pull test); six hairs or more is considered a positive pull test. Special attention should be paid to how easily the hairs break. Easily breakable hair may suggest hair damage caused by overprocessing. Overprocessing can include heat damage from curling irons, straightening, perms, or hair coloring. The diagnosis for this type of hair loss is traumatic alopecia. Pulling from braids, tight hair buns, ponytails, or hair extensions can cause traction alopecia. The treatment for such hair loss is discontinuation of the beauty regimen, addition of biotin supplementation, and adoption of a healthy diet. Other forms of female hair loss to be considered in the differential are listed in Table 1. In searching for an underlying endocrine abnormality, such as hyperandrogenemia or thyroid dysfunction, blood Table 1. Differential diagnosis for female hair loss Alopecia areata Cicatricial alopecia (scarring alopecia) Female pattern hair loss (androgenic alopecia) Telogen effluvium Traction alopecia Traumatic alopecia Trichotillomania Underlying correctable skin condition (e.g., seborrheic dermatitis or psoriasis) Underlying endocrine abnormality (e.g., hyperandrogenemia or thyroid dysfunction)

work should include a complete blood count with differential, serum iron, serum ferritin, thyroid-stimulating hormone (TSH), free thyroxine (T4), antinuclear antibodies, free testosterone, prolactin, 17-hydroxy progesterone, cortisol level, and dehydroepiandrosterone sulfate. Androgenic alopecia

The terms androgenic alopecia and female pattern hair loss may be preferable to female pattern baldness. The word “baldness” may lead to unnecessary panic on the part of the patient. Androgenic alopecia describes hair loss caused by genetically determined sensitivity of hair follicles in the scalp to adult levels of androgens. Androgenic alopecia is the most common cause of hair loss in adult women.1 The diagnosis is made by ruling out other possible diagnoses through lab work, recognition of the distinctive pattern of hair loss (Figure 1), and pathologic analysis of a punch biopsy. The biopsy should be full-thickness (at least 4 mm) sectioned horizontally. Include the differential on the requisition slip that you want to distinguish (e.g., “androgenic alopecia rule out telogen effluvium or alopecia areata”). A sample of at least 6 mm is required to ensure that hair follicles at several stages of the growth cycle are present. Ideally, a dermatopathologist as well as a clinician who is experienced in analyzing hair biopsies should read the hair pathology. For this reason, it may preferable to have the biopsy performed by a local dermatologist who has a working relationship with different pathologists. The pathology is particularly important because androgenic alopecia has a classic presentation of miniaturization of terminal pigmented anagen hairs to fine hypopigmented vellus hairs. Treatment options include topical OTC minoxidil 2% (Rogaine, Theroxidil) applied twice a day1 or hair transplanation. Minoxidil increases the length of time follicles spend in anagen, wakes up follicles in catagen, and enlarges the actual follicles. The most common side effect associated with minoxidil is irritant dermatitis, which is most likely attributable to the vehicle and stabilizers rather than the active ingredient. Unwanted hair growth may be seen in other places on the body. Women who are pregnant or breastfeeding should not use minoxidil, as it can cause hypertrichosis in infants. Patients must use minoxidil for at least four to six months to evaluate efficacy. Many patients report that minoxidil does not lead to new hair growth but simply slows the rate of hair loss. Use of the product must

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female hair loss

In telogen effluvium, some external factor instructs an abnormally large number of hairs to enter the telogen phase and subsequently be shed. be continued for as long as the patient wishes to sustain the results. Hair transplantation is a cosmetic procedure performed in the office under local anesthesia. Hair from the uninvolved area is transplanted to the area with loss. Disadvantages of this treatment option include cost and the appearance of the final result.

normalize) may be the best bet for a patient recovering from a change in his or her health status. Make sure the patient is otherwise healthy, eating a balanced diet, taking a multivitamin containing very little or no vitamin A (too much vitamin A can cause hair loss), and 5 mg/ day of OTC biotin, which has been shown to accelerate hair growth and thicken existing hair.

Telogen effluvium


Hairs are normally shed in the telogen phase. Telogen effluvium is a scalp disorder characterized by increased shedding of undamaged hairs in the telogen phase in response to a change in health status. The process that tells the hair when to enter the anagen, telogen, and catagen phase is complex. In individuals with telogen effluvium, some external factor instructs an abnormally large number of hairs to enter the telogen phase and subsequently be shed (Figure 2). These external factors include, but are not limited to, medications, pregnancy, malnutrition, and stress (Table 2).2 Since it can take up to three months for the hair loss to start or become noticeable, a thorough medical, psychological, and surgical history must cover at least the past six months. The diagnosis of telogen effluvium is one of exclusion combined with analysis of the hair-loss pattern, lab results, and patient history. Laboratory work should include thyroid and chemistry panels, erythrocyte sedimentation rate, antinuclear antibody, and a complete blood count with differential, hematocrit, and ferritin tests. If possible, stop the offending agent/medication or correct the underlying abnormality. Consider recommending counseling and or medication if psychological stress is the underlying cause. The “tincture of time” (that is, waiting for the body to

Individuals with trichotillomania pull out their own hair, including eyebrows and eyelashes. This condition is more commonly seen in women and may be accompanied by such concomitant psychological disorders as depression, psychosis, impulse-control disorders, personality disorders, anxiety, and body dysmorphic disorder. The patches of alopecia caused by the hair pulling often have bizarre sharp, irregular borders, and result in hairs of varying lengths (Figure 3). Some describe confirming the diagnosis by shaving the same patch of scalp weekly to show the normal dense regrowth, but I have rarely seen this in practice. On pathology, distorted follicular anatomy is found, once again supporting the need for a dermatopathologist to read any scalp/hair biopsy. Treatment is a combination of patient realization of the habit, behavior modification, and therapy. Additional use of pharmacologic agents should be decided on a case-by-case basis. If pharmacotherapy is indicated, clomipramine (Anafranil) is the first-line agent.3 Selective serotonin reuptake inhibitors have had limited success. Alopecia areata

Alopecia areata is the most common nonscaring pattern of hair loss that presents as well-circumscribed areas of alopecia.

Table 2. Common causes of telogen effluvium Childbirth, pregnancy, or miscarriage Chronic illness (e.g., HIV, lupus) Endorcine abnormality (e.g., hypothyroidism, hyperthyroidism, hyperparathyroidism) Malnutrition Medications (e.g., retinoids, high-dose vitamin A, anticoagulants [especially heparin], antithyroids, anticonvulsants, interferon, heavy metals, and beta-blockers) Post-febrile/post-infection Post-surgery Psychological stress Rapid weight loss following a crash diet or bariatric surgery Discontinuing oral contraception

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Patients with alopecia areata may also experience such nail changes as ridges, pitting, brittleness, onycholysis, and koilonychia. In this hair-specific autoimmune disease, T-lymphocytes interact with follicular antigens. The clinician can differentiate alopecia areata from tinea capitis by the lack of scalp flaking. A simple fungal culture can confirm the diagnosis. In an adult, a scalp tinea capitis infection is unlikely unless the patient works in a high-risk environment (e.g., an elementary school with a known outbreak) or is immunosuppressed. One out of five patients with alopecia areata report having a family member with the same condition. Classically, alopecia areata presents as round or oval patches of nonscarred hair loss. Short exclamation-point hairs are often seen at the edges of the patch of hair loss. Other patterns of loss include ophiasis (a band of loss around the temporal and occipital scalp), alopecia totalis (loss of all scalp hair), and alopecia universalis (loss of all scalp and body hair). Patients with alopecia areata may also experience such nail changes as ridges, pitting, brittleness, onycholysis, and koilonychia. Approximately 40% of patients with alopecia areata will have allergic rhinitis, atopic dermatitis, or asthma.4 Other associated diseases include autoimmune thyroid disease (e.g., Hashimoto’s thyroiditis, Graves’ disease), vitiligo, inflammatory bowel disease, HLA associations, and autoimmune polyendocrinopathy syndrome type 1. Type

1 diabetes is more prevalent in the relatives of persons with alopecia areata. Typical treatment of alopecia areata involves a combination of intralesional corticosteroids (a concentration of 5 mg/mL of triamcinolone acetonide injected every four to eight weeks is usually sufficient), topical steroids, topical minoxidil, and oral biotin. Bimatoprost ophthalmic solution (Latisse, Lumigan) is an option for eyelash loss and is used off-label for eyebrow regrowth. Treatment options for ophiasis, alopecia totalis, and alopecia universalis are extremely limited. Alopecia areata is most often chronic and relapsing.

FIGURE 2. Stress is a common cause of telogen effluvium (shown).

FIGURE 3. Trichotillomania (shown) results in patches of alopecia.

Underlying skin conditions

© cmsp / a. wilson

© cmsp / wellcome image library

Physical examination will typically reveal such underlying correctable skin conditions as seborrheic dermatitis or psoriasis. Both conditions may have the symptoms of itching and flaking and will impact such other body areas as the face, nasolabial folds, eyebrows, and ears. Seborrheic dermatitis is more diffuse than psoriasis and can have a greasy yellow appearance, particularly on the face. Psoriasis is characterized by sharply marginated plaques with scale. Frequently, there is a family history of psoriasis. Plaques are often symmetric and are typically found on the elbows,

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female hair loss

knees, and groin. Topical steroids are first-line agents for both conditions. Such steroid-sparing agents as ketoconazole shampoo (Nizoral) or cream (Ketozole, Nizoral) are effective for seborrheic dermatitis. For scalp psoriasis, consider OTC coal-tar shampoo and topical calcipotriene (Dovonex, Sorilux). Underlying endocrine abnormalities

Hyperandrogenemia and thyroid dysfunction are the two most common underlying endocrine abnormalities that lead to hair loss in adult females. Patient history, other complaints, review of systems, and a physical examination all contribute to making this diagnosis. Laboratory workup confirms the diagnosis. Thyroid dysfunction can be evaluated with TSH and T4 tests. Symptoms of hypothyroidism can include fatigue, weight gain, decreased appetite, cold intolerance, dry skin, muscle pain, joint pain, weakness in the extremities, depression, emotional lability, mental impairment, forgetfulness, impaired memory, inability to concentrate, constipation, paresthesias, nerve entrapment syndromes, blurred vision, decreased hearing, fullness in the throat, and hair loss.5 Typically, the hair loss associated with thyroid dysfunction is diffuse overall thinning with no scalp changes. The remaining hair can be dry, coarse, and lusterless. Hyperandrogenic disorders include polycystic ovary syndrome (PCOS), adrenal or ovarian tumors, congenital adrenal hyperplasia, hyperprolactinemia, acromegaly, and Cushing syndrome. Signs of PCOS, the most common condition associated with hyperandrogenism, can include irregular menstrual cycle, amenorrhoea, impaired fertility, difficulty getting pregnant, miscarriage, seborrhea, excessive body hair, acne, and obesity.6 The pattern of hair loss seen with hyperandrogenism is typically diffuse and mimics that of androgenic alopecia. Treating hair loss in hyperandrogenic states or thyroid dysfunction requires addressing the underlying abnormality.

The hair loss pattern in individuals with CLE presents as background erythema, variable hypopigmentation, and/or follicular plugging. Other skin lesions of CLE may or may not be present. A thorough evaluation of other signs and symptoms, a family history, and blood work are important pieces of the diagnostic puzzle. Treatments include topical and intralesional steroids, systemic steroids, antimalarials, and thalidomide (Thalomid).7 Lichen planopilaris typically shows perifollicular erythema and scarring with a background violaceous discoloration to the scalp. Intralesional steroids and referral to a dermatology practice are essential aspects in appropriate management of lichen planopilaris. Summary

The workup of the chief complaint of hair loss in the adult female patient is neither quick nor simple. A comprehensive personal history and family history, thorough physical examination, and blood work are crucial elements leading to the proper diagnosis. Find a dermatology practice that you know can offer these patients additional counseling, provide support in the initial workup, and continue your baseline workup with the appropriate referral. n Ms. Jacobson is the past president of the Society of Dermatology Physician Assistants and currently practices at Delaware Valley Dermatology Group in Wilmington, Del. References 1. Thiedke CC. Alopecia in women. Am Fam Physician. 2003;67:1007-1114. Available at 2. Sperling LC, Mezebish DS. Hair diseases. Med Clin North Am. 1998;82:1155-1169. 3. Ninan PT, Rothbaum BO, Marsteller FA, et al. A placebo-controlled trial of cognitive-behavioral therapy and clomipramine in trichotillomania. J Clin Psychiatry. 2000;61:47-50. 4. Huang KP, Mullangi S, Guo Y, Qureshi AA. Autoimmune, atopic, and mental health comorbid conditions associated with alopecia areata in the United States. JAMA Dermatol. 2013;149:789-794.

Cicatricial alopecia

5. Medscape. Hypothyroidism clinical presentation. Available at emedicine.

Cicatricial alopecia, also referred to as scarring alopecia, often results in permanent destruction of the hair follicle. In such cases, a scalp biopsy is almost always necessary to identify the form of cicatricial alopecia and to determine whether there is an underlying treatable condition, such as cutaneous lupus erythematosus (CLE). On pathologic analysis of the biopsy, lymphocytic hair loss can be seen with lichen planopilaris and CLE; neutrophilic hair loss may be associated with folliculitis decalvans or dissecting cellulitis. 6. ACOG Committee on Practice Bulletinsâ&#x20AC;&#x201D;Gynecology. ACOG Practice Bulletin No. 108: Polycystic ovary syndrome. Obstet Gynecol. 2009;114:936-949. 7. Maender JL, Krishnan RS, Angel TA, Hsu S. Complete resolution of generalized lichen planus after treatment with thalidomide. J Drugs Dermatol. 2005;4:86-88. All electronic documents accessed September 15, 2013.

44 the clinical advisor â&#x20AC;˘ october 2013 â&#x20AC;˘

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feature: Debbie Semmel, MSN, FNP-BC

Options for pelvic congestion syndrome This challenging diagnosis presents as a dull, throbbing, and achy pain in the vulvar region and may require referral to an interventional radiologist.


elvic congestion syndrome (PCS) is a poorly understood and often overlooked etiology of chronic pelvic pain. Millions of women worldwide may develop chronic pelvic pain at some time in their life, and the occur­ rence rate may be as high as 39.1%.1 Chronic pelvic pain can be debilitating and accounts for 10% to 15% of all gynecologic visits.1 Managing this complex condition can be a challenge. When clinical and ultrasound examinations are normal, further diagnostic imaging helps in making the diagnosis. Once identified, PCS can be treated successfully with embolization therapy. Etiology

Figure 1. MRI reveals gonadal vein reflux, confirming the diagnosis of PCS.

