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VOL. LVI • NO. 11 NOVEMBER 2015


WHEN SHE INTERVIEWED A REGIONS BUSINESS BANKER, she gave us the third degree about our favorite way to improve her cash flow. You should too. We never shy away from a difficult situation, or a serious challenge. In fact, we hope you pull out all the stops and ask us about what really matters.

1 What process do you use to understand how money flows through my business?

2 Will you be able to offer solutions that maximize my cash flow?

3 Do you have good ideas about how I can expedite collections?

4 How can you help me find that 25th hour in a day?

When every decision feels make or break, you’ll be glad you’re working with a banker who has your back. So interview a Regions Business Banker today to learn how we can help your business move forward, now and down the road.

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VOL. LVI • NO. 11 NOVEMBER 2015

EDITOR Lucius M. Lampton, MD ASSOCIATE EDITORS D. Stanley Hartness, MD Richard D. deShazo, MD

THE ASSOCIATION President Daniel P. Edney, MD President-Elect Lee Voulters, MD

MANAGING EDITOR Karen A. Evers

Secretary-Treasurer Michael Mansour, MD

PUBLICATIONS COMMITTEE Dwalia S. South, MD Chair Philip T. Merideth, MD, JD Martin M. Pomphrey, MD Leslie E. England, MD Ex-Officio and the Editors

Speaker Geri Lee Weiland, MD Vice Speaker Jeffrey A. Morris, MD Executive Director Charmain Kanosky

JOURNAL OF THE MISSISSIPPI STATE MEDICAL ASSOCIATION (ISSN 0026-6396) is owned and published monthly by the Mississippi State Medical Association, founded 1856, located at 408 West Parkway Place, Ridgeland, Mississippi 39158-2548. (ISSN# 0026-6396 as mandated by section E211.10, Domestic Mail Manual). Periodicals postage paid at Jackson, MS and at additional mailing offices. CORRESPONDENCE: Journal MSMA, Managing Editor, Karen A. Evers, P.O. Box 2548, Ridgeland, MS 39158-2548, Ph.: 601-853-6733, Fax: 601-853-6746, www.MSMAonline.com. SUBSCRIPTION RATE: $83.00 per annum; $96.00 per annum for foreign subscriptions; $7.00 per copy, $10.00 per foreign copy, as available. ADVERTISING RATES: furnished on request. Cristen Hemmins, Hemmins Hall, Inc. Advertising, P.O. Box 1112, Oxford, Mississippi 38655, Ph: 662-236-1700, Fax: 662-236-7011, email: cristenh@watervalley.net POSTMASTER: send address changes to Journal of the Mississippi State Medical Association, P.O. Box 2548, Ridgeland, MS 39158-2548. The views expressed in this publication reflect the opinions of the authors and do not necessarily state the opinions or policies of the Mississippi State Medical Association. Copyright © 2015 Mississippi State Medical Association.

SCIENTIFIC ARTICLES Tobacco Use Trends among Mississippi Youth following the 328 1997 Settlement of Mississippi’s Medicaid Lawsuit and Subsequent Tobacco Prevention Initiatives Emily McClelland, MS; Nell Valentine, MS; Robert McMillen, PhD Is Vitamin D Deficiency Contributing to Mississippi’s Persistent 334 Black-White Disparity in Preterm Birth? Charlene Collier, MD, MPH, MHS and Alan Penman, MBChB, PhD, MPH

Top Ten Facts You Need to Know about Clostridium difficile 348 Saira Butt, MD

Clinical Problem-Solving Case: A Rash Decision 350 Laura J. Miller, MD SPECIAL ARTICLE My Immigration Story 337 Heddy-Dale Matthias, MD PRESIDENT’S PAGE Component Society Rescue Program Daniel P. Edney, MD, MSMA President

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EDITORIALS Praise the Lord and Take Away their Ammunition! D. Stanley Hartness, MD; Associate Editor

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The Physician Abuse of Meaningful Use 344 Richard D. deShazo, MD; Mollie R. deShazo, MD; Matthew D. deShazo, MD Psychostimulants: Concerns over Long Term Adverse Side Effects 346 James Gray Adams, MD DEPARTMENTS From the Editor: Are We as Fat as We Can Get? Lucius M. Lampton, MD

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MSMA Physician Leadership Academy: Jonathan Jones, MD

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ABOUT THE COVER- “GILES ISLAND FOGGY SUNRISE IN THE MISSISSIPPI RIVER WOODS, ADAMS COUNTY” This photograph was taken by Joe R. Bumgardner, MD of Starkville, a retired general surgeon who practiced there for 27 years. He writes: “Giles Island is a place of legend and drama, a canvas for history and fame. Once a working plantation on the north bluff of Natchez, today the land at Giles Island is a Mississippi Hardwood Bottom, lush and full of wildlife. In 1933, the Corps of Engineers dredged the Giles cutoff, separating the land from the main land of Mississippi, creating what is now the hunter’s paradise of Giles Island. In the recent past, I have been fortunate to bow-harvest two quality whitetail bucks at Giles Island. Recently (January 2015), I had the opportunity to bow hunt for three and a half days at Giles Island and was most fortunate (on more than one occasion) to experience nature’s spectacular sunrises in the woods adjacent to the mighty Mississippi River. My only camera was my ‘smartphone’ (iPhone 6) and I was compelled to capture this spectacular event. This image is just one of several that depicted breathtaking sunrises.” VOL. LVI • NO. 11 NOVEMBER 2015

Official Publication

MSMA • Since 1959

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F R O M

A

T H E

E D I T O R

Are We as Fat as We Can Get?

ccording to data released in September, Mississippi is no longer the fattest state in the union. Dear Arkansas and West Virginia have elbowed us out of top position, with Arkansas first having an adult obesity rate of 35.9%. Our celebration should be somewhat muted by the fact that our obesity percentage, 35.5%, has not gone down, just leveled off as the nation and other states have continued to trend upwards (22 states are now above 30%!). One fellow physician reflected cynically upon hearing the news that our state was no longer first in obesity: “Are we as fat as we can get?” While there is still much to be done, Mississippi’s leadership, especially in medical, public health, and school circles, does deserve significant credit for decreasing our slope upwards. Even back in 2012, Mississippi had been recognized as one of the few states in the country demonstrating a significant drop in the prevalence of overweight and obesity in children. The Mississippi Healthy Students Act, passed by the Legislature in 2007, was the first major coordinated effort to prevent further increases in the state’s childhood obesity rates. The Act focused on public school students and emphasized improved

nutrition in the cafeterias and vending machines, increased physical activity, and the provision of health education. Mississippi remains first in the country with heart disease, third with hypertension, and second with diabetes, all conditions directly influenced by obesity. As well, our significant poverty and racial diversity place additional hurdles in combating obesity. Although overall rates for obesity and overweight have leveled off among Mississippi’s students, data reveals emerging racial disparities in those rates, home nutrition, and health education. Mississippi is not as obese as we can get, and if our state reduces its emphasis on obesity reduction and improving health education, it can and will get much fatter, and, as a consequence, much sicker. Physician involvement and leadership on local school health councils is one way our profession can make a difference. As well, a renewed commitment to the creation of comprehensive, coordinated school health education would transform the current generation of Mississippi’s children, helping them grow into healthy adults. Contact me at LukeLampton@cableone.net. —Lucius M. Lampton, MD, Editor

JOURNAL EDITORIAL ADVISORY BOARD Timothy J. Alford, MD Family Physician, Kosciusko Medical Clinic Michael Artigues, MD Pediatrician, McComb Children’s Clinic Diane K. Beebe, MD Professor and Chair, Department of Family Medicine, University of Mississippi Medical Center, Jackson Rep. Sidney W. Bondurant, MD Retired Obstetrician-Gynecologist, Grenada Jennifer J. Bryan, MD Assistant Professor, Department of Family Medicine University of Mississippi Medical Center, Jackson Jeffrey D. Carron, MD Professor, Department of Otolaryngology & Communicative Sciences, University of Mississippi Medical Center, Jackson Gordon (Mike) Castleberry, MD Urologist, Starkville Urology Clinic Matthew deShazo, MD, MPH Assistant Professor-Cardiology, University of Mississippi Medical Center, Jackson Thomas E. Dobbs, MD, MPH State Epidemiologist, Mississippi State Department of Health, Hattiesburg Sharon Douglas, MD Professor of Medicine and Associate Dean for VA Education, University of Mississippi School of Medicine, Associate Chief of Staff for Education and Ethics, G.V. Montgomery VA Medical Center, Jackson Bradford J. Dye, III, MD Ear Nose & Throat Consultants, Oxford

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Daniel P. Edney, MD Executive Committee Member, National Disaster Life Support Education Consortium, Internist, The Street Clinic, Vicksburg Owen B. Evans, MD Professor of Pediatrics and Neurology University of Mississippi Medical Center, Jackson Maxie L. Gordon, MD Assistant Professor, Department of Psychiatry and Human Behavior, Director of the Adult Inpatient Psychiatry Unit and Medical Student Education, University of Mississippi Medical Center, Jackson Nitin K. Gupta, MD Assistant Professor-Digestive Diseases, University of Mississippi Medical Center, Jackson Scott Hambleton, MD Medical Director, Mississippi Professionals Health Program, Ridgeland J. Edward Hill, MD Family Physician, North Mississippi Medical Center, Tupelo W. Mark Horne, MD Internist, Jefferson Medical Associates, Laurel Daniel W. Jones, MD Sanderson Chair in Obesity, Metabolic Diseases and Nutrition Director, Clinical and Population Science, Mississippi Center for Obesity Research, Professor of Medicine and Physiology, Interim Chair, Department of Medicine Ben E. Kitchens, MD Family Physician, Iuka

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Brett C. Lampton, MD Internist/Hospitalist, Baptist Memorial Hospital, Oxford Philip L. Levin, MD President, Gulf Coast Writers Association Emergency Medicine Physician, Gulfport Lillian Lien, MD Professor and Director, Division of Endocrinology, University of Mississippi Medical Center, Jackson William Lineaweaver, MD Editor, Annals of Plastic Surgery, Medical Director, JMS Burn and Reconstruction Center, Brandon Michael D. Maples, MD Vice President and Chief of Medical Operations, Baptist Health Systems Heddy-Dale Matthias, MD Anesthesiologist, Critical Care Internist, Madison Jason G. Murphy, MD Surgeon, Surgical Clinic Associates, Jackson Alan R. Moore, MD Clinical Neurophysiologist, Muscle and Nerve, Jackson Paul “Hal” Moore Jr., MD Radiologist, Singing River Radiology Group, Pascagoula Ann Myers, MD Rheumatologist , Mississippi Arthritis Clinic, Jackson Darden H. North, MD Obstetrician/Gynecologist , Jackson Health Care-Women, Flowood

Jack D. Owens, MD, MPH Neonatologist, Newborn Associates, Flowood Michelle Y. Owens, MD Associate Professor, Vice-Chair of Obstetrics and Gynecology, University of Mississippi Medical Center, Jackson Jimmy L. Stewart, Jr., MD Program Director, Combined Internal Medicine/ Pediatrics Residency Program, Associate Professor of Medicine and Pediatrics University of Mississippi Medical Center, Jackson Shou J. Tang, MD Professor and Director, Division of Digestive Diseases, University of Mississippi Medical Center, Jackson Samuel Calvin Thigpen, MD Hematology-Oncology Fellow, Department of Medicine, University of Mississippi Medical Center, Jackson Thad F. Waites, MD Clinical Cardiologist, Hattiesburg Clinic W. Lamar Weems, MD Urologist, Jackson Chris E. Wiggins, MD Orthopaedic Surgeon, Bienville Orthopaedic Specialists, Pascagoula John E. Wilkaitis, MD Chief Medical Officer, Brentwood Behavioral Healthcare, Flowood Sloan C. Youngblood, MD Assistant Medical Director, Department of Anesthesiology, University of Mississippi Medical Center, Jackson


Got Questions MACM Risk Management has answers.

At Medical Assurance Company of Mississippi, we believe protecting our insureds from litigation is just as important as the service we provide after a suit is filed. The primary focus of our physician insureds is the health and well-being of their patients. Our responsibility is to help them keep that focus, while working on issues and topics that affect the delivery of healthcare in Mississippi. All of the programs and services listed below are offered at no cost to MACM insureds. •

Onsite Survey. Through these evaluations, our staff can analyze the risk management systems and documentation within your practice to offer suggestions for improvement.

In-Service Education. With customized presentations and training, our staff can meet the needs of our individual insureds.

Consultations by Telephone and Email. Our consultants are located in Mississippi and available to answer questions from insureds when they need timely assistance.

Publications. Our insureds receive information that is timely through Risk Manager Alert email blasts, as well as more in-depth information through our Risk Manager magazine.

Reference Materials. These written bulletins are available to our insureds and designed to help in specific circumstances that come up daily in a medical practice, such as withdrawal from patient care.

Educational Opportunities. In addition to the knowledge of our in-house staff, MACM has contacts across the U.S. and makes this expertise available to our insureds through webinars and conferences.

Presentations and Speaking Engagements. The Risk Management Staff has been a sought-after source for presentations at conferences on an array of topics related to the practice of healthcare.

If you are not currently insured by Medical Assurance Company of Mississippi, what services and educational opportunities are you missing out on?

Don’t be left out! To take advantage of the many opportunities that MACM offers its insureds, contact Tammi Arrington at (800) 325-4172 or tammi.arrington@macm.net for information and a quote on your medical professional liability needs. NOVEMBER 2015 • JOURNAL MSMA 327


S C I E N T I F I C

A R T I C L E S

Tobacco Use Trends among Mississippi Youth following the 1997 Settlement of Mississippi’s Medicaid Lawsuit and Subsequent Tobacco Prevention Initiatives EMILY MCCLELLAND, MS; NELL VALENTINE, MS; ROBERT MCMILLEN, PHD Tobacco is the leading cause of death in the U.S., and most cigarette smokers begin smoking during middle and high school.1,2 Over the past two decades, Mississippi has implemented several programs and policies to reduce tobacco use among our youth. In the 1990s, a lawsuit and subsequent settlement with the tobacco industry created funds for the development of youth tobacco prevention programs. Starting in 2002, Mississippi began to join other states in passing local smokefree ordinances for indoor public places. To date, more than a hundred Mississippi municipalities have implemented smokefree ordinances. The tax burden on cigarettes has also changed; Mississippi had one of the lowest state taxes on cigarettes prior to raising the tax from 18 cents to 68 cents per pack in 2009. Research ties each of these actions to reductions in youth smoking rates.3-6 Lawsuits & Youth Tobacco Prevention Programs In 1994, then-Mississippi Attorney General Mike Moore filed a groundbreaking lawsuit with the Chancery Court of Jackson. The lawsuit alleged that the tobacco industry had conspired and fraudulently concealed the dangerous nature of tobacco, and the state requested monetary compensation for Medicaid expenses caused by tobacco products.7 Three years later in 1997, the tobacco industry and the state of Mississippi reached a settlement agreement. Based upon this agreement, the tobacco industry was to pay Mississippi $170 million. In addition, beginning in January of 1998 payments were to be made to Mississippi annually in perpetuity calculated with “a formula that had been based upon the estimated costs of smoking to Mississippi taxpayers through the Medicaid program” (with adjustments for any changes in inflation or smoking rates).7 In 1998, the Chancery Court approved the creation of a nonprofit corporation known as the Partnership for a Healthy Mississippi (PHM), which was charged with making the social and cultural climate in Mississippi intolerant of tobacco use by youth. In fiscal year 1999, initial spending on the program was $17 million. The Jackson County Chancery Court ordered continued annual funding for the PHM in December 2000. This order provided for $20 million to be diverted directly to the PHM from tobacco settlement payments annually in perpetuity in order to continue funding anti-tobacco programs in Mississippi.

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From 1998 to 2007, the PHM coordinated the state’s comprehensive tobacco prevention programs, focusing primarily on youth from kindergarten through high school. These programs followed the CDC Best Practices for Tobacco Control Programs8 and included state and community interventions, mass media campaigns, and cessation assistance. In 1998, the Mississippi State Department of Health (MSDH) began administering the Youth Tobacco Survey to middle and high school students in order to perform surveillance and evaluation of the Partnership’s programs. The MSU Social Science Research Center began collaborating with the Health Department to conduct this survey. Despite the Chancery Court funding the PHM’s tobacco prevention programs, there were challenges to this use of state money as allocated by the judicial system. House Bill 1115, passed by the Legislature in 2006, funded the PHM comprehensive tobacco prevention programs via a Legislative appropriation, rather than a judicial action. Governor Haley Barbour, however, vetoed this bill in March of 2006. Prior to this veto, the governor had participated in a legal effort to overturn the Chancery Court’s decision to fund the PHM. Governor Barbour, the state Division of Medicaid, and the Health Care Trust Fund filed motions to vacate the December 2000 order and direct the $20 million away from tobacco prevention and into the Health Care Trust Fund. In May 2006, citing a lack of agreement between the legislative and executive branches regarding funding for tobacco prevention, the Jackson County Chancery Court granted the Governor and Treasurer’s motion, denying the tobacco prevention programs access to further funding. In June 2007, the Mississippi Supreme Court upheld the December 2006 order from the Jackson County Chancery Court that determined only the Mississippi Legislature could appropriate funds to tobacco prevention programs. As of June 1, 2006, counter-marketing campaigns were no longer airing, and the college program for the 18 to 24-year-old market was ended. As of November 30, 2006, the Partnership ceased funding of cessation programs, including a statewide quitline and regional tobacco cessation treatment clinics, a law enforcement program, and numerous statewide and after-school programs.


ABSTRACT Background: Mississippi has implemented several programs and policies to reduce youth tobacco. This study examines trends in youth tobacco use and compares current prevalence rates for cigarettes, cigars, smokeless tobacco, and e-cigarettes. Design/Methods: The Youth Tobacco Survey is a self-administered survey of a multi-stage sample of public high school students.

Conclusion: The state has successfully decreased cigarette and cigar smoking. However, smokeless tobacco use has not changed and e-cigarettes are becoming increasingly popular. Currently, Mississippi youth are at equal risk for cigarette, cigar, smokeless tobacco, or electronic cigarette use. Tobacco prevention efforts, clinician counseling, and policies should address each of these products rather than focus primarily on cigarettes.

Results: Cigarette and cigar smoking decreased from 1998 to 2014. However, current use of smokeless tobacco did not change and e-cigarette use has increased. Currently, there are no significant differences in the prevalence of cigarette, cigar, smokeless tobacco, or electronic cigarette use.

Keywords: Tobacco, Youth

The Senate sought to restore tobacco prevention programs during the 2007 legislative session. SENATE BILL NO. 2764 called for the development, implementation, and funding of a comprehensive and statewide tobacco education, prevention, and cessation program that is consistent with the Best Practices for Tobacco Control Programs of the federal Centers for Disease Control and Prevention. Subsequently, the legislature appropriated (fiscal year FY2008) $9 million for the MSDH to create a state tobacco prevention and cessation program – the Office of Tobacco Control (OTC).

State Tobacco Tax As of July 2015, the average state cigarette tax is $1.60 per pack. The cigarette tax in Mississippi is $0.68 per pack. Mississippi had one of the lowest cigarette taxes in the U.S. prior to raising the tax from $0.18 to $0.68 in 2009. Since raising the tax, the number of packs of cigarettes sold in Mississippi has decreased by more than 30%, while tax revenue from cigarette sales has almost tripled.10 Although Mississippi collected tax revenue on fewer packs of cigarettes, each pack brought in 50 cents more revenue. Research from other states replicates Mississippi’s experience. Every state that has made a meaningful increase in the state cigarette tax has experienced reduced consumption and increased revenue.11 Moreover, surveys have found reductions in youth smoking prevalence following tax increases.

Since 2008, the OTC has supported state and community interventions to encourage and support tobacco-free lifestyles; local tobacco-free coalitions to prevent the initiation of tobacco use among youth, reduce exposure to secondhand smoke, promote tobacco cessation services, and eliminate tobacco-related disparities; youth programs led by the PHM to deter the initiation of tobacco use among school-age youth; and cessation services, including the Mississippi Tobacco Quitline and the ACT Center for Tobacco Treatment, Education, and Research. Local Smokefree Laws Local ordinances and statewide laws prohibiting smoking in indoor public spaces protect nonsmokers from the harmful effects of secondhand smoke. The added benefit is that these laws also reduce youth smoking.6 Their impact comes from both disrupting opportunities for trial/experimentation and by changing social norms such that smoking is perceived as less acceptable. In recognition of these benefits, 24 states and the District of Columbia have passed smokefree laws that apply to indoor restaurants, workplaces, and bars, and 763 municipalities have implemented smokefree ordinances. As of July 2015, 49.5% of the U.S. population is protected by either a state law or local ordinance.9 In Mississippi, Metcalfe became the first municipality to implement a smokefree law in 2002, followed by Mayersville in 2005. Momentum for this initiative increased in 2006 after Starkville passed an ordinance. To date, there are now 116 Mississippi municipalities with smokefree ordinances, protecting 31% of Mississippians.

The tax and regulatory burden on other tobacco products is substantially lighter than on cigarettes. The state tax on cigars and smokeless tobacco is 15% of the manufacturer price and has not increased over the past two decades. Mississippi does not currently tax electronic cigarettes. Federal law prohibits the use of flavors in cigarettes and requires that cigarettes be sold in packs of at least twenty. These regulatory actions reduce the attractiveness of cigarettes to youth who tend to be more price sensitive than adults but are not currently applied to cigars, smokeless tobacco, or e-cigarettes. Electronic Cigarettes Over the past two decades, the social climate of tobacco control in Mississippi has shifted with the implementation of the preceding tobacco prevention initiatives. A relatively new product is also changing the landscape. Electronic cigarettes were introduced to the U.S. market in 2007, and their popularity began to increase after 2010. E-cigarettes are battery-operated devices that heat nicotine, flavor additives, and chemicals in order to release an aerosol that is inhaled by users. Users refer to these devices by several names and typically refer to their use as vaping. These devices are currently not subject to any federal regulation regarding flavors, labeling, or marketing. Mississippi prohibits the sale of the devices to people under the age of 18, but many local smokefree ordinances do not preclude e-cigarette use.