PCS is associated with dilated pelvic varices with reduced venous clearance, most often as a result of retrograde flow in an incompetent ovarian vein. The condition is seen most often in multi­ parous premenopausal women. A relationship between PCS and endogenous estrogen levels is suggested, as estrogen is known to weaken the vein walls.1 The venous congestion stretches the inner surface of the ovarian vein, distorting both the endothelial and smooth-muscle cells. It is postulated that kinking of the ovarian vein leads to venous stasis, flow reversal, and subse­ quent varicosities.2 PCS can also be caused by external compression, such as that seen in nut­ cracker syndrome (compression of the left renal vein between the aorta and superior mesenteric artery) and May-Thurner syndrome (compres­ sion of the left iliac vein beneath the iliac artery. Continues on page 46 • the clinical advisor • october 2013 45

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pelvic congestion syndrome

poll position

Have you ever referred a patient with pelvic congestion syndrome to an interventional radiologist? n=219 10.5%

n Yes n No


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Clinical presentation

PCS is not easy to diagnose. Women typically complain of a dull, throbbing, and achy pain in the vulvar region. This pain often worsens during or after intercourse or just before the onset of menses and/or increases throughout their day. Most women with PCS will not be symptomatic in the morning but will become so with prolonged standing or sitting. The patient may or may not have vulvar varicosities but often has varicose veins, with the left leg presenting greater than the right. The varicosities usually extend along the medial aspect of the medial-to-posterior upper thigh and along the buttocks. The vast array of associated symptoms of PCS include cyclic pain (with menstrual periods), dyspareunia, bladder irritability, GI symptoms, and low-back pain. Hemorrhoids and/or varicose veins of the perineum, buttocks, or lower extremities may also be noted.1 Ovarian point tenderness on examination with a history of postcoital ache is said to be 94% sensitive and 77% specific for PCS.3 PCS is often diagnosed in women younger than age 45 years who have had more than one pregnancy. The ovarian veins increase in size during each pregnancy and do not return to normal in women with PCS. PCS is rarely diagnosed in nulliparous women.

with any of these identifiers will have a higher incidence of somatic complaints and should be treated in conjunction with the assistance of a trained mental-health professional. The review of systems should involve a thorough discussion of the patient’s sleep patterns, lifestyle (e.g., whether the pain affects activities of daily living), menstrual pattern, dyspareunia, urologic dysfunction, and any GI issues. Irritable bowel syndrome (IBS) has been reported in 65% to 79% of women with chronic pelvic pain. All previous consultations, as well as diagnostic or therapeutic interventions, should be reviewed. In addition to an abdominal and pelvic examination, a thorough physical should include the neurologic (evaluating the thoracolumbar spine), cardiovascular, pulmonary, and vascular (evidence of varicosities in the lower pelvis, buttocks, and legs) systems. Further testing should include a complete blood count, a complete metabolic profile, a urinalysis, and an endocervical swab for chlamydia. Differential diagnoses

The differential diagnoses for pelvic pain are numerous. These diagnoses include endometriosis, chronic pelvic inflammatory disease, leiomyoma, adenomyosis, nutcracker syndrome, PCS, IBS, diverticulitis, diverticulosis, Meckel’s diverticulum, interstitial cystitis, abnormal bladder function, chronic urethritis, fasciitis, nerve entrapment syndrome, hernia, scoliosis, spondylolisthesis, osteitis pubis, somatization, psychosexual dysfunction, and depression. Imaging studies

Transvaginal ultrasound helps identify ovarian cysts or uterine leiomyomas. If the ultrasound results are inconclusive, an MRI of the pelvis (with and without contrast) is warranted. MRI is helpful with demonstration of the ovarian vein (Figure 1) and varicosities. Dynamic imaging can confirm the active reflux from the ovarian vein. Bear in mind that the MRI is done in the supine position, which can alter the appearance of the varicosities in the pelvis. Whenever possible, the MRI should be scheduled for later in the day or early evening to coincide with a woman’s increased perception of symptoms.

Patient evaluation

Treatment options

A detailed history and comprehensive examination is of paramount importance. The history should focus on the nature, intensity, pattern, location, duration, and radiation of the pain, as well as any exacerbating and relieving factors. The relationship between the pain and a woman’s menstrual cycle should also be discussed. Screening for depression, personality disorders, and domestic violence should be included. Women

After the diagnosis of PCS has been made, treatment with nonsteroidal anti-inflammatory drugs may help relieve the patient’s pain for the short term. Analgesia is a good firstline option, but if symptoms do not improve, the patient should be referred to an interventional radiologist, who specializes in minimally invasive treatments using imaging for guidance. This clinician will perform a thorough history

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pelvic congestion syndrome

Figure 2. Pelvic venography is the gold standard for diagnosis.

Figure 3. Embolization decreases venous congestion within the pelvis.

and physical and will review the imaging with the patient before scheduling her for pelvic venography. Pelvic venography is an outpatient procedure and remains the gold standard for diagnosis of PCS. Using the jugular vein for access, contrast dye is injected into the veins of the pelvis to make them visible via fluoroscopy. To improve accuracy, the procedure is best performed with the patient placed on an incline. If this is not an option, a Valsalva maneuver is required and is often best achieved by having the patient blow into the tubing of a sphygmomanometer and hold the mercury at approximately 20 mm. If no reflux is present, a diagnosis of PCS is highly unlikely. If pelvic and/or ovarian varicosities are present (Figure 2), embolization of the offending abnormal vein can be performed. In embolization, a small guide wire and catheter are inserted into the faulty vein, which is then embolized with coils, plugs, or sclerosant (Figure 3). Women are discharged home the same day and are able to return to regular activity the next day. Any mild cramping experienced over the ensuing 24 to 48 hours is managed well with ibuprofen.

A study revealed that 83% of patients continued to remain symptom-free four years post-treatment.4 Chronic pelvic pain is a significant health problem for many women. Patients with chronic pelvic pain report a high incidence of anxiety, depression, and physical worries.5 Embolization offers a safe, effective and minimally invasive treatment option that can improve or resolve symptoms in women with chronic pelvic pain caused by PCS. n Ms. Semmel is a family nurse practitioner at Duke University Medical Center, Division of Interventional Radiology, in Durham, N.C. References 1. Ignacio EA, Dua R, Sarin S, et al. Pelvic congestion syndrome: diagnosis and treatment. Semin Intervent Radiol. 2008;25:361-368. 2. Giacchetto C, Catizone F, Cotroneo GB, et al. Radiologic anatomy of the genital venous system in female patients with varicocele. Surg Gynecol Obstet. 1989;169:403-407. 3. Beard RW, Reginald PW, Wadsworth J. Clinical features of women with chronic lower abdominal pain and pelvic congestion. Br J Obstet Gynaecol. 1988;95:153-161.


4. Kim HS, Malhotra AD, Rowe PC, et al. Embolotherapy for pelvic conges-

Embolization is successful in 98% to 100% of all PCS cases, with recurrence rates of less than 8%. Symptom improvement has been documented in 70% to 85% of women studied and can be expected within two to four weeks post-procedure.4

tion syndrome: long-term results. J Vasc Interv Radiol. 2006;17(2 Pt 1):289-297. 5. Walling MK, Reiter RC, O’Hara MW, et al. Abuse history and chronic pain in women: prevalences of sexual abuse and physical abuse. Obstet Gynecol. 1994;84:193-199.

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program outline october 2013

0.5 credits

Page 58 Feature Postmenopausal vulvovaginal atrophy: communication and care Mary Jane Minkin, MD, FACOG, NCMP Mary Jane Minkin, MD, FACOG, NCMP, has no relationships to disclose relating to the content of this article.

■■ Learning objectives: • Describe the impact of vulvovaginal atrophy on sexual health and quality of life and relay this information to postmenopausal patients. • Diagnose vulvovaginal atrophy. • Treat vulvovaginal atrophy in line with evidence-based guidelines. • Counsel patients on the etiology of vulvovaginal atrophy and the efficacy and safety of available therapies.

0.5 credits

Page 83 Dermatology Clinic White facial papules and sparse, brittle hair Audrey Chan, MD Audrey Chan, MD, has no relationships to disclose relating to the content of this article.

Painful, nonbleeding lesion on the ear Kristen Grippe, PA-C Kristen Grippe, PA-C, has no relationships to disclose relating to the content of this article.

■■ Learning objectives: • To identify and diagnose dermatologic conditions and review up-to-date treatment.

Page 89 Dermatologic Look-Alikes Enlarging white patches Kerri Robbins, MD Kerri Robbins, MD, has no relationships to disclose relating to the content of this article.

■■ Learning objective: • To distinguish and properly treat dermatologic conditions with similar presentations.

Page 66, 93 posttest This program has been reviewed and is approved for a maximum of 1 hour of AAPA Category I CME credit by the Physician Assistant Review Panel. Approval is valid for one year from the issue date of October 2013. Participants may submit the self-assessment at any time during that period. This program was planned in accordance with AAPA’s CME Standards for Enduring Material Programs and for Commercial Support of Enduring Material Programs. Nurse Practitioner Associates for Continuing Education (NPACE) is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation. NPACE designates this educational activity for a maximum of 1 contact hour of credit. Participants should only claim credit commensurate with the extent of their participation in the activity. • the clinical advisor • october 2013 57

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n Learning Objectives • Describe the impact of vulvovaginal atrophy on sexual health and quality of life and relay this information to postmenopausal patients. • Diagnose vulvovaginal atrophy. • Treat vulvovaginal atrophy in line with evidence-based guidelines. • Counsel patients on the etiology of vulvovaginal atrophy and the efficacy and safety of available therapies. n complete the post test: Page 66

featured course

n additional CME/CE credit: Pages 83, 89 Turn to page 57 for additional information on this month’s CME/CE courses.

This activity is supported by an educational grant from Novo Nordisk Inc., and jointly sponsored by Medical Education Resources (MER), Nurse Practitioner Associates for Continuing Education (NPACE), and Haymarket Medical Education (HME). Faculty Mary Jane Minkin, MD, FACOG, NCMP Clinical Professor of Obstetrics, Gynecology, and Reproductive Sciences Yale University School of Medicine New Haven, CT Release Date: October 2013 Expiration Date: October 2014 Estimated time to complete the educational activity: 30 minutes Target Audience: This activity has been designed to meet the educational needs of Primary Care Physicians, Physician Assistants, and Nurse Practitioners Educational Objectives: After completing the activity, the participant should be better able to: • Describe the impact of vulvovaginal atrophy on sexual health/quality of life and relay this information to postmenopausal patients. • Diagnose vulvovaginal atrophy. • Treat vulvovaginal atrophy in line with evidence-based guidelines. • Counsel patients on the etiology of vulvovaginal atrophy and the efficacy and safety of available therapies. Physician Credit: This activity has been planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of MER and HME. MER is accredited by the ACCME to provide continuing medical education for physicians. Credit Designation: MER designates this educational activity for a maximum of 0.5 AMA PRA Category 1 credits TM. Physicians should only claim credit commensurate with the extent of their participation in the activity. Nursing Credit: Nurse Practitioner Associates for Continuing Education (NPACE) is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation (ANCC). Credit Designation: NPACE designates this educational activity for a maximum of 0.5 contact hours of credit. Participants should only claim credit commensurate with the extent of their participation in the activity. Disclosure Policy – MER MER ensures balance, independence, objectivity, and scientific rigor in all our educational programs. In accordance with this policy, MER identifies conflicts of interest with its instructors, content managers, and other individuals who are in a position to control the content of an activity. Conflicts are resolved by MER to ensure that all scientific research referred to, reported, or used in a CME activity conforms to the generally accepted standards of experimental design, data collection, and analysis. MER is committed to providing its learners with high quality CME activities that promote improvements or quality in health care and not the business interest of a commercial interest. Disclosure Policy – NPACE NPACE is committed to ensuring all educational activities are balanced and free from bias. All faculty participating in our programs disclose any relationships they may have with a commercial interest whose products or services are related to the content of the activity. NPACE’s status as an accredited provider

of continuing nursing education does not imply endorsement by NPACE or ANCC of any commercial products discussed in conjunction with this program. NPACE maintains content integrity and prevents bias in the presence of commercial support through: 1) disclosure by activity planners, authors and content reviewers of relevant relationships with any commercial interest, or lack thereof; 2) disclosure of commercial support; 3) removal of individuals with conflict of interest from the activity; 4) revising the role of the individual with the conflict so that the relationship is no longer relevant to the activity; 5) not awarding contact hours for a portion or all of the activity; 6) undertaking review of the activity by a content reviewer to evaluate for bias, balance, evidence-based content or other indicators of integrity; 7) monitoring the activity to evaluate for bias; and/or 8) reviewing participant feedback. Faculty Disclosures Mary Jane Minkin MD, FACOG, NCMP is on the advisory boards of Noven, Novo Nordisk, Inc., and Bayer. She is also a consultant for Pfizer and Enzymatic Therapy and on the speakers’ bureau for Shionogi. Staff/Planners Disclosures Joe Kopcha, Marina Galanakis, Krista Sierra, Susan Basilico, and Eileen McCaffrey of HME, have no financial relationships to disclose. MER Content Manager has no financial relationships to disclose. Marjorie Crabtree, MSN, DNP; Karen Windle, RNC, MS, MHNP-BC; and R. Mimi Secor, MS, MEd, FNP-BC, FAANP, of NPACE have no financial relationships to disclose. Method of Participation: There are no fees for participating in and receiving CME/CE credit for this activity. During the period of October 2013 through October 2014, participants must: 1) read the learning objectives and faculty disclosures; 2) study the educational activity; 3) complete the posttest and submit it online (physicians may register at; and 4) complete the evaluation form online. A statement of credit will be issued only upon receipt of a completed activity evaluation form and a completed posttest with a score of 70% or better. Disclaimer: The content and views presented in this educational activity are those of the authors and do not necessarily reflect those of MER, NPACE, HME, or Novo Nordisk. The authors have disclosed if there is any discussion of published and/or investigational uses of agents that are not indicated by the FDA in their presentations. The opinions expressed in this educational activity are those of the faculty and do not necessarily represent the views of MER, NPACE, HME, or Novo Nordisk. Before prescribing any medicine, primary references and full prescribing information should be consulted. Any procedures, medications, or other courses of diagnosis or treatment discussed or suggested in this activity should not be used by clinicians without evaluation of their patients’ conditions and possible contraindications on dangers in use, review of any applicable manufacturer’s product information, and comparison with recommendations of other authorities. The information presented in this activity is not meant to serve as a guideline for patient management.

jointly sponsored by

Commercial support for this activity was provided through an educational grant from


Nurse Practitioner Associates

for Continuing Education

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Mary Jane Minkin, md, facog, ncmp

Postmenopausal vulvovaginal atrophy: communication and care

Guidance for the primary-care clinician to identify and treat this chronic and highly prevalent condition


© BSIP / Phototake

ulvovaginal atrophy (VVA) describes symptoms associated with decreased estrogenization of vulvovaginal tissue. The condition can occur at any time in a woman’s life but is most common postmenopause.1 A recent survey including a large cohort of postmenopausal women with VVA symptoms reported the most common manifestations of this condition as vaginal dryness (55%), dyspareunia (44%), and irritation (37%). More than half of respondents (59%) said the symptoms affected their enjoyment of sex. Roughly one quarter reported interference with sleep (24%), general enjoyment of life (23%), and temperament (23%). 2 Other symptoms associated with VVA are postcoital bleeding, soreness, vaginal discharge, itching, and burning. Urinary symptoms include frequency, urgency, and urge incontinence.1 An estimated 10% to 45% of postmenopausal women have vaginal symptoms. 3,4 Unlike the vasomotor symptoms associated with loss of endogenous estrogen, symptoms of VVA usually are progressive and do not resolve spontaneously.

Caption here Vulvovaginal atrophy can compromise quality of life in many postmenopausal women.

Communicating about VVA: a culture of silence Symptomatic vaginal atrophy usually requires medical treatment.1 However, a number of women do not seek help. Various surveys show that only 25% to 56% of women with VVA have discussed symptoms with a health-care professional.2,3,5 More than 25% of those who did discuss vaginal and • the clinical advisor • october 2013 59

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Vulvovaginal Atrophy

Symptomatic vaginal atrophy requires treatment. However, most affected women do not discuss the issue with their clinician.

Pathophysiology and associated symptoms VVA stems from loss of circulating endogenous estrogen. Figure 1 illustrates the hormonal changes that occur with menopause. Compared with premenopause, the post­ menopausal state is associated with lower levels of estrogen and estradiol, but also with diminished amounts of other hormones.9 Estradiol levels <50 pg/mL have been closely associated with vaginal symptoms.10 Reduced estrogen levels also lead to thinning of the vaginal epithelium and a reduction in the production of vaginal glycogen and glucose. In the premenopausal woman, lactobacilli metabolize vaginal glucose and produce lactic acid, leading to an acidic pH in the vagina. Reduced postmenopausal estrogen levels are associated with a higher, more alkaline vaginal pH, loss of lactobacilli, and overgrowth of other bacteria. These changes can lead to vaginal inflammation and infection.1, 3,11 The urinary tract also contains estrogen receptors, and reduced estrogen levels affect urinary function. Physiologic changes include thinning of the urethral mucosa, atrophy of the bladder trigone, decreased tension of the muscle and connective tissue in the urogenital diaphragm, decreased intraurethral pressure, disordered collagen metabolism, and decreased activity of the α-adrenergic system innervating the bladder neck and urethral sphincter.11

Urinary symptoms associated with reduced estrogen levels include increased frequency, nocturia, urge incontinence, dysuria, and recurrent urinary tract infections (UTIs).1,3,11,12 Diagnosis of VVA Diagnosis of VVA is based on patient-reported symptoms and physical exam findings.12 Table 1 lists the physical findings associated with estrogen loss. Measuring vaginal pH or vaginal maturation index can confirm the diagnosis. Vaginal pH ≥4.6 is consistent with vaginal atrophy in the absence of bacterial vaginosis. (Vaginal pH in premenopausal women is typically <4.5.) Vaginal pH is measured by placing pH paper against the inside vaginal wall.1 The vaginal maturation index assesses the relative proportion of parabasal, intermediate, and superficial vaginal epithelial cells. Proportion of superficial cells is typically <5% superficial cells in postmenopausal women and >15% in premenopausal women. This index is rarely used in clinical practice.1 Conditions to consider in the differential diagnosis of VVA include vaginal infection (e.g., candidal vulvovaginitis, bacterial vaginosis, trichomoniasis), vulvovaginal dermatoses (e.g., lichen sclerosus, lichen planus, and lichen simplex chronicus), contact dermatitis, and cancerous or precancerous lesions.1 Discussing VVA: the patient interview Vaginal and urinary health is one of several topics that are appropriate to incorporate into preventive health exams at midlife.13 Letting women know what to expect regarding 70 Patients reporting symptom (%)

sexual symptoms with a clinician waited more than two years to do so, according to one online survey of 1,043 postmenopausal women.6 Embarrassment and lack of knowledge. Reasons for not seeking medical assistance for VVA include embarrassment, mis­conceptions about symptoms, and a belief that no effective treatment is available.7,8 Few women in one survey of 3,046 postmenopausal U.S. women attributed vulvovaginal symptoms to menopause (24%) or hormonal changes (12%).2 In another survey of postmenopausal U.S. women, nearly half (49%) agreed that the symptoms of VVA are just part of growing older. A similar proportion of women (51%) were unaware that local therapy is available for VVA.8 Nearly one-quarter of women in another survey agreed that “[Painful sexual intercourse] is not an appropriate discussion to have with a health-care provider.” 7 Such findings highlight the need for clinicians to initiate conversations with their patients about VVA.


Estradiol Level (pg/mL) <50 >50

50 40 30 20 10 0

Vaginal dryness

Dyspareunia Pain (frequency) (penetration)


Bothered by symptoms

Figure 1. Association of estradiol level with vaginal symptoms

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changes in vaginal and urinary function can help inform patients before problems develop. Initiating the conversation with patients, informing patients that these changes are common, and encouraging patients to seek treatment may increase the likelihood that women will mention symptoms to a provider. One authority suggests viewing education about vaginal health as similar to informing women about the need for routine mammography at age 40 years.14 The postmenopausal woman should be evaluated for vaginal atrophy even if she has not mentioned symptoms.15 Consider prefacing the discussion with such general statements as, “Many women experience vaginal dryness or itching, pain with sex or urination, or incontinence around and after menopause.”12 It is important to respect a patient’s desire for privacy, however. The clinician can ask at various intervals whether the patient would like more information, or let the patient know that she need not answer questions if she would prefer not to discuss the topic. Consider saying something like,“Tell me only what you are comfortable with sharing.” Take care to ensure that your wording does not include implicit preconceptions about sexual activity, sexual orientation, or other personal issues.14 For some patients, mentioning nonsexual symptoms—such as discomfort while riding a bike or when sitting for extended periods of time—may open the conversation. Treatment The goals of VVA therapy are to relieve symptoms and reverse anatomic changes.3 Options include nonhormonal vaginal lubricants and moisturizers, local estrogen therapy11,16 and a selective estrogen receptor modulator (SERM) that was approved recently for treatment of moderate-to-severe dyspareunia.17

Nonhormonal vaginal lubricants and moisturizers

These agents do not address the underlying pathophysiology of vaginal atrophy and its symptoms (Table 2).3 They can be used to relieve vaginal-dryness symptoms in women with a history of hormone-sensitive cancer (e.g., breast or endometrial) and in those who do not wish to use, or do not respond to, estrogen-based therapies.11 Moisturizers are used every few days on a long-term basis. Their purpose is to replace normal vaginal secretions.1,18 Lubricants are designed to reduce friction associated with sexual activity and are applied at the time of sexual activity. They can be water- , oil-, or silicone-based.1,18 Hyalo-GYN, a hyaluronic acid derivative, is a newer option. A nonprescription, nonhormonal moisturizer and lubricant approved for use in the United States in 2010, it is recommended for use every three days.19 Local estrogen therapy

Both The North American Menopause Society (NAMS) and the International Menopause Society recommend local estrogen therapy as the most effective treatment for postmenopausal vaginal atrophy.11,16 Both of these groups and the FDA recommend local estrogen therapy in women with vaginal symptoms only.16,22 Local estrogen therapy avoids most adverse effects of systemic estrogen.11 Such therapy also Table 2. Nonhormonal therapeutic options Moisturizers20 • Replens • Moist Again • Vagisil • Feminease Water-based Lubricants21

• Thin, dry vestibule, vulva, and vaginal tissues

• Astroglide • FemGlide • Just Like Me • K-Y Jelly • Pre-Seed • Slippery Stuff • Summer’s Eve

• Smooth vagina (fewer rugal folds)


• Mildly erythematous or pale vagina

• Luvena Prebiotic

• Shortened, narrowed, less distensible vaginal canal

Silicone-based Lubricants21

Table 1. Physical findings associated with estrogen loss3

• Flattened or absent rugae • Loss of vulva labial fat pad • Clitoral prepuce decreases • Petechiae in vestibule or vagina

• ID Millennium • Pink • Pjur • Pure Pleasure Hyaluronic acid-based19 • Hyalo-GYN • the clinical advisor • October 2013 61

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Vulvovaginal Atrophy

Evidence-based guidelines recommend local estrogen therapy for the treatment of post­menopausal vaginal atrophy. relieves vulvovaginal symptoms and improves cytologic findings to a greater extent than does systemic estrogen.23 Local (vaginal) estrogen therapy has been shown to improve symptoms of vaginal atrophy and overactive bladder, vaginal tissue appearance, vaginal pH, and the vaginal maturation index.3,16,23 This therapy has reduced the incidence of UTIs and of recurrent UTIs.23,24 A Cochrane systematic review reported that some evidence suggests that local estrogen therapy improves urinary incontinence, while conjugated equine estrogens are associated with worsening urinary incontinence.25 Local estrogen formulations approved in the United States for treatment of vaginal atrophy include a conjugated estrogen cream, an estradiol cream, an estradiol ring, and an estradiol vaginal tablet (Table 3).26 These formulations offer equivalent efficacy for relieving symptoms of vaginal atrophy. All are more effective than nonhormonal gel and placebo.27 Choice of therapy is based on patient needs and preferences. Some patients find dosing of the cream confusing. Active estrogen cream dosing is specified in milligrams, the dose of base cream is in grams, and applicator volume is in proportions. Some women prefer to avoid the messiness of cream.1 The estradiol ring is long-acting (three months), but requires dexterity to insert and remove.1 An online survey of postmenopausal women who had switched to vaginal tablets from the creams or rings found that participants reported a longer duration of tablet use compared with creams or rings, and greater compliance with tablets than with creams.26 Women who had used a vaginal cream reported missing doses at least once a month due to the messiness of filling and inserting the applicator, the general unpleasantness of the cream, the need to wash the applicator, and the leakage of the cream following application. Women also cited these issues as prompting their switch to the vaginal tablet. Women who had delayed filling a prescription for the ring and switched to the vaginal tablet cited difficulty removing and/or inserting the ring; expressed concern about vaginal infection, hygiene, or cleanliness; or mentioned that they or their partner could feel the ring. One woman expressed concern that the ring was not the lowest effective dose of estrogen that could be prescribed.26 The majority of women surveyed (52%) switched formulations at the suggestion of their health-care provider, underscoring the clinician’s role in uncovering issues with adherence and preference for another formulation.26

Safety of local estrogen therapy. The most commonly reported adverse effects associated with vaginal estrogen therapy are vaginal bleeding and breast pain. Nausea and perineal pain also may occur.3 Compared with vaginal tablets, conjugated estrogen cream has been associated with a higher rate of uterine bleeding, breast pain, and perineal pain. It also has been associated with significant endometrial overstimulation compared with the vaginal ring.27 All estrogen products, whether vaginal or systemic, contain warnings about increased risk of stroke, myocardial infarction, invasive breast cancer, pulmonary emboli (PE), deep vein thrombosis (DVT), and probable dementia in postmenopausal women. Unopposed estrogens (i.e., without progesterone) carry warnings about risk of endometrial cancer in women with a uterus.28-33 These warnings are based on findings of the Women’s Health Initiative (WHI) study, evaluating systemic conjugated estrogens plus medroxyprogesterone acetate.34 In addition to contraindications in women with a history of PE, DVT, or thromboembolic disease, systemic and local estrogen products are contraindicated in patients with a history of undiagnosed abnormal genital bleeding, a history breast cancer, known or suspected estrogen-dependent cancer, and liver dysfunction or disease.28-33 Vaginal estrogens are associated with limited absorption of systemic estrogen.1,3 Estradiol exposure with one year of an ultra-low-dose tablet (1.14 mg) is roughly equivalent to that of one day of oral estradiol (1 mg/day).16 Steady-state plasma estradiol levels on the ultra-low-dose tablet (10 mcg) are similar to pretreatment levels.35 A progestogen generally is not indicated with local estrogen therapy at the low, recommended dose that is used for vaginal atrophy.16 Clinical trial data supporting endometrial safety do not extend beyond one year. Women who develop uterine bleeding while using low-dose vaginal estrogen should be evaluated thoroughly; endometrial hyperplasia risk increases with rising dose and duration of estrogen exposure.16 Because of the publicity surrounding the WHI findings regarding systemic estrogen therapy, women may have safety concerns about local estrogen therapy. One international survey (of postmenopausal women) reported that 27% of respondents associated local estrogen therapy with risk for breast cancer and 24% with risk for blood clot or stroke.5 When to expect relief; follow-up. Women generally experience symptom improvement within a few weeks of starting vaginal

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Choice of therapy for vaginal atrophy is based on patient needs and preferences. estrogen therapy.3 Some women may not report relief until four to eight weeks after treatment initiation; those with severe atrophy may require more time before deriving sufficient benefit.3,12 Therapy should be continued as long as discomfort from symptoms persists.3 Patients are typically followed up at two to three months, then annually.12 Selective estrogen receptor modulator

The FDA approved the once-daily oral tablet SERM ospemifene in February 2013 for treatment of moderateto-severe dyspareunia. In two phase 3, randomized, doubleblind, 12-week studies, ospemifene was associated with significantly greater beneficial changes from baseline in percentage of superficial and parabasal cells and vaginal pH when compared with those of placebo.36,37 The first trial measured change in severity of most bothersome symptom (vaginal dryness or dyspareunia) compared with placebo after 12 weeks of therapy; significantly greater benefit was observed with ospemifene.36 The second study reported superior benefit with ospemifene in reducing severity of dyspareunia. 37 Hot f lushes were the most frequently reported treatment-related adverse event in this investigation (ospemifene 6.6% vs. placebo 3.6%).37 A long-term (one-year) safety extension of a randomized, double-blind, placebo-controlled study reported no clinically significant adverse changes, few treatment-emergent

adverse events, and no significant endometrial changes. All treatment-emergent adverse events were mild or moderate in severity. Hot flushes were the most common treatmentemergent drug-related adverse event related to the study drug. No treatment-emergent adverse events of pelvic organ prolapse or venous thromboembolism occurred. No cases of endometrial hyperplasia or carcinoma were observed. Vaginal bleeding or spotting occurred in three participants (1.7%), and was self-limiting. Participants were postmenopausal women with a uterus.38 Like other SERMs, ospemifene carries warnings about risk of stroke and DVT. Ospemifene is contraindicated in women with current or prior DVT or PE.17 Incidence of thromboembolic and hemorrhagic stroke in clinical trials of ospemifene (treatment duration up to 15 months) was 0.72 and 1.45 per 1,000 women, respectively, compared with 1.04 and zero, respectively, with placebo.17 Ospemifene also carries warnings about the risk of endometrial and other uterine cancers.17 Ospemifene is contraindicated in women with severe hepatic impairment; known, suspected, or a history of breast cancer; known or suspected estrogen-dependent neoplasia; and undiagnosed abnormal genital bleeding.17 When to consider referral Primary-care clinicians are well positioned to screen, evaluate, and manage women for vaginal, sexual, and