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Current use of these products among U.S. youth tripled from 2013 to 2014, likely due to the novelty of these devices, their attractive flavors, aggressive marketing, and misperceptions that vaping is safe. Summary The social climate of tobacco control in Mississippi has shifted dramatically over the past two decades. The state initiated and settled a landmark lawsuit against the tobacco industry, funds from which support statewide youth tobacco prevention programs. The state has raised the state cigarette tax and 104 municipalities have implemented smokefree laws. Meanwhile, a novel and unregulated tobacco product has entered the market and become increasingly popular among youth. The purpose of this study is to examine trends in youth tobacco use during this time period and to compare current prevalence rates for cigarettes, cigars, smokeless tobacco, and e-cigarettes. Method The Mississippi Youth Tobacco Survey The Mississippi Youth Tobacco Survey (YTS) is a comprehensive tobacco survey administered annually to Mississippi public high school students. The YTS measures students’ attitudes, knowledge, and behaviors concerning tobacco use. We added questions about electronic cigarette use in 2010. Data from the YTS assist the state in designing, implementing, and evaluating their comprehensive tobacco control program. Cross-sectional data for the Mississippi YTS are available for 1998-2000, 2002-2004, 2006, and 2008-2014. The YTS was not conducted in 2001 and 2007 due to changes in management of tobacco prevention programs, and Hurricane Katrina prevented administration of the survey in 2005. Procedure The Institutional Review Board at Mississippi State University approved these annual surveys. Public high school students in the state of Mississippi were selected for participation using a multi-stage sample design. All public schools containing students in 9th, 10th,11th, or 12th grades were included in the first sampling stage. In order to produce a representative sample of students, schools were selected with a probability proportional to enrollment size. Once a school agreed to participate, classrooms were chosen randomly and all students in selected classes were eligible for participation. Parents were informed of the nature and intent of the survey via permission forms that provided the opportunity for them to opt their child out of participation. Teachers used standardized procedures to group administer the anonymous, self-administered questionnaires during a normal class period. A weighting factor was applied to each student record to adjust for non-response at the school, class, or student level. Weighting the data ensured that all schools would be represented equally and that the sample characteristics would match those of the population of public high school students within the state. Weight = W1 * W2 * f1 * f2 * f3 * f4 W1 = inverse of the probability of selecting the school

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W2 = inverse of the probability of selecting the classroom within the school f1 = a school-level non response adjustment factor calculated by school size (small, medium, large) f2 = a class adjustment factor calculated by school f3 = a student-level non response adjustment factor calculated by class f4 = a post stratification adjustment factor calculated by gender and grade Statistical analyses were conducted using SPSS 22.0 and complex sampling procedures. The use of complex sampling procedures was required because standard statistical analyses are based on the assumption that the data were obtained through simple random sampling. Statistical procedures completed with the assumption that the data was obtained with simple random sampling would have underestimated the error variance due to the homogeneity of students within the same school and the same classroom. Measures Respondents were asked about their use of cigarettes, cigars, smokeless tobacco, and e-cigarettes during the past 30 days. Those who reported using a product on at least one of the past 30 days were categorized as current users of that product. Results Overall response rates range from 59% to 75%. Table 1 provides the school, student, and overall response rates for each year. Sample characteristics for each year did not vary significantly across years. TABLE 1. Response Rates


TABLE 2. Trends in Current Tobacco Use

13.9%, 95% CI [10.6, 17.2]; and electronic cigarettes: 11.3%, 95% CI [8.4, 14.2]), whereas females were much more likely to report cigarette use (9.6%, 95% CI [7.2, 12.0]), cigar use (7.6%, 95% CI [5.0, 10.2]), and electronic cigarette use (9.0%, 95% CI [6.8, 11.2]) than smokeless tobacco use (2.0%, 95% CI [0.9, 3.1]) (see Figure 1). Figure 1. 2014 Current Tobacco Use

FIGURE 1. 2014 Current Tobacco Use 20.0 17.5

18.0 16.0 14.0

14.9

13.9

12.0 10.0 8.0

11.3 10.1

11.0

10.3

9.6

9.5

9.0

8.0

7.6

7.1

13.6

13.3

12.6

12.2

6.4

6.0 4.0

2.0

2.0

2.7

0.0 Cigarettes

Cigars Overall Use

Prevalence of Tobacco Use, 1998-2014 Cross-sectional analyses of cigarette, cigar, and smokeless tobacco use indicate that current cigarette and cigar smoking have decreased both substantially and significantly since 1998. However, current use of smokeless tobacco did not change from 1998 to 2014 (see Table 2). Subsequent demographic analyses found that decreases in current cigarette and cigar smoking occurred across all grades, among males and females as well as black and white students. Smokeless tobacco use did not decline for any of these groups. Current e-cigarette use did not change from 2010 (1.2%, 95% CI [0.4, 2.0]) to 2013 (2.9%, 95% CI [1.9, 3.9]). However, current use increased substantially in 2014 to 10.1% (95% CI [8.1, 12.1]). Further analyses revealed that increased prevalence of use occurred across all grades, among males and females as well as black and white students. Current Use of Cigarettes, Cigars, Smokeless Tobacco, and E-cigarettes, 2014 When tobacco control programs were implemented in Mississippi in 1998, cigarette smoking was much more prevalent among high school students than cigar use, which in turn was more common than smokeless tobacco use (see Table 2). As cigarette and cigar use declined over the next 16 years, these differences diminished. By 2014, there were no significant differences between cigarette, cigar, smokeless tobacco, or e-cigarette use (see Figure 1). The prevalence for past 30 day use was approximately 10% for each of these products. Prevalence of cigarette, cigar, and e-cigarette use did not differ between males and females, but males were more likely to report past 30 day use of smokeless tobacco. Analyses by sex indicated that prevalence for use among males was consistent across products (cigarettes: 14.9%, 95% CI [11.6,18.2]); cigars: 12.6%, 95% CI [10.1, 15.1]; smokeless tobacco:

Male

SLT Female

Black

E-Cigarettes White

Prevalence of cigar use use did not differ between black and white students, but white students were more likely to report past 30 day use of cigarettes, smokeless tobacco, and e-cigarettes. Analyses by race revealed similar prevalence rates for white students across products (cigarettes: 17.5%, 95% CI [13.2, 21.8]); cigars: 9.5%, 95% CI [7.5, 11.5]; smokeless tobacco: 13.3%, 95% CI [10.7, 15.9]; and electronic cigarettes: 13.6%, 95% CI [9.9, 17.3]). Black students, however, were more likely to use cigarettes (7.1%, 95% CI [5.4, 8.8]), cigars (11.0%, 95% CI [7.8, 14.2]), or e-cigarettes (6.4%, 95% CI [4.7, 8.1]) than smokeless tobacco (2.7%, 95% CI [1.6, 3.8]). Discussion The social climate for tobacco control in Mississippi experienced several important changes over the past 16 years. Statewide tobacco prevention programs have educated Mississippi youth about the harms of tobacco and prepared them to resist tobacco use, an increase to the state cigarette tax has raised the cost of a pack of cigarettes, and smokefree ordinances at the municipal level deter youth initiation of tobacco use. Each of these social climate shifts is strongly linked to reductions in youth smoking.3-6 The introduction and aggressive marketing of unregulated and untaxed e-cigarettes, however, has added another factor to the social climate. Cigar and cigarette smoking decreased dramatically as these social climate shifts were implemented over the past 16 years. These declines occurred across sex, grade, and race, and will lead to long-term healthcare savings and increased lifespan for young Mississippians.1 However, use of smokeless tobacco has remained constant and e-cigarette use experienced substantial growth over the past year. Tobacco prevention efforts should consider the current landscape of product use. Overall, Mississippi high school students are equally as likely to use e-cigarettes, smokeless tobacco, and cigars as to smoke cigarettes. Prevention programs, tobacco control policies, and clinical

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counseling could more effectively reduce tobacco use by targeting each of these products. Efforts to reduce tobacco use among females and black students could place less emphasis on smokeless tobacco, than on other tobacco products.

Acknowledgement We appreciate the efforts of Rhonda Lampkin, Partnership for a Healthy Mississippi, and Roy Hart, Office of Tobacco Control, Mississippi State Department of Health, to review the Introduction of this article.

Reductions in the prevalence of youth combustible tobacco use following Mississippi’s tobacco prevention efforts are exciting, but the stagnant prevalence of smokeless tobacco use and increased e-cigarette use is alarming. Although noncombustible tobacco products are less harmful than those that are combustible, noncombustible tobacco products are not safe alternatives.13,14 Smokeless tobacco use presents numerous health risks, including cancer, oral disease, and heart disease,1,15 and emerging research illustrates risks for e-cigarette use.13,16-18 Electronic cigarettes can produce volatile organic compounds, heavy metals, and other toxins in the aerosol released, albeit in lower levels than combustible tobacco.18-21 E-cigarettes also have the potential for toxic effects from inhaled flavorings.22 Although many of the flavors used in e-cigarettes have been categorized as Generally Recognized as Safe (GRAS) for human consumption, this classification applies only to ingestion of these products, not inhalation.

References

In addition to the potential harm from inhaling e-cigarette aerosol, use of these products could lead to use of more harmful combustible tobacco products. Two recent studies of youth and young adults found that never-smoking e-cigarette users were much more open than nonusers to try cigarette smoking,23,24 while a study of southern California 11th and 12th graders suggested that a favorable social climate towards e-cigarettes could lead to the renormalization of tobacco use.25 Tobacco prevention programs have successfully reduced rates of combustible tobacco use and need to proactively counteract favorable perceptions created by unregulated marketing. Conclusion Over the past two decades, Mississippi has implemented several programs and policies to reduce tobacco use among youth. The state has had remarkable success in decreasing cigarette and cigar smoking. However, smokeless tobacco use has not changed and e-cigarettes are becoming increasingly popular. Currently, Mississippi youth are at equal risks for cigarette, cigar, smokeless tobacco, or electronic cigarette use. Tobacco prevention efforts and clinician counseling should address each of these products rather than focus primarily on cigarettes. Moreover, regulatory action to prohibit e-cigarette use in places where smoking is not allowed and eliminate flavors and marketing that target youth are needed to curb the growth of e-cigarette use among youth. Finally, e-cigarettes are not subject to a state tobacco tax, while smokeless tobacco and cigars have a much lower tax burden than cigarettes. Equalizing the tax on each of these products could reduce the appeal of the less expensive products to youth. n Support for this article has been provided in part by the Office of Tobacco Control of the Mississippi State Department of Health and the Partnership for a Healthy Mississippi. The information, views, and opinions contained herein are those of the authors and do not necessarily reflect the views and opinions of these organizations.