Table 3.Vaginal estrogens approved in the United States for postmenopausal vaginal atrophy Composition




Vaginal cream



Initial 2-4 g/day for one to two weeks Maintenance: 1 g/day (0.1 mg active ingredient/g), one to three weeks

Conjugated estrogens


0.5-2.0 g/day (0.625 mg active ingredient/g) for 21 days, off for seven days

Estradiol acetate


Device containing 2 mg; releases 7.5 μg/day for 90 days


Two options: device containing 12.4 mg of estradiol releases equivalent to 0.05 mg/days for 90 days; device containing 24.8 mg releases equivalent to 0.10 mg /day for 90 days


10.3 μg of estradiol hemihydrate equivalent to 10 μg of estradiol Initial: One tablet/day for two weeks Maintenance: One tablet twice a week

Vaginal ring

Vaginal tablet

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Vulvovaginal Atrophy

urinary symptoms of VVA. Clinicians may wish to consider referral to a gynecologist, urologist, or urogynecologist, with an interest in atrophic symptoms if the patient’s vulva or vagina appearance is atypical, if the patient does not respond to therapy, if the patient has contraindications to estrogen use, or if the clinician is uncomfortable with treating urogenital symptoms.12 Summary Although common among postmenopausal women, VVA is often not diagnosed because the symptoms are not mentioned to a clinician. Clinicians may detect more cases of VVA by including the condition in the patient interview and in the physical examination during preventive health screenings. Misconceptions about VVA also may lead to women not seeking medical assistance. Educating women age 40 years and older about the signs and symptoms of VVA and the availability of effective therapy may open the door for women to mention vaginal, sexual, or urinary symptoms. n References 1. M  acBride MB, Rhodes DJ, Shuster LT. Vulvovaginal atrophy. Mayo Clin Proc. 2010;85:87-94. Available at PMC2800285/. 2. K  ingsberg SA, Wysocki S, Magnus L, Krychman ML. Vulvar and vaginal atrophy in postmenopausal women: findings from the REVIVE (Real Women’s VIews of Treatment Options for Menopausal Vaginal ChangEs) survey. J Sex Med. 2013;10:1790-1799. 3. T  he North American Menopause Society. The role of local vaginal estrogen for treatment of vaginal atrophy in postmenopausal women: 2007 position statement of The North American Menopause Society. Menopause. 2007;14:355-369. 4. S antoro N, Komi J. Prevalence and impact of vaginal symptoms among postmenopausal women. J Sex Med. 2009;6:2133-2142. 5. N  appi RE, Kokot-Kierepa M. Vaginal Health: Insights, Views & Attitudes (VIVA) - results from an international survey. Climacteric. 2012;15:36-44. 6. H  ealthy Women. New survey reports that some postmenopausal

therapy, treatment regimens. In: Katz VL, Lentz GM, Lobo RA, Gershenson DM, eds. Comprehensive Gynecology. 6th ed. Philadelphia, PA: Elsevier Mosby; 2012. 10. S arrel PM. Effects of hormone replacement therapy on sexual psychophysiology and behavior in postmenopause. J Womens Health Gend Based Med. 2000;9(Suppl 1):S25-32. 11. S turdee DW, Panay N. Recommendations for the management of postmenopausal vaginal atrophy. Climacteric. 2010;13:509-522. 12. Minkin MJ, Guess MK. Diagnosis and treatment of the non–sex-related symptoms of vulvovaginal atrophy. Female Patient. 2012;37:33-41. 13. C  hism LA. Overcoming resistance and barriers to the use of local estrogen therapy for the treatment of vaginal atrophy. Int J Womens Health. 2012:4:551-557. Available at /articles/PMC3474153/. 14. Reiter S. Barriers to effective treatment of vaginal atrophy with local estrogen therapy. Int J Gen Med. 2013;6:153-158. Available at www.ncbi. 15. G  oldstein I. J Womens Health (Larchmt). Recognizing and treating urogenital atrophy in postmenopausal women. 2010;19:425-443. 16. T  he North American Menopause Society. The 2012 Hormone Therapy Position Statement of The North American Menopause Society. Menopause. 2012;19:257-271. Available at www.ncbi.nlm.nih .gov/pmc/articles/PMC3443956/. 17. Osphena [package insert]. Florham Park, NJ: Shionogi Inc.; February 2013. 18. T  an O, Bradshaw K, Carr BR. Management of vulvovaginal atrophyrelated sexual dysfunction in postmenopausal women: an up-to-date review. Menopause. 2012;19:109-117. 19. H  yalo-GYN 510k summary. May 4, 2010. 20. B  achmann G, Santen R J. Vaginal dryness (Beyond the Basics). Available at: Last updated March 2012. 21. The North American Menopause Society. Vaginal and vulvar comfort: lubricants, moisturizers, and low-dose vaginal estrogen. Available at­vaginal-estrogen. 22. U  .S. Food and Drug Administration. FDA updates hormone therapy

women endure vaginal and sexual symptoms of menopause for more

information for postmenopausal women. Available at

than two years before discussing with a health care professional.


Available at

htm. Updated March 29, 2013. Additional information and links

7. R  EVEAL REvealing Vaginal Effects At mid-Life: Surveys of postmenopausal women and health care professionals who treat postmenopausal women. Madison, NJ: Wyeth; 2009. 8. N  appi RE, Kokot-Kierepa M. Women’s voices in the menopause: results from an international survey on vaginal atrophy. Maturitas. 2010;67:233-238. 9. Lobo RA. Menopause and care of the mature woman: endocrinology, consequences of estrogen deficiency, effects of hormone replacement

available at: 23. S anten RJ, Allred C, Ardoi SP, et al. Executive summary: Postmenopausal hormone therapy: An Endocrine Society scientific statement. J Clin Endocrinol Metab. 2010;95(7 Suppl 1):s1-s66. Available at 24. P  errotta C, Aznar M, Mejia R, et al. Oestrogens for preventing recurrent urinary tract infection in postmenopausal women. Cochrane Database Syst Rev. 2008;(2):CD005131.

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25. C  ody JD, Jacobs ML, Richardson K, et al. Oestrogen therapy for urinary incontinence in post-menopausal women. Cochrane Database Syst Rev.

33. Premarin (conjugated estrogens) vaginal cream [package insert]. Philadelphia, PA: Pifzer Inc.; May 2012. 34. U.S. Food and Drug Administration. Estrogen and estrogen with pro-

2012,10:CD001405. 26. M  inkin MJ, Maamari R, Reiter S. Improved compliance and patient satisfaction with estradiol vaginal tablets in postmenopausal women previously treated with another local estrogen therapy. Int J Womens Health. 2013:5:133-139. Available at

gestin therapies for postmenopausal women. Updated June 22, 2010. Available at: ucm135318.htm. 35. Eugster-Hausmann M, Waitzinger J, Lehnick D. Minimized estradiol absorption with ultra-low-dose 10 μg 17β-estradiol vaginal tablets.

articles/PMC3604875/ 27. Suckling J, Lethaby A, Kennedy R. Local oestrogen for vaginal atrophy

Climacteric. 2010;13:219-227. 36. B achmann GA, Komi JO; Ospemifene Study Group. Ospemifene

in postmenopausal women. Cochrane Database Syst Rev.

effectively treats vulvovaginal atrophy in postmenopausal women:

2006;4:CD001500. 28. E strace [package insert]. Rockaway, NJ: Warner Chilcott (USA) LLC;

results from a pivotal phase 3 study. Menopause. 2010;17:480-486. 37. P  ortman DJ, Bachmann GA, Simon JA; Ospemifene Study Group.

December 2011. 29. Estraderm [package insert]. East Hanover, NJ: Novartis Pharmaceuticals

Ospemifene, a novel selective estrogen receptor modulator for treating dyspareunia associated with postmenopausal vulvar and vaginal atrophy.

Corp.; March 2007. 30. E string [package insert]. New York, NY Pfizer Inc.; August 2008. 31. Femring [package insert]. Rockaway, NJ: Warner Chilcott (USA) LLC;

Menopause. 2013;20:623-630. 38. S imon JA, Lin VH, Radovich C. One-year long-term safety extension study of ospemifene for the treatment of vulvar and vaginal atrophy in

May 2006. 32. Premarin (conjugated estrogens) tablets [package insert]. Aphena

postmenopausal women with a uterus. Menopause. 2013;20:418-427.

Pharma Solutions—Tennessee, Inc.: August 2012. Available at:

All electronic documents accessed September 15, 2013. • the clinical advisor • October 2013 65

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posttest Expiration date: October 2014

MER is accredited by the ACCME to provide continuing medical education for physicians. MER designates this educational activity for a maximum of 0.5 AMA PRA Category l Credit™. Nurse Practitioner Associates for Continuing Education (NPACE) is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation. NPACE designates this educational activity for a maximum of 0.5 contact hours of credit. Participants should only claim credit commensurate with the extent of their participation in the activity. A statement of credit will be issued only upon receipt of a completed activity evaluation form and a completed posttest with a score of 70% or better. Posttest must be completed and submitted online. Please go to credits: 0.5

Postmenopausal vulvovaginal atrophy: communication and care page 58

1. Which of the following is true of postmenopausal vulvovaginal atrophy (VVA)? a. Most women with VVA (>75%) have discussed symptoms with a health-care professional b. Symptoms can affect the urinary tract as well as the vulvovaginal area c. Symptoms resolve without treatment in about half of affected women d. Most women attribute symptoms of VVA to hormonal changes 2. Which of the following choices most comprehensively describes symptoms of VVA and their impact on quality of life? a. Vaginal dryness; dyspareunia; irritation; interference with sleep, general enjoyment of life, and temperament b. Urinary frequency, urgency, and urge incontinence c. Vaginal dryness, dyspareunia, irritation d. A and B

4. Which of the following is the most effective treatment for postmenopausal vaginal atrophy, according to The North American Menopause Society and the International Menopause Society? a. Vaginal moisturizers or lubricants b. Local estrogen therapy c. Systemic estrogen therapy d. Selective estrogen receptor modulator therapy 5. Which of the following choices best describes the efficacy and safety of local estrogen therapy? a. Relieves vulvovaginal symptoms and improves cytologic findings to a greater extent than systemic estrogen b. Relieves vaginal symptoms but not urinary symptoms associated with VVA c. Requires coadministration of a progestogen in most patients d. Equivalent efficacy but superior safety profile when compared with systemic estrogen therapy for the treatment of VVA

3. Diagnosis of VVA: a. Is based on patient-reported symptoms and physical exam findings b. Requires confirmation with measurement of vaginal pH ≥4.6 without bacterial vaginosis, or vaginal maturation index (<5% superficial cells) c. Requires confirmation of postmenopausal status by measuring estradiol levels <50 pg/mL d. A and C

To take the Posttest please go to

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Advisor Forum These are letters from practitioners around the country who want to share their clinical problems and successes, observations, and pearls with their colleagues. Responding consultants are identified below. We invite you to participate.

Inside the Forum o c to b e r 2 0 1 3

Consultations Testosterone and belly fat in women . . . . . . . . . . . . . . . . . . . 70 Cast vs. splint for a child with a buckle fracture . . . . . . . . . . . . . . . 71 Reactivation of HPV. . . . . . . . . . . . . 71 Acute pharyngitis in an adult. . . . . . . 71

Clinical Pearls A cocktail for uncomplicated urinary tract infection . . . . . . . . . . . 72 Punch out a pilar cyst. . . . . . . . . . . . .72 When to lance a skin abscess . . . . . . . 72

Send us your letters with questions and comments to: Advisor Forum, The Clinical Advisor, 114 West 26th Street, 4th Floor, New York, NY 10001. You may also fax (646) 638-6117, or contact us by e-mail at letters@ If you are writing in response to a published letter, please indicate so by including the number in parentheses at the end of each item. Letters are edited for length and clarity. The Clinical Advisor’s policy is to print the author’s name with the letter. No anonymous contributions will be accepted.

Consultations Testosterone and belly fat in women A patient recently told me that she wanted to have her testosterone level checked because she had heard that belly fat was in part related to low testosterone levels in men and in women. Is there any truth to this? And if it is true, what is the appropriate way to treat low testosterone in a woman?— KEIRA DILLON, FNP, Vista, Calif. Physiologic studies indicate that, for reasons not well understood, the usual low-level processes of androgen conversion seen in fat cells is turned off in female abdominal adipose tissue, specifically in the presence of abdominal visceral obesity (J Clin Endocrinol Metab. 2003;88:5944-5950, available at, accessed September 15, 2013). In a position statement on postmenopausal testosterone supplementation, The North American Menopause Society (NAMS) stated that women with decreased sexual desire associated with personal distress and with no other identifiable cause may be candidates for testosterone therapy. The NAMS statement went on to recommend that laboratory testing of testosterone levels should be used only to monitor for supraphysiologic levels before and during therapy, not to diagnose testosterone insufficiency. Transdermal patches and topical gels or creams are preferred over oral products because of first-pass hepatic effects documented with oral formulations. Finally, testosterone therapy

Our Consultants

Rebecca H. Bryan, APRN, CNP,

Eileen Campbell, MSN, CRNP,

Philip R. Cohen, MD,

is a lecturer in the Family Health NP Program, University of Pennsylvania School of Nursing, Philadelphia.

is associate program director, Family Health NP Program, University of Pennsylvania School of Nursing, Philadelphia.

is clinical associate professor of dermatology, University of Texas Medical Center, Houston.

Deborah L. Cross, MPH, CRNP, ANP-BC, is associate program

director, Gerontology NP Program, University of Pennsylvania School of Nursing, Philadelphia.

Maria Kidner, DNP, FNP-C,

is a nurse practitioner with Cheyenne Cardiology Associates in Cheyenne, Wyo.

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is contraindicated in women with breast or uterine cancer and in those with cardiovascular or liver disease (Menopause. 2005;12:496511).—Sherril Sego, FNP-C, DNP (180-1)

Cast vs. splint for a child with a buckle fracture Do all pediatric patients with a simple buckle fracture need to be treated with a cast? It likely depends on the site of the injury, but a fracture of the distal radius/ulna is very stable. A cast is often mostly for symptomatic care, such as pain control, more than immobilization. How long is it generally acceptable to keep a young patient in a cast?—MIKE DAHL, PA-C, Springville, Utah Except for very young children or those with special health-care needs, a removable splint is preferable to a cast in children with these types of fractures (Int Emerg Nurs. 2009:17:173-178). The children in this study were typically kept in the splints for three to four weeks, depending on symptoms.—Julee B. Waldrop, DNP (180-2)

Reactivation of HPV A woman had HPV-caused cervical cancer removed via loop electrosurgical excision procedure (LEEP) two years ago. All subsequent Pap smears and HPV tests have been negative. What is the likelihood of HPV returning? Is it safe to assume that the virus will not return if the woman and her male partner are monogamous? Is there a chance that the man still has HPV even if he does not have any signs or symptoms?—KANDACE McCARVER, PA-C, Tucker, Ga. A LEEP is primarily a treatment for women diagnosed with cervical intraepithelial neoplasia (CIN)—most often CIN 2/3—or

Debra August King, PhD, PA,

is senior physician assistant at New York-Presbyterian Hospital, New York City.

Mary Newberry, CNM, MSN

provides well-woman gynecologic care as a midwife with Prima Medical Group, Greenbrae, Calif.

premalignant cervical disease. Although invasive cancer can be diagnosed from the specimen obtained from a LEEP, unless this patient had a radical hysterectomy, radiation, or chemotherapy, I suspect she had CIN rather than invasive cervical cancer. The prognosis for the patient described is good (she has only a 1.8% chance of recurrence). However, she cannot be 100% sure that she has completely cleared the virus. Furthermore, compared with the general population, this woman still has an increased risk of being diagnosed with invasive cervical cancer (56 per 100,000 vs. 5.6 per 100,000). HPV infections can persist and recur. Even women in long-term monogamous relationships can get reinfected. In a randomized clinical trial, HPV-associated lesions regressed at higher rates when male partners of women with such lesions used condoms (Int J Cancer. 2003;107:811-816). Men are not routinely checked for HPV, but it is known that 75% to 80% of sexually active women and men carry, and thus are capable of transmitting, the virus, despite not having any signs or symptoms. Because HPV can be transient, a negative test is not a guarantee of total clearance of the virus. The recommendation for this patient would be a semiannual Pap smear with HPV testing for two years following her LEEP. If all tests are negative, she can increase the interval to every three years until age 65 years. Although condom use would likely decrease the chance of the virus being passed back and forth between her and her partner, many HPV infections are attributed to reactivation of previously acquired infections, which a condom would not be able to prevent.—Mary Newberry, CNM, MSN (180-3)

Acute pharyngitis in an adult A woman, aged 20 years, with no known drug allergies, no current medications, and no medical history presented with a sore throat, “clogged” ears, and possible fever for the past three to four days. At the time of her visit, however, she

Claire O’Connell, MPH, PA-C,

teaches in the PA Program at the New Jersey Medical School and Rutgers University, Piscataway, N.J.

Sherril Sego, FNP-C, DNP,

is a primary-care nurse practitioner at the Department of Veterans Affairs Medical Center in Kansas City, Mo.

Julee B.Waldrop, DNP,

is associate professor at the University of Central Florida (UCF), and practices pediatrics at the UCF Health Center. • the clinical advisor • october 2013 71

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Advisor Forum reported feeling better overall and just wanted to make sure she did not have the flu. Clinical examination revealed a smiling, pleasant, conversational, afebrile patient with normal tympanic membranes; nonpainful sinuses, and tonsils that were inflamed, red, and covered with exudates. Minimal cervical lymphadenopathy was noted. Instead of treating immediately, a throat culture was obtained. The throat culture indicated streptococci. The student returned for her results two days later, and her throat looked normal with no exudates or inflammation. She was treated with a 10-day course of penicillin VK because of the possibility of recurrence and the complications resulting from streptococcus (e.g., endocarditis, glomerulonephritis). Was this the right decision?—KATHY P. MCGOVERN, CRNP, Glenside, Pa. This was absolutely the right decision. Symptoms of streptococcal pharyngitis will resolve even without antibiotic treatment in a normal healthy young woman. The goal of antibiotic therapy is to prevent the occurrence of sequelae. The CDC has a fact sheet that provides useful information on the background, diagnosis, and treatment of acute pharyngitis in adults (available at campaign-materials/info-sheets/adult-acute-pharyngitis.html, accessed September 15, 2013).—Julee B. Waldrop, DNP (180-4)

“That’s the gist of what I want to say. Now get me some statistics to base it on.”

Clinical pearls

“Do you think you could get your scandalobsessed butt out of your chair and feed me?”

Punch out a pilar cyst When removing an epidermoid cyst, consider a 5-mm punch biopsy if the cyst is firm, mobile, and small enough. This is particularly effective for pilar cysts. The wound will heal well with minimal scarring.—KATHLEEN HAYCRAFT, DNP, FNP/PNP-BC, DCNP, Hannibal, Mo. (180-6) when to lance a skin abscess I use an 18-guage needle on a 3-cc syringe to tap a skin abscess. If I can extract more than 1 cc of pus, I know I need to lance and pack the abscess.—VICKIE HELMANDOLLAR, FNP, Lancaster, Calif. (180-7) n

“And exactly how is the peanut-butterand-jelly prepared?”

© The New Yorker Collection 2013 from All Rights Reserved.

A cocktail for uncomplicated UTI I recommend use of a probiotic, vitamin C, and purified cranberry solution to women with uncomplicated urinary tract infection (UTI). This boosts the immune system and acidifies the urine to help prevent future UTIs.—CINDY ADAMS, WHNP-BC, Spokane, Wash. (180-5)

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Derm Dx

exclusive to the web

Interact with your peers by viewing the images and offering your diagnosis and comments. To post your answer, obtain more clues, or view similar cases, visit Learn more about diagnosing and treating these conditions, and see how you compare with your fellow colleagues.

Jaw osteomas and a family history of colon cancer A woman, aged 28 years, presents to the dermatology clinic complaining of lumps on her jaw that are causing an asymmetric appearance. An x-ray demonstrates that these lumps are actually osteomas. What is your diagnosis?

• Muir-Torre syndrome • Brooke-Spiegler syndrome • Gorlin syndrome • Gardner syndrome

● See the full case at

Facial lesions in a young patient with seizures A 6-year-old boy presents with cutaneous lesions on his forehead and face. The boy’s mother reports that he has a history of seizures. What is your diagnosis?

• Neurofibromatosis type 1 • Neurofibromatosis type 2 • Tuberous sclerosis • Noonan syndrome ● See the full case at

Have you missed any recent Derm Dx cases? Go to for a complete archive of past quizzes as well as additional images of last month’s other cases.

Translucent “bump” on the eyelid

Itchy eruption after a whirlpool

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A battery charge dogs a clinician

© cmsp / jbsi

A young NP performs a routine procedure against the patient’s express wishes and winds up in court.

By Ann W. Latner, JD

Ms. C, aged 25 years, was a nurse practitioner in the emergency department (ED) of a small medical center that served a busy community. Since she was the new employee on staff, she was first assigned to work on the night shift. Considering she had been working in private practice—in a pediatric setting—Ms. C was thrilled to have a more expansive set of duties. Working in private practice was too routinized for her taste and she preferred a little more variety on a day-to-day basis. Very early one morning when Ms. C was on duty, she got just that. Police officers and emergency medical personnel came rushing in at approximately 3 a.m. holding a man with a gunshot wound. According to a police statement taken in the triage room, an officer on foot patrol had witnessed the man, Mr. O, driving erratically near a convenience store and had attempted to flag the driver down. The officer suspected that the driver was under the influence. But instead of pulling over, Mr. O drove directly into the officer. The officer fired his gun at the car, striking Mr. O in the left shoulder. When the

In the emergency department, Mr. O was asked to consent to a blood draw by the police for evidentiary purposes.

car finally came to a stop, two backup officers arrested Mr. O and brought him to the hospital. In the ED, Mr. O was asked to consent to a blood draw by the police for evidentiary purposes, and he refused the request. The officer told Mr. O that he would get a warrant, but never did so. Mr. O was rushed off for emergency surgery, and afterward, Ms. C was assigned to care for him in the recovery unit. Pending investigation, Mr. O’s room was guarded by several armed police officers. When Ms. C left the patient’s room, the officers entered and again tried to get Mr. O to consent to a blood draw. He refused once more. One of the officers pulled Ms. C aside and asked her surreptitiously if she would be willing to obtain a blood sample from the patient for them. Ms. C looked down the hall, but didn’t see her supervisor or an Cases presented are based on actual occurrences. Names of participants and details have been changed. Cases are informational only; no specific legal advice is intended. Persons pictured are not the actual individuals mentioned in the article. • the clinical advisor • october 2013 77

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LEGAL ADVISOR attending physician. After a moment of thought, she decided the request was probably valid and took the empty vial that the officer gave her. Ms. C quietly entered the room where Mr. O was now resting comfortably. She asked the patient how he was feeling, checked his vital signs, adjusted his IV drip, made a few notes in his chart, and took the blood sample, which she then gave to the police after she left the room. Mr. O recovered and was transferred to police custody shortly thereafter. Because it was a busy night in the ED, Ms. C quickly moved on to treat her other patients. She never saw Mr. O again and was not aware that he had been brought to the precinct. Several months later, Ms. C was served with papers notifying her that she was being sued by Mr. O for medical battery.

In some states, health-care providers who choose to comply with police requests are not ­immune from liability. In a panic, Ms. C immediately contacted the defense attorney her insurance company recommended. At a lengthy consultation with her lawyer, Ms. C reviewed her chart notes on this patient and recounted her quiet conversation with the officer who had asked her to do him a favor. Ms. C’s attorney reassured her that in all probability this charge of medical battery would not stick. “We will move for summary judgment,” the lawyer said. “We will ask the court to dismiss the case based on the fact that you were acting on instructions from the police officers and had no reason to believe their request was improper.” The attorney moved to have the case dismissed on these grounds, and the trial court agreed with him, granting summary judgment. Ms. C was relieved until she was notified that the plaintiff was appealing the case. At the appeal, Mr. O’s attorney argued that although their client was awake and alert, Ms. C never informed him that she was taking blood so the police could assess his alcohol level at the time he hit the pedestrian policeman. Instead, the plaintiff’s counsel argued that Ms. C led Mr. O to believe that she was taking his blood for medical purposes. The plaintiff’s attorney further argued that in the absence of consent, the drawing of Mr. O’s blood constituted medical battery. Ms. C’s attorney countered that Mr. O never objected to the blood draw, and thus he tacitly consented. The appeals court sided with the plaintiff and held that Ms. C’s actions constituted medical battery. Specifically, the

court said that consent for medical treatment is not the same as consent to a blood draw for law-enforcement purposes. The court also noted that the legislature of this state—in opposition to that of several other states—does not expressly require clinicians to comply with law-enforcement requests in a medical setting. Therefore, health-care providers who choose to comply with police requests are not immune from liability. Ms. C settled the case with Mr. O for an unspecified amount. Legal background

Medical malpractice cases require an injury in order for a lawsuit to be filed. In other words, making a mistake isn’t enough to be sued, unless that error resulted in an injury. However, medical battery does not require an injury. In common law, a medical professional who performs a procedure that a patient has not consented to is liable for battery. Battery is defined as unlawful touching or contact with another person—including touching someone without consent. If an unconscious person is brought into the ED, treating him or her would not constitute battery because there is implied consent. However, a conscious person must consent to medical treatment and any procedure that involves physical contact. In this case, although Mr. O consented to medical treatment, he clearly did not consent to a blood draw for law-enforcement purposes. In fact, Mr. O specifically refused to have his blood drawn for that purpose on two separate occasions. Protecting yourself

One of the arguments that the defense attorney made was that Ms. C was not aware that Mr. O had previously refused the blood draw from the police. However, even if Ms. C did not know that the patient had refused to comply, she was still obligated to inform him that the blood draw was for law-enforcement—and not medical—purposes, and ask for his consent. It is important to remember that consent for medical treatment is limited. Such consent cannot be interpreted as permission for a practitioner to draw blood for other purposes or to do anything to the patient that is not treatment-related. Check particular state statutes to find out whether your state has enacted any law protecting providers who comply with police requests. Some states, Illinois and Pennsylvania for example, do protect medical personnel in such instances. However, according to common law—and in states in which no such protective legislation has been enacted—a clinician will not be protected from a lawsuit if he or she assists police in an unconsented blood draw. n

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Stat Consult

A quick review of common conditions, using the best global evidence


Acute sinusitis in adults By Alan Drabkin, MD

Dr. Drabkin is a clinical editor for DynaMed ( dynamed), a database of comprehensive updated summaries covering more than 3,200 clinical topics, and Assistant Clinical Professor of Population Medicine at Harvard Medical School.

• Inflammation of mucosa of paranasal sinuses, typically infectious Incidence/prevalence

• Common Causes

• Viral upper-respiratory infection usually initiates sinusitis. • Bacteria ——Streptococcus pneumoniae ——Haemophilus influenzae ——Moraxella catarrhalis ——Other streptococcal species ——Staphylococcus aureus • Fungal (rare) Likely risk factors

• Smoking • Anatomic abnormalities • Allergic rhinitis • Asthma Complications

© science source / living art enterprise

• Orbital cellulitis • Venous sinus thrombosis • Bacterial meningitis • Brain abscess • Osteomyelitis • Superior orbital fissure syndrome • Pott puffy tumor (frontal bone osteomyelitis and subperiosteal abscess) History

MRI shows bilateral maxillary sinus mucosal thickening and opacification consistent with sinusitis.