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1. U.S. Department of Health and Human Services. The health consequences of smoking - 50 years of progress: A report of the Surgeon General.; 2014. 2. U.S. Department of Health and Human Services. Preventing tobacco use among youth and young adults: A report of the Surgeon General.; 2012. 3. Fichtenberg CM, and Glantz SA. Effect of smoke-free workplaces on smoking behaviour: systematic review. Bmj. 2002;325(7357):188. 4. Tauras JA, Chaloupka FJ, Farrelly MC, Giovino GA, Wakefield M, Johnston LD, O’Malley PM, Kloska DD, and Pechacek TF. State tobacco control spending and youth smoking. American Journal of Public Health. 2005;95(2):338-344. 5. Levy DT, Chaloupka F, and Gitchell J. The effects of tobacco control policies on smoking rates: a tobacco control scorecard. Journal of Public Health Management and Practice. 2004;10(4):338-353. 6. Wakefield MA, Chaloupka FJ, Kaufman NJ, Orleans CT, Barker DC, and Ruel EE. Effect of restrictions on smoking at home, at school, and in public places on teenage smoking: cross sectional study. BMJ. 2000;321(7257):333-337. 7. Givel M. Politcal Reform and Tobacco Control Policy Making in Mississippi From 1990 to 2001. 2002:1-61. 8. OSH-Graphics. Best Practices for comprehensive tobacco control programs. 1999. 9.  Summary of 100% Smokefree State Laws and Population Protected by 100% U.S. Smokefree Laws. Summary of 100% Smokefree State Laws and Population Protected by 100% U.S. Smokefree Laws. 2015. 10. Orzechowski, and Walker. The Tax Burden on Tobacco, Volume 49, 2014. 11. Chaloupka F, Levy D, and Huang J. The Impact of Tax and Smoke-Free Air Policy Changes. Robert Wood Johnson Foundation; 2011. 12. Chaloupka FJ, Yurekli A, and Fong GT. Tobacco taxes as a tobacco control strategy. Tob Control. 2012;21(2):172-80. doi:10.1136/tobaccocontrol-2011-050417. 13. McGrath-Morrow SA, Hayashi M, Aherrera A, Lopez A, Malinina A, Collaco JM, Neptune E, Klein JD, Winickoff JP, Breysse P, Lazarus P, and Chen G. The effects of electronic cigarette emissions on systemic cotinine levels, weight and postnatal lung growth in neonatal mice. PLoS One. 2015;10(2):e0118344. doi:10.1371/ journal.pone.0118344. 14.  Jensen RP, Luo W, Pankow JF, Strongin RM, and Peyton DH. Hidden Formaldehyde in E-Cigarette Aerosols. N Engl J Med. 2015;372(4):392-394. doi:10.1056/NEJMc1413069. 15.  IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans.; 2007. 16. Bekki K, Uchiyama S, Ohta K, Inaba Y, Nakagome H, and Kunugita N. Carbonyl Compounds Generated from Electronic Cigarettes. Int J Environ Res Public Health. 2014;11(11):11192-11200. doi:10.3390/ijerph111111192. 17. Callahan-Lyon P. Electronic cigarettes: human health effects. Tob Control. 2014;23 Suppl 2:ii36-ii40. doi:10.1136/tobaccocontrol-2013-051470. 18. Schober W, Szendrei K, Matzen W, Osiander-Fuchs H, Heitmann D, Schettgen T, Jörres RA, and Fromme H. Use of electronic cigarettes (e-cigarettes) impairs indoor air quality and increases FeNO levels of e-cigarette consumers. Int J Hyg Environ Health. 2013. doi:10.1016/j.ijheh.2013.11.003. 19. Czogala J, Goniewicz ML, Fidelus B, Zielinska-Danch W, Travers MJ, and Sobczak A. Secondhand Exposure to Vapors From Electronic Cigarettes. Nicotine Tob Res. 2013. doi:10.1093/ntr/ntt203. 20. Goniewicz ML, Knysak J, Gawron M, Kosmider L, Sobczak A, Kurek J, Prokopowicz A, Jablonska-Czapla M, Rosik-Dulewska C, Havel C, Jacob P, and Benowitz N. Levels of selected carcinogens and toxicants in vapour from electronic cigarettes. Tob Control. 2013. doi:10.1136/tobaccocontrol-2012-050859.


21.  Schripp T, Markewitz D, Uhde E, and Salthammer T. Does e-cigarette consumption cause passive vaping? Indoor Air. 2013;23(1):25-31. doi:10.1111/ j.1600-0668.2012.00792.x. 22. Barrington-Trimis JL, Samet JM, and McConnell R. Flavorings in Electronic Cigarettes: An Unrecognized Respiratory Health Hazard? JAMA. 2014. doi:10.1001/jama.2014.14830. 23. Coleman BN, Apelberg BJ, Ambrose BK, Green KM, Choiniere CJ, Bunnell R, and King BA. Association Between Electronic Cigarette Use and Openness to Cigarette Smoking Among U.S. Young Adults. Nicotine Tob Res. 2014. doi:10.1093/ ntr/ntu211. 24. Bunnell RE, Agaku IT, Arrazola RA, Apelberg BJ, Caraballo RS, Corey CG, Coleman BN, Dube SR, and King BA. Intentions to Smoke Cigarettes Among Never-Smoking U.S. Middle and High School Electronic Cigarette Users, National Youth Tobacco Survey, 2011-2013. Nicotine Tob Res. 2014. doi:10.1093/ ntr/ntu166. 25. Barrington-Trimis JL, Berhane K, Unger JB, Cruz TB, Huh J, Leventhal AM, Urman R, Wang K, Howland S, Gilreath TD, Chou CP, Pentz MA, and McConnell R. Psychosocial Factors Associated With Adolescent Electronic Cigarette and Cigarette Use. Pediatrics. 2015. doi:10.1542/peds.2015-0639.

Author Information Data Management Coordinator, Mississippi Health Policy Research Center, Social Science Research Center, Mississippi State University. Emily McClelland performs analyses and manages various datasets and projects

related to the prevalence of youth and adult tobacco use in Mississippi. These datasets and projects are surveillance services for the Office of Tobacco Control of the Mississippi State Department of Health (Ms. McClelland). Project Coordinator, Social Science Research Center, Mississippi State University. Nell Valentine leads the Mississippi Youth Tobacco Survey and is the Co-Principal Investigator for the Tobacco Surveillance project for the Office of Tobacco Control of the Mississippi State Department of Health (Ms. Valentine). Associate Professor, Department of Psychology & Associate Director, Social Science Research Center, Mississippi State University. Robert McMillen serves as the Principal Investigator for the Data Sets Project of the American Academy of Pediatrics Julius B. Richmond Center of Excellence and provides surveillance services for the Office of Tobacco Control of the Mississippi State Department of Health (Dr. McMillen). Corresponding Author Robert McMillen, One Research Park, Suite 103, Starkville, MS, 39759 (rcm19@msstate.edu)

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A R T I C L E S

Is Vitamin D Deficiency Contributing to Mississippi’s Persistent Black-White Disparity in Preterm Birth? CHARLENE COLLIER, MD, MPH, MHS AND ALAN PENMAN, MBCHB, PHD, MPH

Key words: Infant mortality; preterm birth; vitamin D In Mississippi there is a considerable racial disparity in the infant mortality rate (IMR): in 2014 the IMR was 5.9 deaths per 1,000 live births in white women and 11.2 deaths per 1,000 live births in black women.1 Although the IMR in Mississippi has decreased markedly over the decades in both white and black women, the racial disparity persists, with black women consistently having an IMR that is more than double that of white women (Figure). The specific reasons for this intractable disparity remain unclear despite decades of research and improvements in socioeconomic conditions, education levels, and health care access. Preterm birth is a primary contributor to infant mortality, with significantly higher rates among black women. In recent years evidence has emerged that maternal vitamin D deficiency may be a risk factor for preterm birth and other adverse pregnancy outcomes, and that differences in the prevalence of vitamin D deficiency between black and white women may account for at least part of the disparity in IMR.2 Below we set out the evidence and rationale for this thinking. FIGURE. IMR- Mississippi 1980-2013 (3 year moving average)

Figure. Infant mortality rate (IMR), Mississippi 1980-2013 (3-year moving average) Black (upper axis)

White (lower axis)

30.0

IMR per 1,000 live births

25.0

20.0

15.0

10.0

5.0

0.0 1980 1982 1984 1986 1988 1990 1992 1994 1996 1998 2000 2002 2004 2006 2008 2010 2012 2014

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Preterm birth as a major cause of infant mortality in Mississippi Mississippi’s high IMR is in large part driven by a higher than average rate of preterm births (defined as birth <37 gestational weeks) – 12.9% in 2014,1 compared to the 9.6% national average. In Mississippi, over the period 2010-2014, 16.0% of births to black women were premature compared to 11.3% for white women. The lower the gestational age of an infant at birth, the greater the risk for medical complications including death. In Mississippi in 2012, the IMR among infants born at less than 37 weeks of gestation was 31.6 per 1,000, compared to 4.4 among infants born at 37‐39 weeks of gestation.1 Pregnant women (particularly black women) and vitamin D deficiency Vitamin D deficiency affects 94-97% of pregnant black women.3-5 In the general population, vitamin D deficiency has increased in prevalence due to low vitamin D intake in the diet and diminished exposure to UV sunlight through protective sun behaviors.6,7 Among pregnant women, vitamin D deficiency persists in spite of prenatal vitamin intake because 25-hydroxyvitamin D (25(OH)D) levels found in prenatal vitamins are insufficient to correct preexisting deficient levels.3,8 The problem is compounded by obesity, which is common in Mississippi. Women with a body mass index greater than 30 are at increased risk of vitamin D deficiency because adipose tissue serves as a repository for vitamin D that does not get into the circulation.9 In 2009 an estimated 48.6% of pregnant women in Mississippi were overweight or obese prior to pregnancy.10 Vitamin D and the maternal-fetal immune response to infection There is growing evidence that vitamin D deficiency influences the risk of preterm birth through its effect on the maternal immune system. A key function of vitamin D during pregnancy is to support normal immune responses and thereby minimize the detrimental effects of inflammation at the fetal–maternal interface. Vitamin D functions within the placenta as a modulator of cytokine production and the immune response to infection. In general, 1,25-dihydroxyvitamin D (1,25(OH)2D) reduces the activity of the adaptive immune system and enhances the activity of the innate immune system.11-13 A deficiency in vitamin D is, therefore, thought to allow for inflammation