• Chief concern ——Purulent nasal discharge ——Facial pain, pressure, or fullness ——Nasal obstruction • History of present illness ——Worsening signs or symptoms following initial improvement (referred to as “double sickening”) • Medication history ——Poor response to nasal decongestants • the clinical advisor • october 2013 79

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Stat Consult • Medical history ——Ask about ■■ Trauma ■■ Viral upper-respiratory infection ■■ Allergic rhinitis ■■ Asthma ■■ Immunodeficiency • Social history ——Ask about smoking or secondhand-smoke exposure. Making the diagnosis

• Criteria for clinical diagnosis of acute sinusitis ——Presence of at least two major or one major plus two or more minor symptoms ■■ Major symptoms »»Nasal congestion/obstruction »»Facial congestion/fullness »»Facial pain/pressure »»Purulent anterior nasal discharge »»Purulent/discolored posterior nasal discharge »»Hyposmia/anosmia »»Fever ■■ Minor criteria »»Headache »»Ear pain, pressure, or fullness »»Halitosis »»Dental pain »»Cough »»Fatigue ——Sinus aspiration and culture (gold standard, but rarely indicated or performed) Differential diagnosis

• Viral upper-respiratory infection • Allergic rhinitis • Migraine Imaging studies

• American Academy of Otolaryngology–Head and Neck Surgery Foundation (AAO-HNSF) recommendations for adult sinusitis ——Routine radiographic imaging not recommended ——Options include ■■ Plain film radiography ■■ CT ■■ MRI, only if complications suspected • Infectious Diseases Societ y of America (IDSA) recommendations

——Routine radiographic confirmation of sinusitis not necessary and not advised ——CT preferred over MRI if suppurative complications suspected Other diagnostic testing

• Bacterial cultures (IDSA recommendations) ——Not recommended for initial diagnosis ——Obtain if unresponsive to empiric treatment with first- and second-line agents • Fiberoptic nasal endoscopy • Nasal-swab cytology Medications

• Analgesics and antipyretics ——Consider for symptomatic relief • Empiric antibiotic treatment ——IDSA recommendations ■■ Start empiric antimicrobial therapy as soon as clinical diagnosis is established. ■■ Treat uncomplicated acute bacterial rhinosinusitis with five to seven days of antibiotics. ■■ Initial empiric therapy if no risk for antibiotic resistance »»First-line agent is amoxicillin-clavulanate (Amoclan, Augmentin) 500 mg/125 mg orally three times daily or 875 mg/125 mg orally b.i.d. »»Alternative options ◊ H igh-dose a mox ici l l in-clav u lanate at 2,000 mg/125 mg orally b.i.d. ◊ Doxycycline 100 mg orally twice daily or 200 mg orally once daily ■■ If risk of antibiotic resistance or if failed initial therapy, use any of »»High-dose amoxicillin-clavulanate 2,000 mg/ 125 mg orally b.i.d. »»Levofloxacin (Levaquin) 500 mg orally once daily »»Moxifloxacin (Avelox) 400 mg orally once daily ■■ If beta-lactam allergy, use any of »»Doxycycline 100 mg orally or 200 mg orally once daily »»Levofloxacin 500 mg orally once daily »»Moxifloxacin 400 mg orally once daily ■■ For severe infection requiring hospitalization, use any of »»Ampicillin-sulbactam (Unasyn) 1.5-3 g IV every six hours »»Levofloxacin 500 mg orally or IV once daily

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Stat Consult »»Moxifloxacin 400 mg orally or IV once daily »»Ceftriaxone (Rocephin) 1-2 g IV every 12 to

24 hours »»Cefotaxime (Claforan) 2 g IV every four to six hours ■■ Antibiotics not recommended for initial empiric therapy. »»Macrolides »»Trimethoprim-sulfamethoxazole (Bactrim, Septra, Sulfatrim) »»Second- and third-generation oral cephalosporin monotherapy »»Coverage for usual or methicillin-resistant S. aureus ——AAO-HNSF recommendations for adult sinusitis ■■ Antibiotics not recommended for acute viral rhinosinusitis. ■■ For acute bacterial rhinosinusitis »»Consider watchful waiting without antibiotics in patients with uncomplicated mild illness (mild pain and temperature <101° F [38.3° C]) with assurance of follow-up. ◊ Defer antibiotics for up to seven days after diagnosis. ◊ Limit management to symptomatic relief. »»If decision made to treat with antibiotic ◊ Amoxicillin is considered first-line therapy for most adults. ◊ Consider trimethoprim/sulfamethoxazole or macrolide if penicillin allergy ◊ Consider using an alternate antibiotic if risk of resistance ◊ No evidence to suggest difference in clinical outcomes with different dose or duration • Efficacy of antibiotics (vs. no antibiotics) ——Antibiotics improve symptoms at seven to 15 days, but high rate of clinical improvement without antibiotics ——Antibiotics are associated with a slightly higher improvement or cure rates at seven to 15 days in patients with mild-to-moderate sinusitis. ——Amoxicillin does not provide clinically meaningful symptom improvement in sinusitis patients at three days but improves self-reported symptoms at seven days. ——Moxifloxacin does not appear to clearly improve clinical cure rate in adults with acute bacterial sinusitis. • Comparative efficacy of antibiotics ——No antibiotic clearly superior for treatment if seven or more days of symptoms

——Fluoroquinolones do not appear to be more effective than beta-lactams for acute bacterial sinusitis. • Duration of antibiotics ——Appropriate duration of antibiotic course not established ——May have equal efficacy with ■■ Trimethoprim/sulfamethoxazole for either three or 10 days ■■ Amoxicillin/clavulanate for either five or 10 days • Nasal steroids ——Evidence suggests statistically significant but clinically small improvement in symptoms with nasal steroid sprays. • Oral steroids ——Oral steroids may hasten symptom improvement in adults with acute sinusitis. • Pelargonium sidoides ——Pelargonium sidoides preparation may reduce sinusitis severity in patients with presumed acute bacterial rhinosinusitis. • Saline nasal irrigation ——Conflicting evidence for efficacy • Decongestants ——Neither topical nor oral decongestants recommended as adjunct therapy • Antihistamines ——No role for symptom relief in nonatopic patients • Mucolytics ——Effectiveness not demonstrated Surgery and procedures

• Functional endoscopic sinus surgery may be used if refractory to medical treatment. Other management

• Most cases resolve without treatment. • Neither baseline signs and symptoms nor x-ray appear to predict disease course. • Facial ultrasound is associated with similar improvement in pain and congestion compared with amoxicillin. Prevention

• Educate patients with chronic rhinosinusitis or recurrent acute rhinosinusitis about control measures ——Washing hands regularly with soap or alcohol-based rub ——Smoking cessation, if applicable ——Saline nasal irrigation. n

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Dermatology Clinic n Learning objectives: To identify and diagnose dermatologic conditions and review up-to-date treatment. n complete the posttest: Page 93

n additional CME/CE: Pages 58, 89

Turn to page 57 for additional information on this month’s CME/CE courses.


White facial papules and sparse, brittle hair Audrey Chan, MD

A boy, aged 13 months, presented for evaluation of white papules on his face. The boy’s mother explained that the lesions had appeared several months earlier and did not seem to be painful or pruritic. The mother also reported that her son does not perspire. Physical examination revealed approximately 30 1-mm-to-2-mm white papules scattered on the face. Similar papules were noted on the face of the child’s mother as well. Sparse and brittle hair was also noted on the boy’s scalp and eyebrows. Examination of the mother’s scalp revealed hypotrichosis. What is your diagnosis? Turn to page 84


Painful, nonbleeding lesion on the ear Kristen Grippe, PA-C

A woman, aged 72 years, presented to the dermatology clinic with complaints of a persistent lesion located on the helix of her right ear. The lesion, which had been present for seven months, was extremely tender but had not bled or changed in size since its initial appearance. The woman reported that the pain was most severe when she slept on her right side and occasionally woke her up at night. Unfortunately, the patient was unable to sleep in a different position due to a previous spinal surgery. Pertinent dermatologic history included a squamous cell carcinoma on her left cheek and multiple actinic keratoses. What is your diagnosis? Turn to page 85 • the clinical advisor • october 2013 83

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Dermatology Clinic

Bazex-Dupré-Christol syndrome

Bazex-Dupré-Christol syndrome (BDCS), also known as Bazex syndrome, is a rare genodermatosis characterized by the triad of hypotrichosis, basal cell carcinoma (BCC), and follicular atrophoderma. As of 2006, only 138 cases of BDCS have been reported.1 Because of the rarity of this disease, the incidence or prevalence has not been wellestablished. Males and females can be affected. A large number of families with this syndrome originate from Central Europe, primarily France and Belgium.2 BDCS is thought to be inherited in an X-linked dominant fashion, as no male-to-male transmission has been reported and almost all daughters of affected fathers are affected.1 The gene mutation has been previously linked to Xq24-q27; however, more recent studies have narrowed the candidate region to chromosome Xq25-27.1. The pathogenic mutation has yet to be identified.3,4 The diagnosis of BDCS can be difficult because clinical findings present at different ages. Hypotrichosis is a congenital feature and is one of the earliest signs of this genodermatosis. Hair abnormalities may be seen on the scalp, eyelashes, eyebrows, and axillary and pubic areas. It is estimated that 85% of all patients with BDCS demonstrate some hair-shaft abnormality. Microscopic examination

The most worrisome characteristic of Bazex-Dupré-Christol syndrome is the association with basal cell carcinoma. of the hair can reveal broken shafts, trichorrhexis nodosa, and/or pili bifurcati.5 Hair can become more abundant with age but often remains sparse and fragile.5 Milia are present in 66% of patients and can appear in infancy. The number of milia can range from a few isolated lesions to hundreds of papules on the face and trunk. Follicular atrophoderma is seen in the majority of, but not all, cases and presents as atrophic ice-pick follicular depressions, most commonly on the dorsal hands. Follicular atrophoderma may also be seen on the dorsal feet, face, and extensor surfaces of the elbows

and knees. It is unclear whether follicular atrophoderma is present at birth, but it does tend to present in early childhood. The most worrisome characteristic of BDCS is the association with BCC. Although part of the classic clinical triad describing BDCS, BCC develops only in 28% of patients.5 BCCs typically develop in the second to third decade of life, but the onset may range from age 9 years to age 50 years. The most common location of BCC is on the face.6 Hypohidrosis is another characteristic finding but may only be present in 25% of patients. Hypohidrosis may be generalized or localized to the face. In approximately 10% of patients, basal cell nevi and trichoepitheliomas may be seen. These neoplasms are usually seen on the face; however, trichoepitheliomas on the genitalia have been reported.7 The diagnosis of BDCS is made clinically, as genetic testing is not available at this time. Hair samples are rarely obtained because the microscopic findings are nonspecific and highly varied. It is rather the qualitative findings of hair sparsity and brittleness that characterize BDCS. Skin biopsies may be performed to confirm clinical findings. The histology of milia is that of tiny epidermoid cysts. The cystic spaces seen on skin biopsy are located in the superficial dermis and are lined by stratified squamous epithelium. The cyst contains varied amounts of lamellated keratin. On skin biopsy, follicular atrophoderma is notable for a depression in the epidermis with the absence of hair structures.6 Suspected BCCs require biopsy. The characteristic histologic findings of BCC include islands of basaloid cells with peripheral palisading and stromal retraction. Trichoepitheliomas are also notable for islands of basaloid cells and peripheral palisading, but these neoplasms lack the stromal retraction seen in BCCs. Trichoepitheliomas also can be distinguished from BCCs by the presence of keratin-filled cysts and papillary-mesenchymal bodies, which are rudimentary follicular papillae. The differential diagnosis varies based on the time of presentation. If a patient presents in infancy, only such early findings as hypotrichosis, follicular atrophoderma, or milia may be present. The differential diagnosis in infancy includes Rombo syndrome and X-linked dominant chondrodysplasia punctata. Rombo syndrome is a genodermatosis inherited in an autosomal-dominant fashion. Rombo syndrome is also characterized by hypotrichosis, milia, and BCCs; however, unlike BDCS, this syndrome is notable for hyperhidrosis and vermicular atrophoderma (atrophic scarring on the cheeks); cyanotic redness of the face, lips, and hands; and short stature.1 X-linked chondrodysplasia punctata also presents with follicular atrophoderma and abnormal hair, but such highly

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characteristic findings as asymmetric shortening of the limbs, striated hyperkeratosis, and pigmentary defects of the skin make the clinical distinction from BDCS relatively easy. If a patient presents later in life with multiple BCCs, the differential diagnosis would include Gorlin syndrome. Gorlin syndrome, also known as nevoid BCC syndrome, is notable for multiple BCCs. Patients with Gorlin syndrome often have characteristic macrocephaly, frontal bossing, hypertelorism, and palmar pits, which are not seen in BDCS. The early diagnosis of Gorlin syndrome is especially important due to the increased risk for the development of medulloblastoma in early childhood. Because of the risk of BCC, individuals with BDCS should be evaluated at least once per year. Typically, the only findings patients seek treatment for are BCC and milia. Treatment of BCC depends on several factors, including histologic type, patient preference, and tumor size and location. The preferred methods of treatment for most BCCs include curettage or local excision. Superficial BCCs may be treated with topical imiquimod 5% (Aldara) cream applied five nights a week for six weeks. High-risk histologic types (i.e., infiltrative, morpheaform, micronodular), recurrent BCCs, or lesions on cosmetically sensitive areas should be referred for Mohs micrographic surgery or to a plastic surgeon. Milia can be treated with incision with a cuttingedge needle and manual expression. There is a case report of eruptive milia successfully being treated with tretinoin 0.1% cream b.i.d. for six weeks.8 This patient’s family history, hypotrichosis, milia, and hypohidrosis were consistent with BDCS. Due to the patient’s young age, no treatment for milia was initiated. He will be monitored for the development of BCCs. Dr. Chan is a third-year dermatology resident at Baylor College of Medicine in Houston. References 1. Torrelo A, Sprecher E, Mediero IG, et al. What syndrome is this? BazexDupre-Christol syndrome. Pediatr Dermatol. 2006;23:286-290. 2. Kidd A, Carson L, Gregory DW, et al. A Scottish family with BazexDupré-Christol syndrome: follicular atrophoderma, congenital hypotrichosis, and basal cell carcinoma. J Med Genet. 1996;33:493-497. 3. Vabres P, Lacombe D, Rabinowitz LG, et al. The gene for BazexDupré-Christol syndrome maps to chromosome Xq. J Invest Dermatol. 1995;105:87-91. 4. Parren LJ, Abuzahra F, Wagenvoort T, et al. Linkage refinement of Bazex-Dupré-Christol syndrome to an 11·4-Mb interval on chromosome Xq25-27.1. Br J Dermatol. 2011;165:201-203.

5. Barcelos AC, Nico MM. Bazex-Dupré-Christol syndrome in a 1-year-old boy and his mother. Pediatr Dermatol. 2008;25:112-113. 6. Goeteyn M, Geerts ML, Kint A, De Weert J. The Bazex-Dupré-Christol syndrome. Arch Dermatol. 1994;130:337-342. 7. Yung A, Newton-Bishop JA. A case of Bazex-Dupré-Christol syndrome associated with multiple genital trichoepitheliomas. Br J Dermatol. 2005;153:682-684. 8. Connelly T. Eruptive milia and rapid response to topical tretinoin. Arch Dermatol. 2008;144:816-817.