in response to bacterial infection that leads to preterm labor or preterm rupture of amniotic membranes. Vitamin D deficiency, bacterial vaginosis, and inflammationmediated preterm birth Pregnant women with low 25(OH)D levels have an increased risk of bacterial vaginosis and lower birth weight infants.14,15 Bacterial vaginosis, characterized by overgrowth of particular aerobic and anaerobic vaginal flora and elevation of the vaginal pH, increases the risk of preterm delivery >2-fold.16-18 Placental colonization by bacterial species common in bacterial vaginosis has been linked to an increased risk of premature birth.19-21 Black women, particularly low-income women, have higher rates of bacterial vaginosis both before and during pregnancy.18 Vitamin D deficiency is more strongly associated with bacterial vaginosis during pregnancy in black women than White women.18 This association is believed to translate to a higher risk of inflammation-mediated spontaneous preterm birth. In a recent study including women of multiple ethnicities, among nonwhite mothers, but not white mothers, serum 25(OH)D levels <30 nmol/L were associated with increased risk of spontaneous preterm birth. This association was driven by inflammation-mediated cases of spontaneous preterm birth and spontaneous preterm birth cases without placental lesions.21 Vitamin D deficiency and preterm birth In a case-cohort study of 3,453 women attending a teaching hospital in Pittsburgh, PA, the incidence of preterm birth at less than 37 weeks of gestation was 11.3% in women with a serum 25(OH)D levels <50 nmol/L and 7.3% in women with a serum 25(OH)D levels ≥75 nmol/L; the adjusted risk of preterm birth was 80% higher in the former compared to the latter.22 In a multicenter U.S. cohort of twin pregnancies, preterm birth at less than 35 weeks of gestation occurred in 49.4% of women with 25(OH)D levels concentrations less than 75 nmol/L compared with 26.2% among those with concentrations of ≥75 nmol/L; after adjustment, maternal 25(OH)D concentration of ≥75 nmol/L was associated with a 60% reduction in the odds of preterm birth compared with concentrations less than 75 nmol/L.23 Among nonwhite mothers serum 25(OH)D levels of 30-<50, 50-<75, and ≥75 nmol/L were associated with reductions of 1.0-1.6 cases of spontaneous preterm birth per 100 live births and 20%-30% reductions in risk of spontaneous preterm birth compared with 25(OH)D levels less than 30 nmol/L. This same association was not seen for White mothers with similar serum 25(OH)D levels.21 Two other recent studies reported no association between maternal vitamin D levels at 10-14 weeks24 or 15-21 weeks of gestation25 and preterm birth. Schneuer et al studied 5,109 women attending first trimester Down Syndrome screening in Australia.24 Thorp et al studied women with prior spontaneous preterm birth participating in a randomized trial of omega-3 fatty acid supplementation to prevent recurrent preterm birth.25 There are a number of reasons that could account for the failure to find an association between maternal vitamin D levels and preterm birth in these studies. For example, Schneuer et al admit that “our findings are relevant to sun-rich latitudes with a low

prevalence of vitamin D deficiency and may not be applicable to other settings.”24 In the study of Thorp et al, the majority of the mothers did not have serum 25(OH)D concentrations <50 nmol/l.25 Preterm birth: a syndrome with many causes and phenotypes Preterm birth is a complex syndrome with a heterogeneous pathophysiology, yet most studies have not attempted (or been able) to distinguish between different subtypes. The need to identify more homogenous phenotypes is now recognized. For example, in an international multiethnic, cross-sectional study of 60,058 births (including 5,828 preterm births), Barros et al identified 12 preterm birth phenotypes associated with different patterns of neonatal outcomes. In 22% of all preterm births, parturition started spontaneously and was not associated with any of the phenotypic conditions considered.26 Future studies will need to focus more on specific subtypes (such as spontaneous preterm birth with no obvious risk factors such as extrauterine infection, pre-eclampsia, multiple pregnancy, or fetal anomaly) and be powered to detect differences in preterm birth rates according to maternal vitamin D status. Clinical trials of vitamin D supplementation in pregnant women The few clinical trials of maternal supplementation with vitamin D during pregnancy conducted to date have confirmed the safety and efficacy of supplementation, but were not powered to detect reductions in preterm birth rates.27-30 There was suggestive evidence of a reduction in risk of infection, preterm labor, and preterm birth as supplementation dose increased.29,30 Future randomized clinical trials of maternal vitamin D supplementation to prevent preterm birth should have sufficient power to detect differences in preterm birth rates between trial arms. However, these should probably be conducted only after agreement has been reached on defining more homogenous phenotypes, as discussed above. Significance for Mississippi, and next step Confirmation of an association between vitamin D deficiency in pregnancy and preterm birth has major public health implications for antenatal care and infant mortality in Mississippi: widespread antenatal vitamin D screening and supplementation among pregnant women are relatively simple and inexpensive interventions that could reduce the intractable racial disparity in preterm birth and infant mortality in the state. There are no population data available for Mississippi on the prevalence of vitamin D deficiency in pregnancy; data are also lacking on the association between vitamin D levels in pregnancy and the risk of preterm birth in Mississippi women. As Mississippi has the highest rate of preterm birth in the country and as there is strong biologic plausibility for a link between vitamin D deficiency and preterm birth, it is both important and urgent that we obtain state-specific populationbased data on vitamin D levels in pregnant women and determine whether low vitamin D levels in pregnancy increase the risk of preterm birth, particularly in black women. n

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Author Information Alan Penman, MBChB, PhD, MPH, Professor, Center of Biostatistics and Bioinformatics and SOM-Preventive Medicine, University of Mississippi Medical Center, Jackson, MS. Charlene Collier, MD, MPH, MHS, Assistant Professor, SOM-Obstetrics and Gynecology, University of Mississippi Medical Center, Jackson, MS, Perinatal Health Policy and Research Consultant, Mississippi State Department of Health, Jackson, MS. References 1.  Mississippi Infant Mortality Reports. Available at: http://msdh.ms.gov/ msdhsite/index.cfm/29,0,299,324,html. Accessed 12/13/15. 2. Bodnar LM, Simhan HN. Vitamin D may be a link to black-white disparities in adverse birth outcomes. Obstet Gynecol Surv. 2010;65(4):273-84. 3. Ginde AA, Sullivan AF, Mansbach JM, Camargo CA Jr. Vitamin D insufficiency in pregnant and nonpregnant women of childbearing age in the US. Am J Obstet Gynecol. 2010;202(5):436.e1-8. 4. Hamilton SA, McNeil R, Hollis BW, Davis DJ, Winkler J, Cook C, Warner G, Bivens B, McShane P, Wagner CL. Profound Vitamin D Deficiency in a Diverse Group of Women during Pregnancy Living in a Sun-Rich Environment at Latitude 32°N. Int J Endocrinol. 2010;2010:917428. 5. Johnson DD, Wagner CL, Hulsey TC, McNeil RB, Ebeling M, Hollis BW. Vitamin D deficiency and insufficiency is common during pregnancy. Am J Perinatol. 2011;28(1):7-12. 6. Looker AC, Pfeiffer CM, Lacher DA, Schleicher RL, Picciano MF, Yetley EA. Serum 25-hydroxyvitamin D status of the US population: 1988–1994 compared with 2000–2004. Am J Clin Nutr. 2008;88:1519–27.

18. Foxman B, Wen A, Srinivasan U, Goldberg D, Marrs CF, Owen J, Wing DA, Misra D. Mycoplasma, bacterial vaginosis-associated bacteria BVAB3, race, and risk of preterm birth in a high-risk cohort. J Obstet Gynecol. 2013: S00029378(13)01041-7. 19. Onderdonk AB, Hecht JL, McElrath TF, Delaney ML, Allred EN, Leviton A; ELGAN Study Investigators. Colonization of second trimester placenta parenchyma. Am J Obstet Gynecol. 2008; 199(1): 52.e1–52.e10. 20. Fichorova RN, et al. Maternal microbe-specific modulation of inflammatory response in extremely low-gestational-age newborns. mBio2. 2011(1):e0028010). 21. Bodnar LM, Klebanoff MA, Gernand AD, Platt RW, Parks WT, Catov JM, Simhan HN. Maternal Vitamin D Status and Spontaneous Preterm Birth by Placental Histology in the US Collaborative Perinatal Project. Am J Epidemiol. 2014;179(2):168-76. 22. Bodnar LM, Platt RW, Simhan HN. Early-pregnancy vitamin D deficiency and risk of preterm birth subtypes. Obstet Gynecol. 2015;125(2):439-47. 23. Bodnar LM, Rouse DJ, Momirova V, Peaceman AM, Sciscione A, Spong CY, Varner MW, Malone FD, Iams JD, Mercer BM, Thorp JM Jr, Sorokin Y, Carpenter MW, Lo J, Ramin SM, Harper M; Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) Maternal-Fetal Medicine Units (MFMU) Network. Maternal 25-hydroxyvitamin D and preterm birth in twin gestations. Obstet Gynecol. 2013;122(1):91-8. 24. Schneuer FJ, Roberts CL, Guilbert C, Simpson JM, Algert CS, Khambalia AZ, Tasevski V, Ashton AW, Morris JM, Nassar N. Effects of maternal serum 25-hydroxyvitamin D concentrations in the first trimester on subsequent pregnancy outcomes in an Australian population. Am J Clin Nutr. 2014;99(2):287-95. 25. Wetta LA, Biggio JR, Cliver S, Abramovici A, Barnes S, Tita AT. Is midtrimester vitamin D status associated with spontaneous preterm birth and preeclampsia? Am J Perinatol. 2014;31(6):541-6.

8. Heaney RP, Davies KM, Chen TC, Holick MF, Barger-Lux MJ. Human serum 25-hydroxycholecalciferol response to extended oral dosing with cholecalciferol. Am J Clin Nutr. 2003;77:204–10.

26. Barros FC, Papageorghiou AT, Victora CG, Noble JA, Pang R, Iams J, Cheikh Ismail L, Goldenberg RL, Lambert A, Kramer MS, Carvalho M, CondeAgudelo A, Jaffer YA, Bertino E, Gravett MG, Altman DG, Ohuma EO, Purwar M, Frederick IO, Bhutta ZA, Kennedy SH, Villar J; International Fetal and Newborn Growth Consortium for the 21st Century. The distribution of clinical phenotypes of preterm birth syndrome: implications for prevention. JAMA Pediatr. 2015;169(3):220-9.

9. Wagner CL, Taylor SN, Dawodu A, Johnson DD, Hollis BW. Vitamin D and its role during pregnancy in attaining optimal health of mother and fetus. Nutrients. 2012;4(3):208-30.

27. Hollis BW, Johnson D, Hulsey TC, Ebeling M, Wagner CL. Vitamin D supplementation during pregnancy: double-blind, randomized clinical trial of safety and effectiveness. J Bone Miner Res. 2011;26(10):2341-57.

10. Office of Health Data and Research, Mississippi State Department of Health. Mississippi PRAMS Surveillance Report, Year 2009 Births, Jackson, MS: Mississippi Department of Health, 2013. Available at: http://msdh.ms.gov/ msdhsite/_static/resources/5604.pdf. Accessed 4/23/15.

28. Thorne-Lyman A, Fawzi WW. Vitamin D during pregnancy and maternal, neonatal and infant health outcomes: a systematic review and meta-analysis. Paediatr Perinat Epidemiol. 2012;26 Suppl 1:75-90.

7. Ginde AA, Liu MC, Camargo CA Jr. Demographic differences and trends of vitamin D insufficiency in the US population, 1988-2004. Arch Intern Med. 2009;169(6):626-32.

11. Shin JS, Choi MY, Longtine MS, Nelson DM. Vitamin D effects on pregnancy and the placenta. Placenta. 2010;31(12):1027-34. 12. Liu NQ, Hewison M. Vitamin D, the placenta and pregnancy. Arch Biochem Biophys. 2012;523(1):37-47. 13.  Hewison M. An update on vitamin D and human immunity. Clinical Endocrinology. 2012;76, 315–325. 14. Bodnar LM, Krohn MA, Simhan HN. Maternal vitamin D deficiency is associated with bacterial vaginosis in the first trimester of pregnancy. J Nutr. 2009;139(6):1157-61. 15. Hensel KJ, Randis TM, Gelber SE, Ratner AJ. Pregnancy-specific association of vitamin D deficiency and bacterial vaginosis. Am J Obstet Gynecol. 2011;204(1):41.e1-9. 16. Leitich H, Bodner-Adler B, Brunbauer M, Kaider A, Egarter C, Husslein P. Bacterial vaginosis as a risk factor for preterm delivery: a meta-analysis. Am J Obstet Gynecol. 2003;189(1):139-47. 17. Donders GG, Van Calsteren K, Bellen G, Reybrouck R, Van den Bosch T, Riphagen I, Van Lierde S. Predictive value for preterm birth of abnormal vaginal flora, bacterial vaginosis and aerobic vaginitis during the first trimester of pregnancy. BJOG. 2009;116(10):1315-24.