Chondrodermatitis nodularis helicis

The patient was diagnosed clinically with chondrodermatitis nodularis helicis (CNH). This condition presents as one or more inflamed nodules on the helix or antihelix of the ear and is most commonly seen in middleaged or elderly populations. Men are more frequently affected than women. The nodules will spontaneously appear as flesh-colored or pink lesions measuring 3 mm to 20 mm and can have a central crust. Once they appear, the lesions will typically remain stable in size and are usually quite tender. One or both ears can be affected at the same time. The lesions will occur on the part of the ear with the most outward projection. Men are more at risk on the helix, whereas women are more affected on the antihelix. In general, the apex of the helix is the most common site.1 The exact cause of CNH is unknown, but lesions are thought to occur due to ischemia of the dermis. The ear has relatively little subcutaneous tissue for insulation and padding, and only small dermal blood vessels supply the epidermis, dermis, perichondrium, and cartilage. These anatomic features of the ear prevent adequate healing and lead to perichondritis. Ischemia can be increased due to favoring one side during sleep, as the ear is crushed into the pillow. Other causes may include pressure from piercings and use of earphones, cell phones, and hands-free phone devices with ear attachments. Actinic damage, repetitive trauma, or previous frostbite may predispose patients to easier breakdown of dermal tissue.2 CNH may occasionally be associated with autoimmune or connectivetissue disorders, including autoimmune thyroiditis, lupus • the clinical advisor • october 2013 85

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Dermatology Clinic

erythematosus, dermatomyositis, and scleroderma. Such cases may be more common in pediatric or young-adult female patients.3 Diagnosis of CNH can be made clinically based on patient history and symptoms. A shave biopsy can be performed to rule out such similarly appearing conditions as basal cell carcinoma, squamous cell carcinoma, actinic keratoses, atypical fibroxanthomas, and pseudocysts.3 Basal cell and squamous cell carcinomas are caused by chronic sun damage or radiation, will typically continue to enlarge, and can bleed easily if traumatized. Actinic keratoses are premalignant scaly or crusted papules or plaques with scale that will often appear on sun-exposed skin and can be tender or bleed. Atypical fibroxanthomas are rapidly growing pink or red nodules on sun-exposed skin that are frequently mistaken for malignancies.4 Pseudocysts present as a noninflamed and painless swelling of the pinna and typically occur in men in the third or fourth decade of life. Pseudocysts also may occur from repeated minor trauma or pressure.5 Because of the similar presentations of these conditions, a biopsy is often needed to secure the correct diagnosis. Histologic changes include those similarly seen in a decub­ itus ulcer but on a smaller scale. These changes include epidermal ulceration and dermal homogeneous acellular collagen degeneration with fibrin deposition. Granulation tissue flanks the zone of necrosis on both sides.6 A workup for autoimmune conditions should be performed if the patient presents with lesions at a younger age or if otherwise suspected from the patient’s history. Treatments for CNH are varied and can be challenging. The main objective of therapy is to relieve pressure being exerted on the ear and may include removing piercings or discontinuing use of electronic devices that pinch the ear. Sleeping on the opposite side of the head can be helpful but is not always possible, and there is a risk that the patient will develop a CNH nodule on the other ear. Special pillows have been designed to alleviate pressure on the ear during sleep. These pillows work by creating an air space in which the ear can rest while the other parts of the head are supported. Intralesional injections of triamcinolone acetonide and twice-daily topical betamethasone valerate cream 0.025% for six weeks have been shown to be effective in approximately 25% of patients studied.7 Antibiotics can be used if infection is suspected. Cryotherapy and CO2 laser ablation are third-line options.7 When CNH lesions are recalcitrant and the patient is willing to undergo a more invasive approach, excision of

the nodule and surrounding cartilage can be performed by a surgeon. The most common method is to perform a wedge excision of the nodule with reconstruction of the skin and cartilage margins. It is important that the cartilage edges are smooth so as not to create any additional pressure points on the ear. While a punch excision can also be performed to encompass the entire nodule,8 this approach is less favored because it will likely require a skin graft. The prognosis after excision is generally good, but lesions may recur in the same or different areas unless chronic pressure is relieved. Reassurance that the lesion is not a tumor may put the patient’s mind at ease and no treatment may be desired.9 The woman in this case was initially treated with an intralesional injection of triamcinolone acetonide, which decreased the size of the lesion by approximately half. After reporting moderate pain at her follow-up appointment, the patient opted to use a pillow designed to alleviate pressure on the ear during sleep. She will be reevaluated in six months. n Ms. Grippe is a physician assistant at Dermatology Associates of Erie in Erie, Pa. References 1. Yaneza MM, Sheikh S. Chondrodermatitis nodularis chronica helicis excision and reconstruction. J Laryngol Otol. 2013;127:63-64. 2. Chrondrodermatitis nodularis chronica helicis. In: James W, Berger T, Elston D, eds. Andrew’s Diseases of the Skin, 10th Ed. Philadelphia, Pa.: Saunders; 2006:610. 3. Medscape. Chondrodermatitis nodularis helicis. Available at emedicine. 4. Medscape. Atypical fibroxanthoma. Available at emedicine.medscape .com/article/1056204. 5. Vano-Galvan S. Dermacase. Auricular pseudocyst. Can Fam Physician. 2009;55:271-272. Available at 6. Chung HJ, Cam K, Schwartz L. Firm papules on the auricular helix. Weathering nodules (WNs) of the ear. JAMA Dermatol. 2013;149:475-480. 7. Beck MH. Treatment of chondrodermatitis nodularis helicis and conventional wisdom? Br J Dermatol. 1985;113:504-505. 8. Rajan N, Langtry JA. The punch and graft technique: a novel method of surgical treatment for chondrodermatitis nodularis helicis. Br J Dermatol. 2007;157:744-747. 9. Lawrence, C. Chondrodermatitis nodularis helicis chronica. In: Lebwohl M, Heymann W, eds. Treatment of Skin Diseases, 3rd ed. Philadelphia, Pa.: Saunders; 2010:139-141. All electronic documents accessed September 15, 2013.

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alternative meds update

What you should know about the herbs and supplements patients use

By Sherril Sego, FNP-C, DNP. Ms. Sego is a staff clinician at the VA Hospital in Kansas City, Mo., where she practices adult medicine and women’s health. She also teaches at the nursing schools of the University of Missouri and the University of Kansas.


© Science Source / Rod Planck

Rhodiola rosea, or roseroot, is native to the arctic regions of Europe,Asia, and North America.With a long history of medicinal use in Scandinavia, Russia, and ancient Greece, rhodiola has been employed to treat ailments of the nervous system, including depression, muscle weakness and muscle fatigue, and altitude sickness.1 Rhodiola is commonly referred to as an adaptogen, a type of plant purported to decrease cellular sensitivity to stress.1 Practitioners of complementary and alternative medicine assert that adaptogens allow the body to adapt to—or even resist—physical, chemical, and environmental stressors.

Background R. rosea is a perennial plant that grows to a typical height of less than 3 ft.2 It yields delicate yellow flowers but has a thick rhizome structure.2 These rhizomes, which have a rose fragrance when cut, are harvested for medicinal use.2 Researchers have identified at least six specific categories of antioxidative, stress-mediating compounds within the plant’s roots.1

Science Most of R. rosea’s medical utility stems from two specific mechanisms of action. Scientists believe that the plant’s effects are related to optimizing serotonin and dopamine levels as a result of monoamine-oxidase inhibition and its influence on such opioid peptides as beta-endorphins. However, these specific neurochemical mechanisms have not been clearly documented.2,3 One 2009 study examined R. rosea’s effect in blocking two different enzymes within the monoamine

oxidase family. Both enzymes showed a statistically significant inhibitory effect >80%.2 Stress-related fatigue and depression have been widely studied in connection with R. rosea supplementation. In one trial, researchers randomized 60 healthy adults to a daily treatment of R. rosea extract.4 Pre- and post-study scores on two assessment scales (the Montgomery-Asberg Depression Scale and the Pines’ burnout scale), the Conners’ Computerized Continuous Performance Test II (CCPT II), and awakening salivary cortisol levels were evaluated for efficacy. After a 28-day treatment period, improvements over placebo were seen in the Pines’ burnout scale and the CCPT II. Post-treatment salivary cortisol levels to awakening stress were also blunted by as much as 30% over pretreatment levels. In a pilot study exploring the effect of R. rosea in generalized anxiety disorder, 10 volunteers were given daily doses of R. rosea extract for 10 weeks.5 Pre- and post-treatment assessments using the Hamilton Anxiety Rating Scale (HARS), the four-dimensional anxiety and depression scale, and the • the clinical advisor • october 2013 87

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alternative meds update Clinical Global Impression scales of severity and improvement were made. The post-treatment scores on the HARS were significantly lower than pretreatment, with corresponding improvements in anxiety indices.5 The potential neuroprotective action of a multiherb compound containing R. rosea was explored in patients with Parkinson disease.6 A total of 32 patients were evaluated pre- and post-treatment for impairments to motor function. The threemonth trial allowed participants to continue their established regimen of antiparkinson therapies while being given two courses of the experimental herb compound during that time. By adjusting for previous levels of steady state or decline, the post-treatment data showed an improvement in such symptoms as tremor, rigidity, and gait. A literature review of randomized clinical trials of R. rosea identified 11 placebo-controlled trials.7 Physical and mental performance measures were identified as assessment criteria in each, with single-compound R. rosea as the experimental agent. Across-the-board findings supported a possible mild benefit from R. rosea intervention but indicated a need for larger, more robust and replicable clinical data. In a 2012 literature review, the same performance measures were evaluated but subjected to more rigid scientific criteria.8 In all 11 trials, efficacy of R. rosea was considered contradictory.8 These findings also suggest that more rigorous testing is needed to evaluate R. rosea’s clinical utility.8 The systematic review shows some evidence suggesting that the herb may help alleviate mental fatigue and increase physical stamina, but methodologic flaws in the studies to date limit accurate assessment of efficacy.8

Dose, how supplied, cost R. rosea is typically available as a capsule, and doses range from 200 mg to more than 400 mg orally b.i.d. Since the bulk of this herb is found in challenging climates, harvesting the pure product increases cost. In the United States, most formulations and strengths are available for less than $40 for a one-month supply.

Summary Historically, R. rosea has been used to treat depression.

Researchers have identified at least six specific categories of antioxidative, stress-mediating compounds within the plant’s roots.

Safety, interactions

As adequate safety and efficacy data is lacking at present, R. rosea should not be recommended as a reliable supplement. n References 1. Khanum F, Bawa, AS, Singh B, Rhodiola rosea: A versatile adaptogen. Comprehensive Reviews in Food Science and Food Safety. 2005;4:55-62. 2. van Diermen D, Marston A, Bravo J, et al. Monoamine oxidase inhibition by Rhodiola rosea L. roots. J Ethnopharmacol. 2009;122:397-401. 3. Edwards D, Heufelder A, Zimmermann A. Therapeutic effects and safety of Rhodiola rosea extract WS® 1375 in subjects with life-stress symptoms—results of an openlabel study. Phytother Res. 2012;26:1220-1225. 4. Olsson EM, von Schéele B, Panossian AG. A randomized, double-blind, placebo-controlled, parallel-group study of the standardized extract shr-5 of the roots of Rhodiola rosea in the treatment of subjects with stress-related fatigue. Planta Med. 2009;75:105-112. 5. Bystritsky A, Kerwin L, Feusner JD. A pilot study of Rhodiola rosea (Rhodax) for generalized anxiety disorder (GAD). J Altern Complement Med. 2008;14:175-180. 6. Bocharov EV, Ivanova-Smolenskaya IA, Poleshchuk VV, et al. Therapeutic efficacy of the neuroprotective plant adaptogen in neurodegenerative disease (Parkinson’s disease as an example). Bull Exp Biol Med. 2010;149:682-684. 7. Hung SK, Perry R, Ernst E. The effectiveness and efficacy of Rhodiola rosea L.: A systematic review of randomized clinical trials. Phytomedicine. 2011;18:235-244. 8. Ishaque S, Shamseer L, Bukutu C, Vohra S. Rhodiola rosea for physical and mental fatigue: A systematic review. BMC Complement Altern Med. 2012;29:12-70. Available at All electronic documents accessed September 15, 2013.

© thinkstock

All studies cited only mild side effects, including sedation and nausea. No serious adverse effects were documented. However, these trials are relatively small, so safety factors are still in question. Allergic reactions are always a possibility, and pregnant or nursing women, infants, and children should not use R. rosea without discussing this move with a health-care provider. 88 the clinical advisor • october 2013 •

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Dermatologic Look-Alikes n Learning objective: To distinguish and properly treat dermatologic conditions with similar presentations. n complete the posttest: Page 93

n additional CME/CE: Pages 58, 83

Turn to page 57 for additional information on this month’s CME/CE courses.

Enlarging white patches Kerri Robbins, MD



A Hispanic male, aged 12 years, was brought to the clinic with a complaint of white patches on his face. The lesion began four months ago as a white patch around the boy’s mouth. Since that time, the lesion had continued to enlarge, and new lesions had developed around both eyes within the past month. The lesions were asymptomatic, and no prior treatment had been attempted. Review of systems and medical history was otherwise negative. On physical examination, depigmented patches were appreciated in a periocular and perioral distribution.

A white woman, aged 51 years, presented with a mildly pruritic white patch on her left shoulder. The lesion had been present for three months and was slowly enlarging. The woman had been applying OTC hydrocortisone without relief. No history of prior trauma was reported, and there were no alleviating or aggravating factors. Physical examination revealed a white, atrophic plaque with surrounding erythema and hyperpigmentation on the left posterior shoulder. A similar lesion was also appreciated on the woman’s left hip. • the clinical advisor • october 2013 89

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Dermatologic Look-Alikes


Vitiligo was first described in 1500 B.C. and may have been derived from the Latin word vitium, meaning “blemish” or vitelilus, meaning the “white, glistening flesh of calves.”1 Throughout history, confusion with such disorders as leprosy continually provoked discrimination and segregation for vitiligo sufferers. Unfortunately, it was not until the late 19th century that significant progress was made in the understanding of vitiligo and the melanocyte was discovered as the causative factor. Vitiligo affects approximately 0.5% to 2% of the population worldwide.2 It may appear at any age throughout life, with the average age of onset being approximately 20 years. The pathogenesis of vitiligo is largely unknown but is thought to be multifactorial. Many believe that vitiligo results in the destruction and loss of histochemically recognizable melanocytes. However, others have proposed that melanocytes may still be present in very small numbers or in an undifferentiated state without melanogenic activity.

Vitiligo most commonly presents as an amelanotic macule or patch that is surrounded by normal-appearing skin. The importance of genetics in the development of vitiligo has been demonstrated in various twin and family studies. Interestingly, these genetic associations seem to be strongest in families with various vitiligo-associated autoimmune diseases rather than in those with only localized or generalized vitiligo. Many hypotheses surrounding the destruction of melanocytes exist. These include such theories as an autoimmune destruction, an intrinsic defect of melanocytes, a defective free-radical defense, reduced melanocyte survival, destruction by autocytotoxic metabolites, membrane lipid alterations, a deficiency of unidentified melanocyte growth factors, destruction by neurochemical substances, and a viral cause. A convergence theory has also been proposed, in which several of these factors are thought to contribute in some way to the phenomenon of vitiligo.