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29. Wagner CL, McNeil R, Hamilton SA, Winkler J, Rodriguez Cook C, Warner G, Bivens B, Davis DJ, Smith PG, Murphy M, Shary JR, Hollis BW. A randomized trial of vitamin D supplementation in 2 community health center networks in South Carolina. Am J Obstet Gynecol. 2013;208(2):137.e1-13. 30. Wagner CL, McNeil RB, Johnson DD, Hulsey TC, Ebeling M, Robinson C, Hamilton SA, Hollis BW. Health characteristics and outcomes of two randomized vitamin D supplementation trials during pregnancy: a combined analysis. J Steroid Biochem Mol Biol. 2013;136:313-20.


S P E C I A L

A R T I C L E

My Immigration Story HEDDY-DALE MATTHIAS, MD

I

’m not certain when I first met Sofia or how I came to know her.  She has been my once-a-week housekeeper for around five years.  She is paid well and does a good job, including my laundry.  My house is large, multileveled, uncluttered, and mostly unused.  My Golden Retriever, Luka, adds his abundant shedding blonde hair to her labors.   Sofia usually cleans alone, but sometimes her mother, Emma, accompanies her to help.  Sofia is twenty-four, and her mother, Emma, is fifty-five.  Sofia has a threeyear old daughter, Elisa Cruz, who was born in the United States.  Sofia was three when her mother brought her and her five-year-old sister, Fernanda, to the U.S.  Although her mother was here legally on a visa for a while, she sent for Sofia and her sister after their father died in Mexico and the girls entered the U.S. without authorization. 

According to Sofia, her father was a well-to-do attorney in Mexico.  She says that his siblings were able to finesse the legal system in Mexico to garner the bulk of his estate, leaving his immediate family with nothing but their house.  Emma sold the house and came to the U.S. on a visa, and subsequently brought her two daughters here.    Emma entered into a new live-in relationship in Mississippi and her partner became a step-father, of sorts, to her children.  However, Emma’s partner proved to be an unfit alcoholic, and frequently assaulted her. At that time, Emma consulted Patricia Ice, an immigration attorney in Jackson, Mississippi.  By this time Emma had overstayed her authorized time limit in the United States and she was living with expired immigration documents in Mississippi.  Ms. Ice was able to help convince the United States Citizenship and Immigration Services

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(USCIS), a unit of the Department of Homeland Security, to allow Emma to stay legally in this country after the conviction, arrest, and deportation of her abusive partner.  Emma is now a lawful permanent resident.  She would one day like to become a citizen, but she must wait five years before she can even apply.  After that she must wait a few more months to pass naturalization tests and take the oath of allegiance.   Because Sofia and her sister came into this country without authorization, they were in undocumented status for a long time. For that reason, they were unable to visit relatives in Mexico.  Of course, since they are Mexican citizens, they could go to Mexico at any time.  But they would not have been able to return to the United States.  The girls were students in school in metro Jackson and their mother had made a life for them here.  Leaving would have disrupted everything they had all worked for.  In June 2012 President Barack Obama issued an executive order called the Deferred Action for Childhood Arrivals (DACA) program.  Pursuant to this executive order Sofia was able to get an employment authorization card from the USCIS for two years with an option to renew. Although she continues to have permission to work here, according to USICS, Sofia has no immigration status, but is considered lawfully present in the U.S. If this sounds confusing, it is.  Her sister, Fernanda, has U nonimmigrant status because she, too, like her mother, was a victim of severe domestic violence.    I thought, until recently, that Sofia was married to the father of her daughter, but she is not.  She was vague when I asked her why she wasn’t, and suggested that they wanted to marry in Mexico, but couldn’t return there at this time.  The father of her daughter, Elisa Cruz, is undocumented in the U.S., and works for cash for his brother who runs a framing crew in the Jackson area. I suspect they cannot marry here because of his unauthorized status.   Sofia is presently enrolled at Hinds Community College in a paralegal program, and, according to her, receives “straight A” grades.  Since Sofia does not have lawful permanent residence status, she must pay almost twice the tuition that American citizen students pay to attend Hinds.  This is a cruel irony because Sofia attended and graduated from public elementary, middle and high schools in Mississippi like most of her community college classmates.  As a result of the U.S. Supreme Court case Plyler v. Doe (1982) all children, regardless of immigration status, have the constitutional right to attend U.S. public K-12 schools. The Mississippi Immigrants Rights Alliance (MIRA), where Patricia Ice is the legal project director, in collaboration with other organizations, is actively advocating for tuition equity, which would allow undocumented college students who attended high school in Mississippi to pay the same tuition as permanent resident and American citizen students. Earlier this year during the regular Mississippi state legislative session, a state representative introduced a bill for tuition equity.  The committee chair refused to bring the bill to a vote; therefore, it did not move forward.  According to the National Conference of State Legislatures, twenty states offer in-state tuition to post-secondary unauthorized immigrant students.   When Sofia is finished with her paralegal studies, she plans to attend Jackson

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State University to compile credits to apply for law school; her ultimate goal is to become an attorney like her father.  I have told her I would do anything possible to help her fulfill her dream.  Sofia is uncertain whether she’d like to practice law in the U.S. or Mexico.   As long as Sofia remains unmarried, her mother, Emma, as a lawful permanent resident or a U.S. citizen, can petition for Sofia to also become a permanent resident.  However, after the petition is filed, Sofia could wait up to 21 years to become a permanent resident. Her sister Fernanda’s “U nonimmigrant status (or U visa)” allows her to apply for lawful permanent residence this year.   Sofia told me that she is ambivalent about whether she wants to become a U.S. citizen and remain here, or, at some time in the future, return to Mexico.  If she ever becomes a U.S. citizen, according to current policy, Sofia can also keep her Mexican citizenship.  I asked her why she remains here and doesn’t return to Mexico now.  She replied, “Presently, there is no work for me in Mexico, and I couldn’t make the type of money that I and my family make here.  If I returned to Mexico now, I probably would have to wait at least five years to re-enter the U.S. to see my mother.  In addition, I left Mexico when I was three and I don’t have a home there, nor do I know anything about Mexico, although I would like to see my relatives and extended family.”   I have grown to love and admire Sofia and her mother.  I trust them both with the keys to my house and everything in it.  Most of the time no one is in the house, or even in town, when she comes to clean.  When I broke my femur last year and was depressed and disconsolate about being in a wheelchair and confined to one room in my house for six months, Emma would often volunteer to stay overnight to keep me company and lighten my spirits.  She would often pray for my recovery. Sofia and Emma both are lovely, kind, intelligent, spiritual, and, especially, hard-working women.   Why have I taken the time to write about Sofia and Emma?   Prior to knowing them, and, actually, until recently, I have been a severe “hardliner” on illegal immigration, especially Hispanic immigration from Mexico.  I have often said, “I love immigrants.  My father was a German Jew who was fortunate to immigrate here prior to the Nazi takeover of Germany, before Kristallnacht in 1938, before the SS began spying on everyone, and before the concentration camps began operations, incinerating some of my relatives.   But our country should welcome all immigrants equally, irrespective of geography.  Mexicans should not have a “leg up” because of the serendipity of their geography.  Immigrants must come here legally, in an orderly fashion, and from countries far and wide.  Immigrants must be fully vetted prior to acceptance.  And those who choose to walk across bridges, or swim rivers, or be shuttled in dark vans should not then or now be able to become citizens ahead of others who legally apply for citizenship.”   I still do believe that quote.  I do, but…What are we to do with all the Sofias and Emmas in this country?  Sofia knows nothing of Mexico, as she’s been raised and schooled here her whole life.  Her daughter, Elisa Cruz, is a three-year old U.S. citizen.  Sofia did not come here to have a child. She had a child in the same


fashion and for the same reasons as most U.S. women do after living here for the entirety of her adult life. As a U.S. citizen, Elisa Cruz receives Medicaid and SNAP like many other Mississippi children of hard-working parents.

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Am I still concerned about the porosity of our borders? Absolutely yes. Am I adamant that the U.S. must control its borders and immigration process? Yes. Am I angry that the federal government has allowed unauthorized and seemingly unlimited immigration for at least three decades? Yes. But my experience with Sofia, Emma, and Elisa Cruz has moderated and nuanced my understanding of the complexities of “illegal immigration” by putting human faces on the problem.

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Acknowledgment: The women in this article are compilations of many undocumented immigrants. All names and facts have been altered in protection. Heddy-Dale Matthias, MD is an anesthesiologist in Jackson and a new member of the Journal MSMA Editorial Advisory Board. For further information you can visit her Facebook page at http://www.facebook.com/profile. php?id=556186285

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This is the first installment in a spotlight series on the MSMA Physician Leadership Academy class of 2016.

Jonathan Jones, MD As a freshman at the University of Florida, Dr. Jonathan Jones had plans to become a teacher. Those plans began to change when he joined some pre-med classmates for an afternoon of volunteering at a free medical clinic. “The undergraduate students took some brief histories on the patients and vital signs. Though I knew nothing about medicine, I loved it. I realized that doctors do a lot of teaching, not only students but patients as well.” Today, he continues to enjoy teaching and spending time with patients as an associate professor and program director of Emergency Medicine at the University of Mississippi Medical Center. Finding his path as a physician was not always easy: Dr. Jones hated medical school and regrets not having a mentor during those four years. As a resident at UMMC, he found guidance from Dr. LouAnn Woodward, who was the residency program director at the time and is now the Vice-Chancellor. She helped him navigate changing residencies from Internal Medicine to Emergency Medicine, which he found was a much better fit. “I realized that my favorite part of medicine was the diagnosis. In Emergency Medicine, we deal with complaints (chest pain, abdominal pain, etc.) instead of diseases (heart attacks, appendicitis, etc.). I love trying to figure out what is wrong. I also enjoy the diversity of pathology and of patients and that I get to treat everyone without regard to their finances, insurance, or anything else.” Dr. Jones has always enjoyed the education component 340

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of medicine, and he entered academia immediately after completing residency. As a teacher at heart, the most satisfying aspect of his job is working with the residents. “My proudest moment every year is resident graduation. Seeing an eager, novice student or intern develop into a competent physician is incredibly satisfying and is definitely my greatest achievement.” In addition to his work with students and residents, Dr. Jones serves as a mentor to two assistant professors in the Division of Emergency Medicine in UMMC’s Department of Pediatrics. Through the Physician Leadership Academy, he hopes to gain skills and strategies to better communicate with his colleagues, with policy makers, and with the general public. He is passionate about physician advocacy because, though physicians make decisions for their patients, many of the “big” decisions are made at the Capitol. “Politicians make health policy and this will never change. If we want smart and effective policy, then doctors need to either become politicians or to educate politicians,” he says. “That’s what organized medicine can accomplish. If doctors don’t speak up for and support policy that protects patients, then we are not truly treating our patients appropriately.” Beyond medicine, Dr. Jones loves his wife and their dogs and spends most of his free time running. He’s completed 14 marathons and has several scheduled for 2016, including the Mississippi Blues Marathon which he has run four times.


P R E S I D E N T ’ S

P A G E

Component Society Rescue Program DANIEL P. EDNEY, MD, MSMA PRESIDENT

I

n my inaugural address, I challenged our MSMA to get into the groove of organized medicine. As physicians practicing in an ever-changing healthcare environment, we owe it to each other and to our patients to unite and speak with one voice, which starts in our local component societies.

Each one of our component societies has the potential to serve as a powerhouse within our Association. Unfortunately, the attendance and activity at many of our local county societies has begun (or continued) to wane in the past few years. In my own experience, our component society planned to set up a meeting, and suddenly six months had passed and we still had not put one together. Then, it took another three to get one scheduled. MSMA’s new Component Society Rescue program can help take some of the hassle out of planning a meeting and jumpstart renewed activity so you can once again enjoy the camaraderie with your colleagues at your local component society. MSMA can ease the administrative burden on officers by organizing meetings, sending invitations, lining up speakers and arranging CME events. I believe this can reignite interest in your local component society. MSMA will oversee a smooth transition between officers to avoid the lapse in communication many societies experience during that time. For a flat annual fee, our staff will create a customized Component Society Rescue plan tailored to your society’s needs. Need speakers or CME events? Just let us know how we can help. To learn more or discuss your society’s needs, contact me at President@MSMAonline.com or General Counsel Conner Reeves at CReeves@MSMAonline.com. We welcome your thoughts, questions and ideas.

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E D I T O R I A L

Praise the Lord and Take Away their Ammunition! D. STANLEY HARTNESS, MD; ASSOCIATE EDITOR

T

he all-too-familiar voice of the ubiquitous trial lawyer interrupted the music on my car radio, but the ad that followed made it difficult for me to keep my vehicle between the ditches.

“According to the prestigious Journal of the American Medical Association, medical malpractice is the 3rd leading cause of death in the United States.” Say what? He then proceeded to cite a 2000 JAMA article authored by Barbara Starfield, M.D., of Johns Hopkins School of Public Health in which she stated, “The total estimated number of deaths caused by medical treatment in the U.S. every year is 225,000. Thus, the U.S. medical system is the third leading cause of death, after heart disease and cancer.” In researching this disturbing information, I came across an article from the Center for Medical Consumers attributing the death of Dr. Starfield at age 78 about four years ago to her medical care, implicating the drug Plavix which she had been prescribed following a coronary artery stent. However, it was significant to note she had died while swimming alone in a pool with “pool drowning” listed as the immediate cause of death and “cerebral hemorrhage” as the underlying condition. Interestingly, autopsy also showed a bruise of Dr. Starfield’s scalp to which her husband responded that he suspected a bump against the bend in the pool could have precipitated the bleeding. But I digress. As far as I’ve been able to discover, of all the causes of death in the U.S., the leading top 10 account for about 75% of all deaths, and the top three account for over 50% with the main culprits remaining consistent for at least the last five years: 1. Heart disease 2. Cancer 3. Chronic lower respiratory disease 4. Stroke 5. Accidents 6. Alzheimer disease 7. Diabetes 8. Influenza/pneumonia 9. Kidney disease 10. Suicide

Even though to me this list seems to reflect more accurate (and certainly more palatable) statistics, our medical profession can ill afford a cavalier attitude which leads to statements such as, “Even more significantly, the medical system has played a large role in undermining the health of America” which appeared in the World Health Education Initiative and again was attributed to Dr. Starfield. While blaming the traditional medical paradigm for failure to provide decent medical care for America, the same article then states paradoxically that as many as 40 million people in the U.S. do not have access to this deplorable health care which, it stands to reason, would result ultimately in their deaths anyway! Considering the tremendous strides made in the tort reform arena over the past ten years, we cannot allow a claim set forth by a plaintiff ’s attorney (much less a member of own profession) which purports to list medical malpractice as the third leading cause of death in our country to go unchallenged when this erroneous information cannot be corroborated by any other data, including that from the CDC. Rather, we must continue to produce well-educated, superbly trained young physicians who regularly participate in CME so as to stay abreast of current developments in their specialties. Perhaps even more critical but much less teachable is that special “bedside manner” which has been responsible for defusing many potentially litigious situations. Oh, I still hear the radio ad and my knuckles turn a little white on the steering wheel but I’ve redoubled my efforts to keep my team out of the Top 10.

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The Physician Abuse of Meaningful Use RICHARD D. DESHAZO, MD;1,2 MOLLIE R. DESHAZO, MD;3 AND MATTHEW D. DESHAZO, MD1 from the Departments of Medicine1 and Pediatrics,2 the University of Mississippi Medical Center, Jackson, MS, and the Department of Medicine, School of Medicine University of Alabama-Birmingham, AL3

Another Day Off? We often spend nights and weekends churning away in an electronic medical record (EMR) doing work we did not have time to complete in clinic. Although we have been using an EMR for several years, new clicks and check boxes are endlessly added. Now much of the interaction we have with the EMR has nothing to do with the care of the patients we enjoy providing. We now provide inputs to make billing, collections, audits, and compliance more efficient and fight with prescription writing functions that argue with us. If the inputs we make in the EMR resulted in more efficient and higher quality patient care, the extra work and time might be worth it. So far, we are not convinced.  Another Harangue? This essay seems headed toward another harangue against the EMR.  You may be right or wrong about that. It troubles us that our experiences across institutions are so familiar and disappointing.  Have we entered a phase of learned helplessness in medicine?  EMR Effects on Diagnosis and Treatment Staring at a computer during clinic visits leaves less time to develop rapport and demonstrate empathy for patients, much less pick up all important diagnostic clues. As consultants, we function as diagnosticians. We obtain and review large volumes of medical records from colleagues who ask us for advice and assistance. That used to be fun. Now it is less so. Patient data documented in EMR templates make it difficult to understand the way the patient looked and felt, much less the specific timing and response to the treatment. Moreover, symptoms and signs are difficult to synthesize in check boxes and the ICD-10-compliant problem lists required for billing. In that regard, the problem lists from electronic medical records are often erroneous, as many problems and symptoms are forced to reside in the “not otherwise specified” category because the patients don’t fit available categories. The system of rewards and punishment for EMR users seems to be directed toward generating a list of the most billable conditions and services rather than recording the most accurate, appropriate, and useful clinical information. Fed-Speak: Meaningful Use for Whom? “Meaningful Use” is government jargon, i.e. “Fed-Speak,” for the behaviors physicians and institutions must demonstrate to receive financial assistance to buy EMRs and ultimately to participate in federal health care programs.1 And now, with the progression from Meaningful Use 1 to 2 and eventually to “2.5” and 3, these data, at least some of which are innately erroneous, are being used to generate electronically synthesized narratives and critiques on quality and safety data. Moreover, there is increasing pressure for public disclosure of aggregate data on physician groups and hospitals.2 Obama-Momma? Many doctors we hear blame the whole thing on “Obamacare” and “government intervention,” but we disagree. Electronic medical records were developed and deployed long before the Obama presidency and with the strong support and encouragement of the insurance industry, which was already collecting data on individual physician behavior and patient outcomes to pick physician panels for their health maintenance organizations (HMOs). The proprietary EMRs which now predominate the market (there are now over 700 of them) were developed by American industry using IT personnel working with physician consultants and sold to American health systems, most of which were hospital-based. The EMRs were built with an eye to the financial considerations and a wink and a nod to the medical care. “Cost savings” were promised to sell them but have yet to materialize. And, the decisions as to which systems were purchased were made for the most part by hospital administrators who budgeted for them out of enhanced hospital revenues promised but never materialized. Now we are stuck with EMRs that require endless updates and fixes, and generate huge fixed and variable costs. True, the government did encourage nationwide implementation of and certifies the EMRs it will accept for use with federal insurance programs. However, there was no mandate on how best to meet their requirements in the process of developing specific EMRs.3 344

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It’s All About the Money Anybody who uses the current EMRs knows that their focus is to capture specific information to optimize billing and compliance and not to serve as facilitators of disease diagnosis and treatment. That is far from all bad as money is tight. Physician payment by insurance programs continues to shrink and hospitals have lost disproportionate share (DISH) payments so important in offsetting financial losses in caring for those without private insurance. Hospitals, especially those that provide care to underserved populations, need more money to survive. But studies now show that “physicians spend more time entering data into medical record than any other activity, including direct patient care.”4 The choices in the proprietary institutional templates are often inappropriate to the clinical situation, and the provider medical data collection side of EMRs is expensive, slow, or impossible to fix. Promised features like voice activated operation have never appeared or, where present, have not been supported by the information technology (IT) services from the vendors. And since these automated transcription programs are “add-ons,” not “add-ins,” the EMR vendors have limited interest in optimizing them. The newest EMR systems are already antiques in the modern voice-to-print world. Moreover, since you do not need check boxes when you dictate and check boxes facilitate billing and audits by non-medical personnel, physicians don’t get much support from administrators for requests to implement voice-to-print EMR functions. It’s all about the money. One Answer We think that EMRs have great promise to improve patient care and prevent medical errors. However, the present ones, rather than improving safety, care and patient satisfaction, are guilty of promoting physician and patient dissatisfaction, disinformation, plagiarism, intellectual dishonesty, and huge costs. One answer is interactive voice activated interfaces between the EMR and the provider, like those with Apple’s Siri and Dragon (if improved). Physicians talk faster than we can type or write, and with decent technology we can audit and correct what comes up in text as it pops up and be done with it. Meaningful data for patient care could then become real “Meaningful Use.” Until this occurs (hopefully), EMRs need to be interfaced by scribes, not physicians. “Meaningful Data” for patient care would then become real “Meaningful Use.”   Acknowledgement: The authors thank Leigh Baldwin Skipworth, BA and William F. Brown, BA for their assistance in the preparation of this manuscript. References 1. 2.

MSMA

3. 4.

Fiorillo AB, MD, FACP. Meaningful Use: Stage 1, Stage 2, and Stage 3. Internal Medicine. Meaningful use 2012. Practical Reviews in Internal Medicine (Audio Series) Oakstone Publishing, Birmingham, AL 35242. (Practicalreviews.com). Kidwell RP, JD. EHRs: Data Integrity and common mistakes impacting patient safety. Electronic Health Records, 2015. Practical Reviews in Internal Medicine (Audio Series) Oakstone Publishing, Birmingham, AL 35242. (Practicalreviews.com). Centers for Medicare and Medicaid. Care Objectives for Meaningful Use (2011-present) CMS.gov. Hill RC, Jr, MD, Sears LM, MBA, Melanson SW, MD. 4000 Clicks: A productivity analysis of electronic medical records in a community hospital ER. The Am J Emer Med 2013; 31: 1591-1594.