Vitiligo most commonly presents as an amelanotic macule or patch that is surrounded by normal-appearing skin. Lesions of vitiligo expand centrifugally and the borders are usually convex, making it appear as if the depigmented areas are invading the normal skin. The macules and patches of vitiligo usually have well-defined borders and range from a few millimeters to several centimeters in size. Lesions may be round, oval, or linear in shape. Vitiligo may also display the Koebner phenomenon, which is defined as the development of vitiligo at the sites of trauma. Patients are usually asymptomatic; however, pruritus may occasionally be present. In individuals with fair skin, the lesions of vitiligo may be difficult to appreciate. However, visualization may become more apparent with the help of a Wood’s lamp or after tanning of uninvolved skin. Vitiligo can be classified into localized, generalized, and universal types. The localized type includes such variants as focal, segmental, and mucosal. Focal vitiligo affects one nondermatomal site (e.g., the glans penis). Segmental, or unilateral, vitiligo presents with one or more macules involving a unilateral segment of the body. Segmental vitiligo tends to appear at an earlier age and is resistant to treatment. In mucosal vitiligo, only mucosal-membrane lesions exist. The generalized pattern is the most common and includes such variants as vulgaris, acrofacial, and mixed. Vitiligo vulgaris features scattered patches of vitiligo that are widely distributed. In acrofacial vitiligo, patients present with lesions that are limited to the distal extremities and face. Mixed vitiligo may present as several combinations of the above subtypes. Universal vitiligo results in complete or nearly complete depigmentation. Most patients with vitiligo are otherwise healthy. However, there has been an association with various autoimmune endocrinopathies, in particular thyroid dysfunction. Most studies on the subject point to an increased risk in individuals with increasing age.3 However, these studies are controversial, and most recommend that clinicians be aware of the increased risk and be attentive to symptoms of thyroid disease. On histopathology of well-established lesions, a complete absence of melanocytes will be noted. Although most lesions do not demonstrate an inflammatory infiltrate, early lesions may show a superficial perivascular and occasionally lichenoid mononuclear cell infiltrate at the border. The differential diagnosis for vitiligo includes chemical leukoderma, postinflammatory hypopigmentation, halo nevi, tinea versicolor, leprosy, leukoderma associated with scleroderma, late stages of treponematosis or onchocerciasis

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(river blindness), hypopigmentation associated with topical corticosteroid use, and lichen sclerosus. Treatment of vitiligo is aimed at stabilizing the depigmenting process and gaining repigmentation. There are a number of treatment options (many of which are off-label); however, there is no single therapeutic approach that works in all patients. The areas that tend to have the highest degree of repigmentation are the face, mid-extremities, and trunk. The treatment of choice for generalized vitiligo is narrowband UVB. Excimer laser phototherapy can also be effective on limited areas. Potent or superpotent topical corticosteroids may be useful for localized areas, but patients should be advised to discontinue treatment after two months if there is no visible improvement and should be warned about the possibility of atrophy. Systemic corticosteroids can halt rapidly progressing vitiligo but cannot be used long-term due to their toxicity. Topical 0.1% tacrolimus (Protopic) ointment has also resulted in repigmentation of vitiligo and is often used on the face and genitals. For recalcitrant stable vitiligo, such surgical therapies as autologous transplantation may be performed. If more than 50% to 80% of the body surface area is affected, consider depigmentation with monobenzone (Benoquin) 20%. The course of the disease is very unpredictable. Every individual is different, and while some degree of spontaneous repigmentation is not uncommon, complete and stable repigmentation is rare. The boy in this case was treated with tacrolimus 0.1% ointment. Some repigmentation was noted at a follow-up appointment two months later.


Lichen sclerosus

Ferdinand Jean Darier made the first histologic description of lichen sclerosus in 1882.4 In 1887, Francois Henri Hallopeau reported the first clinical description and named the entity lichen plan atrophique. Other terms that have been used include lichen sclerosus et atrophicus, kraurosis vulvae, and balanitis xerotica obliterans. As proposed by the International Society for the Study of Vulvar Disease, today the entity is now most commonly known as lichen sclerosus.

Lichen sclerosus is relatively uncommon, and the prevalence in the female population is thought to be approximately 1.7%. All ages may be affected by the disorder; whites tend to be preferentially affected, and females predominate at all ages. Females also tend to have a bimodal age distribution, with peaks occurring in prepubertal girls and postmenopausal women. In both sexes, the anogenital area is affected in approximately 85% of cases. The pathogenesis of lichen sclerosus is poorly understood. Inflammation seems fundamental for the initiation of lichen sclerosus; however, the mechanisms leading to subsequent sclerosis remain unknown. A genetic predisposition is thought to contribute to the development of lichen sclerosus, and an association with MHC class II antigen HLA-DQ7 has been observed.5 Interestingly, this same region is also associated with an increased risk of autoimmune diseases. Immunoglobulin G autoantibodies to extracellular matrix protein 1 have been found in approximately 80% of individuals with lichen sclerosus.6 Although detection of the antibody may be helpful in diagnosing the disorder, it has no role in quantifying the extent of the disease. Other proposed causal factors include oxidative stress, infections, and hormonal influences. Lichen sclerosus can affect both anogenital and extragenital skin. In women, anogenital involvement is most commonly observed on the vulva and the perianal region. The lesion will often encircle both the genitalia and the perianal region, forming a figure-eight configuration. Lesions in women begin as areas of sharply demarcated and slightly raised erythema. Areas may then become eroded and eventually evolve into a dry and hypopigmented sclerotic patch. Early lesions may occasionally appear bruised, hemorrhagic, or eroded. Girls and women who present for treatment of this complaint may be misdiagnosed as victims of sexual abuse. Patients frequently complain of severe pruritus and pain. Due to the fissuring and erosions, patients may also complain of dysuria, dyspareunia, and/or pain with defecation. Constipation is a common complaint in children with lichen sclerosus. If left untreated, the atrophy may become so severe that it leads to shrinkage or obliteration of the labia major, labia minora, and/or clitoris. In males, lesions usually only involve the glans penis; however, they can extend onto the penile shaft and scrotum. The lesions are atrophic and markedly hypopigmented or depigmented. Phimosis and paraphimosis are common complications. Most men with lichen sclerosus are uncircumcised. However, circumcision in these patients does not â&#x20AC;˘ the clinical advisor â&#x20AC;˘ october 2013 91

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universally “cure” the disease. If left untreated, urethral meatal stenosis may occur. Extragenital lichen sclerosus is more common in older age groups and is often asymptomatic. Patients may occasionally complain of dryness or pruritus. The extragenital lesions occur most commonly on the neck, flexural surfaces of the wrists, and sites of physical trauma or continuous pressure such as the shoulder or hip. The tongue and oral mucosa are rarely involved. Lesions begin as bluish-white shiny papules that may coalesce into plaques or patches and eventually develop into a scarlike atrophy with an ivory color. Telangiectasias and follicular plugging may be seen in advanced stages, and lesions may occasionally develop hemorrhagic bullae. Histologically, lesions of lichen sclerosus show a trilayered appearance, often described as the “red, white, and blue” sign. The first zone is the compact hyperorthokeratotic scale and atrophic epidermis (red) with vacuolar degeneration. The second, deeper zone is the pale edematous dermis (white) and subjacent is a variably dense interstitial lymphocytic inflammatory infiltrate (blue). Established lesions demonstrate hyperkeratosis with an atrophic epidermis, pale superficial dermal stroma, and rare inflammatory cells. A cleftlike space often separates the atrophic epidermis from the pale dermis. Extragenital lichen sclerosus must be differentiated from vitiligo, morphea, anetoderma, discoid lupus erythematosus, idiopathic guttate hypomelanosis, post-inflammatory hypopigmention, and chemical leukoderma. Genital lichen sclerosus may mimic lichen planus, lichen simplex chronicus, vulvar intraepithelial neoplasia, erythroplasia of Queyrat, vitiligo, and extramammary Paget disease. Early aggressive treatment with such superpotent topical steroids as clobetasol has been shown to prevent disease progression.7 In most relevant studies, clobetasol propionate 0.05% cream was applied for 12 to 24 weeks.8 The majority of patients undergoing this treatment showed a significant improvement in pruritus and burning, but the visible white and atrophic skin is often only minimally improved. Long-term side effects have not been seen, even with long-term and maintenance use of clobetasol. Topical tacrolimus 0.1% and 0.03% ointments, along with pimecrolimus (Elidel) 1% cream, have also been proven effective, but should only be used when topical steroids are not effective or are not tolerated. In refractory cases, such off-label treatments as hydroxychloroquine (Plaquenil), topical calcitriol (Vectical), topical calcipotriol, cyclosporine (Gengraf, Neoral, Sandimmune), topical tretinoin,

acitretin (Soriatane), and hydroxyurea (Droxia, Hydrea) may be tried. Phototherapy and surgery are other options. Circumcision is the treatment of choice for genital lichen sclerosus in males. Persons with lichen sclerosus have a lifetime risk of approximately ≤5% of developing squamous cell carcinoma. Patients should be educated on this risk and monitored on a regular basis for progression. As for the woman in this case, biopsy confirmed the diagnosis of lichen sclerosus, and the patient was treated with clobetasol 0.05% ointment daily for three months. On follow-up, the patient reported no pruritus, but the lesion had only improved minimally. n Dr. Robbins is an instructor in the Department of Dermatology at Baylor College of Medicine in Houston. References 1. Millington GW, Levell NJ. Vitiligo: the historical curse of depigmentation. Int J Dermatol. 2007;46:990-995. 2. Krüger C, Schallreuter KU. A review of the worldwide prevalence of vitiligo in children/adolescents and adults. Int J Dermatol. 2012;51:1206-1212. 3. Vrijman C, Kroon NW, Lipens J, et al. The prevalence of thyroid disease in patients with vitiligo: a systematic review. Br J Dermatol. 2012;167:1224-1235. 4. Darier J. Lichen plan sclereux. Ann Derm Syph. 1892;23:833. 5. Marren P, Yell J, Charnock FM, et al. The association between lichen sclerosus and antigens of the HLA system. Br J Dermatol. 1995;132:197-203. 6. Oyama N, Chan I, Neill SM, et al. Autoantibodies to extracellular matrix protein 1 in lichen sclerosus. Lancet. 2003;362:118-123. 7. Tausch TJ, Peterson AC. Early aggressive treatment of lichen sclerosus may prevent disease progression. J Urol. 2012;187:2101-2105. 8. Lorenz B, Kaufman RH, Kutzner SK. Lichen sclerosus. Therapy with clobetasol propionate. J Reprod Med. 1998;43:790-794.

© The New Yorker Collection 2013 from All Rights Reserved.


“If you have to do time, can I have your desk set?”

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posttest Expiration date: October 2014

Nurse Practitioner Associates for Continuing Education (NPACE) is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation. The Nurse Practitioner Associates for Continuing Education designates this educational activity for a maximum of 0.5 contact hours of credit. Participants should only claim credit commensurate with the extent of their participation in the activity. Posttests must be completed and submitted online. NPs may register at no charge at must receive a score of 70% or better on each test taken to obtain credit.

credits: 0.5

Dermatology Clinic

Dermatologic Look-Alikes

page 83

page 89

Case #1: Bazex-Dupré-Christol syndrome

Case #1: Vitiligo

1. Bazex-Dupré-Christol syndrome is characterized by a. Hypotrichosis b. Basal cell carcinomas c. Follicular atrophoderma d. All of the above

1. Lesions of vitiligo display the Koebner phenomenon, which is defined as a. An urticarial flare caused by rubbing b. Pinpoint bleeding when scraped c. Development of new lesions at the sites of trauma d. Blister formation with light rubbing

2. What is a characteristic of Gorlin syndrome? a. Macrocephaly b. Cyanotic redness of the face c. Hyperhidrosis d. Vermiculate atrophoderma

2. What is the treatment of choice for generalized vitiligo? a. Systemic corticosteroids b. Narrow band UVB c. Monobenzone (Benoquin) 20% d. Topical tacrolimus (Protopic) 1%

Case #2: Chondrodermatitis nodularis helicis 3. In the differential diagnosis of chondrodermatitis nodularis helicis (CNH), atypical fibroxanthomas are described as a. Lesions that typically continue to enlarge and bleed easily if traumatized b. Rapidly growing pink or red nodules on sun-exposed skin c. Premalignant scaly or crusted papules or plaques d. Noninflamed and painless swellings on the pinna

Case #2: Lichen sclerosus

4. What treatment has been shown to be approximately 25% effective in patients with CNH? a. Intralesional triamcinolone acetonide and twice-daily topical betamethasone b. Cryotherapy c. CO2 laser ablation d. Wedge excision of the nodule

4. Patients with lichen sclerosus have a lifetime risk of approximately ≤5% of developing a. Malignant melanoma b. Basal cell carcinoma c. Squamous cell carcinoma d. Merkel cell carcinoma

3. What is the location of lichen sclerosus in approximately 85% of patients? a. Anogenital region b. Flexural surfaces c. Tongue and oral mucosa d. Shoulder or hip

To take the Posttest please go to • the clinical advisor • october 2013 93

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COMMENTARY Sharon Fruh, PhD, RN, FNP-BC, an associate professor at the University of South Alabama College of Nursing in Mobile, Ala., does research in family meals in health-disparity populations.

We can impact the obesity epidemic Health-care providers are struggling in the nation’s war against obesity, but as a nurse practitioner (NP) or physician assistant (PA), you can make a difference by providing weight-loss guidance on an ongoing basis to your patients. Patients want us to get involved and give them individualized and detailed weight-loss plans. For example, one study found that 82% of persons who are either overweight or obese would like help from their family physicians (Diabetes Educ. 2006;32:557-561). But other research has shown that providers can be reluctant to discuss weight reduction, and have avoided the subject due to

Quality of clinician counseling can influence patient motivation to lose weight and intentions to change behavior.

fear of offending the patient ( J Am Acad Nurse Pract. 2009;21:454-460). Providers may feel discouraged and perhaps ineffective in the area of weight-loss counseling and may shy away from engaging in this practice. However, quality of clinician counseling can influence patient motivation to lose weight and intentions to change behavior (BMC Health Serv Res. 2010;10:159, available at; accessed September 15, 2013). NPs and PAs need to be familiar with effective weight-loss strategies and comfortable discussing these tactics with patients. It is also important for clinicians to calculate and discuss with the patient the patient’s BMI, waist circumference, and waist-to-hip ratio. A person with a BMI >25 is considered overweight, and a person with a BMI >30 is considered obese. Waist circumference >40 inches for men and >35 inches for women is considered high. Waist-to-hip ratios >0.85 for women and >1.0 for men fall into the high-risk category. Encourage patients to become acquainted with calorie counts of foods and explain to them how making small changes each day can lead to significant weight loss over time. For example, cutting out just 100 calories a day can lead to a 10-lb. weight loss in a year. In June 2013, the American Medical Association officially recognized obesity as a disease. The Centers for Medicare and Medicaid

Services already (as of December 2011) reimburses for behavioral counseling of obese patients (defined as a BMI ≥ 30) delivered in the primarycare setting. NPs and PAs can bill for these services. Reimbursable benefits include weekly face-to-face counseling for a month, then everyother-week counseling for five months. Patients who have lost at least 6.6 lbs at the end of six months are entitled to receive six more monthly counseling sessions. Behavioral counseling must be consistent with the five As: assess, advise, agree, assist, and arrange. NPs and PAs can make a difference in fighting obesity. We must be willing to take the following steps: • Familiarize ourselves with successful weightloss strategies. • Talk about weight issues with patients. • Obtain physiologic measurements from the patient on an ongoing basis. • Use every opportunity to employ successful strategies to help patients lose weight. • Stay current on effective weight-counseling techniques. • Refer patients to a nutritionist when needed. As clinicians, we can better engage in the weight-loss battle if we are aware and equipped to make a difference in the lives of the patients we serve. Additional information on this topic is available at (accessed September 15, 2013). n

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October 2013 Clinical Advisor  

The Clinical Advisor is a monthly journal for nurse practitioners and physician assistants in primary care. Its mission is to keep practitio...

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