Physician

Leadership

Academy

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E D I T O R I A L

Psychostimulants: Concerns over Long Term Adverse Side Effects JAMES GRAY ADAMS, MD

Psychostimulant prescriptions for children have dramatically increased worldwide, bolstered by a large volume of medical literature supporting their safety and effectiveness short term, if not long term, in addressing attention problems and hyperactive behavior.1 In truth, a growing body of remote and current medical literature raises clear and unsettling risk versus benefit issues and exposes a disturbing disconnect between our comfortable prescribing habits and the wisdom of using addictive, mind altering drugs during any age, especially during the formative, developmental age in young children.2 Use of psychostimulants (PS) in 6-year-olds with attention deficit hyperactive disorder (ADHD) has become more commonplace, and, more disturbingly but not surprisingly, current literature clearly exposes increasing use for performance enhancement.3,4 Given the vagueness inherent in the observation-based criteria for the diagnosis of attention deficit and hyperactivity disorder in the DSM IV and DSM V, it is not hard to understand the surge in diagnosis of this condition, coming from all levels of medical specialization. Methods of excluding other mental health, social and medical conditions that mask as ADHD are equally vague, though guidelines and warnings do exist in obscurity and in theory but not necessarily in common practice.5 Studies exposing the frequency of diversion of PS for recreational abuse are hardly surprising. This article does not condemn necessary, restricted PS use, especially in the worst ADHD cases where there are few alternatives in urban areas and practically none for physicians practicing in rural areas of Mississippi. These sad cases are the children who incessantly move, talk or jump from the exam table, disturbed children for whom there are, in the real world of medicine today, no reasonable alternatives. Nevertheless, we must recognize that PS are too often abused and are habit forming drugs that exert their therapeutic effects and side effects in the central nervous system. It is surprising then that articles exploring long term, mental effects of the routine, prescription use of PS in children during periods of early brain development are hard to find and, as I propose later, may be impossible to design for future prospective studies. Adverse effect literature on the use of PS does exist, but it is skewed towards positive reviews of safety based on assessments of mostly physical side effects, not long term, serious mental adverse effects or long term performance outcomes. This problem is compounded by the fact that studies are often funded by manufactures of PS and reviewers who lack adequate long term study data from drug manufacturers on the adverse effects of psychostimulants.6 There is ample, concrete evidence that abuse of PS is a causative or a precipitating agent in serious mental disorders such as severe anxiety disorders, schizophrenia, and bipolar disorder. Literature concerning mental adverse effects in routine prescribed doses does exist, however, including predisposition to adult drug habituation and alcoholism.7 Numerous animal studies and some human studies exist. Some recent studies show both chemical and structural brain alterations associated with the use of PS in standard doses, these alterations being long term and with functional consequences.8,9,10 Animal studies matched by relative age and PS dosing to human childhood may or may not apply to humans with absolute correlation, but who among us is willing to completely ignore the warnings from this formidable body of research? The critical issue is brain structure “plasticity,” the remodeling of dendritic connections and the alteration or death of nerve cells in response to pharmacological insults. This information was not discussed 45 years ago when I started medical school. Yet I, like both my younger and older colleagues as well as nurse practitioners in Mississippi, have the legal right to diagnose and treat children with drugs that, based on a large body of scientific literature, may alter brain structure to the detriment of the patient’s best interest. This is where those in charge of the delivery of health care have to address limits and ultimate goals of medical intervention. Are we acting in the best interest of our patients, especially children, to prescribe cognitive enhancing drugs to meet the demands of our current educational system? Are we treating disease, or have we entered the murky arena of social engineering? We have to grapple with long-term outcome benefits to justify risks, and there are risks. There is a sentinel study addressing the issue of cognitive outcomes, but the study is lengthy, complicated and ultimately evokes philosophical and ethical issues, since the crux of this matter reaches the very foundation of the practice of medicine, risks versus benefits, primum non nocere, first do no harm.11 The study, in fact, questions the magnitude of the cognitive benefits of using PS, the results mixed and not overly impressive, the long term outcomes mostly unknown. It is possible we will never be able to design prospective studies defining long-term problems with children treated with standard dosing of PS. This problem has multiple, complex considerations. The diagnosis of ADHD is observational, sometimes theoretically collaborated from multiple sources such as teachers, psychologists, parents but, nevertheless observational. Imagine a study 20 years later of children who, let’s say for example, took PS from the first grade through high school. How would you design a study to detect subclinical mental issues? By this I refer to the adult

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ADHD patient who doesn’t seek medical attention for a mental disease, though they have mental issues that impact the life of the patient and the patient’s family. Could you access health admissions for anxiety, depression, schizophrenia or bipolar disorder? These would represent overt, clinical disease, but then, without a control group, a skeptic would justly point out that the study pertains to people who were placed on PS to begin with because there minds were “not normal.” There is no large, randomized pool of children with ADHD who do not receive treatment, only those whose parents decline to accept the medication for voluntary reasons or by dropouts from therapy. Studies could use questionnaires if adult subjects could be trailed and identified, but there is always the stigma of mental illness, making problematic any reasonably accurate response rate. In Scandinavia, accessing medical records and accumulating data are easier, but even in the most ideal situation, how large and complex would a study have to be sorting through all the variables of genetics, environment, erroneous diagnoses, chance misfortune…in essence all the vicissitudes of human existence? We are now back to first base: our duty as physicians to assess risk versus benefits with the best available evidence. Summary The personal rewards are substantial for the healthcare provider who can make teachers and parents happy. There are evolving, alternative methods of dealing with ADHD, but PS are relatively cheap and quick when they work (roughly 70% of the time) and readily accessible.12 We have no social or educational structures currently to deal with the extreme ADHD cases. In cases of less dramatic, attention problems, poor grades, where PS boost attention, physicians are unlikely to abandon their patients willingly, unless compelled to sacrifice short term goals over the unanswered questions about what is best in the long run. How can we know if it’s the child and not the educational system that needs diagnosis and treatment? Psychiatric literature consistently suggests the prevalence of attention deficit in children is roughly 5% of the child population. Do 5% of our children need to take PS? This is where risks versus benefits enters the decision making process, and this is where this article aims to intentionally plant a healthy dose of scientific scrutiny. Ultimately, the doctor in charge makes a decision…sometimes based on intangibles that cannot be legislated or defined by even the best scientific studies. It is not clear or scientifically established that the use of PS, especially in young, developing minds of children, is safe or meaningfully beneficial in the long run. There is much information in human and animal studies to question the wishful thinking that using mind altering drugs in children is the right thing to do. There are risks, and there are benefits. In this case, the risks are less obvious, cloaked in the inadequacy of our current state of knowledge, potentially threatening the quality of the lives we seek to enhance. References

1.

Olfson M, Blanco C, Wang S, et al. National trends in the mental health care of children, adolescents, and adults by office-based physicians. JAMA Psychiatry 2014;71(1):8190.

2.

Clavenna A, Bonati M. Safety of medicines used for ADHD in children: a review of published prospective clinical trials. Arch Dis Child 2014;99(9):866-872.

3.

Fanton J, Gleason MM. Psychopharmacology and preschoolers: a critical review of current conditions. Child Adolesc Psychiatr Clin N Am 2009;18(3):753-771.

4.

Weyandt LL, Oster DR, Marraccini ME, et al. Pharmacological interventions for adolescents and adults with ADHD: stimulant and nonstimulant medications and misuse of prescriptions stimulants. Psychol Res Behav Manag 2014;7:223-249.

5.

Diagnosis and treatment of attention deficit hyperactivity disorder in school-age children and adolescents 2012 clinical practice guideline 2012. National Guidelines Clearinghouse, U. S. Department of Health and Human Resources Web Site. http://www.guideline.gov/content.aspx?id=38620&search=psychostimulants. Updated Mar 2012. Accessed May 2015.

6.

Aagaard L, Hansen EH. The occurrence of adverse drug reactions reported for attention deficit hyperactivity disorder (ADHD) medications in the pediatric population: a qualitative review of empirical studies. Neuropsychiatr Dis Treat 2011;7:729-744.

7.

Dalsgaard S, Mortensen PB, Frydenberg M, et al. ADHD, stimulant treatment in childhood and subsequent substance abuse in adulthood - a naturalistic long-term follow-up study. Addict Behav 2014;39(1):325-328.

8.

Gulley JM, Juraska JM. The effect of abused drugs on adolescent development of corticolimbic circuitry and behavior. Neuroscience 2013;249:3-20.

9.

Teixeira-Gomes A, Costa VM, Feio-Azevedo R, et al. The neurotoxicity of amphetamines during the adolescent period. Int J Dev Neurosci 2015;41:44-62.

10. Berman SM, Kuczenski R, McCracken JT, et al. Potential adverse effects of amphetamine treatment on brain and behavior: a review. Mol Psychiatry 2009;14(2): 123-142. 11. Smith ME, Farah MJ. Are prescription stimulants “smart pill”? The epidemiology and cognitive neuroscience of prescription stimulant use by normal healthy individuals. Psychol Bull 2011;137(5):717-741. 12. Holtmann M, Pniewski B, Wachtlin D, et al. Neurofeedback in children with attention-deficit/hyperactivity disorder (ADHD) – a controlled multicenter study of a non-pharmacological treatment approach. BMC Pediatrics 2014;14:202.

Author information: Dr. Adams did general practice in Bolivar County, Mississippi for 19 years before becoming the medical director of Occupational Health Services for The King’s Daughters Hospital in Greenville, Mississippi for six years followed by two years solo. For the last 16 years, he has devoted all his time performing disability exams for the Social Security Disability system in Mississippi. He is a past board member of the American Academy of Disability Evaluating Physicians and continues to serves the organization in various ways, including lecturing and audiovisual education. Correspondence: Jim Adams 208 S Pearman Ave. Cleveland, MS 38732

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Top Ten Facts You Need to Know About Clostridium difficile Saira Butt, MD Introduction Clostridium difficile is a gram positive, anaerobic, spore forming bacillus and the causative organism of Clostridium difficile infection (CDI). CDI can range from asymptomatic colonization to diarrhea, colitis, pseudo-membranous colitis and death.1 Any antibiotic class can cause CDI but most likely culprits are clindamycin, cephalosporins, penicillins and fluoroquinolones. Even one dose of an antibiotic can lead to CDI. 2

1 2

Clostridium difficile is now the most common cause of hospital acquired infection in the United States. Morbidity and mortality have increased in the past decade. The age-adjusted death rate for CDI is 2.3 deaths per 100,000 population. After diagnosis, attributable mortality is 6.9% at 30 days and 16.7% at one year. The estimated cost per infection is $6,000 to $9,000, and the estimated total cost per year is $3.2 billion.3

There is an epidemic is the community acquired CDI (CA-CDI), which is seen in presumed low risk patients who are not on antibiotics (children, peripartum women and healthcare workers).4 In the last two decades there has been dramatic increase in CDI, and mortality has increased from 1.5% to 6.9%. This is due to emergence of BI/ NAP/027 strain, which has increased binary toxin production and increased mortality of 16.7%. This toxin increases the risk for recurrent disease and has lower susceptibility to metronidazole.5,6

3 4 5 6 7

Clostridium difficile Infection (CDI) is classified as hospital acquired (HA-CDI) or community acquired (CA-CDI). Risk factors for initial HA-CDI are age < 65 years, antibiotic exposure, health care exposure, chemotherapy, enteral feedings, gastrointestinal surgery, impaired immunity, smoking and underlying comorbidities.7 Risk factors of initial CA-CDI is age < 50 years, female gender, less antibiotic exposure, less comorbid conditions but recurrence is similar to HA-CDI.8 Recurrent infections average around 20%. Risk factors for recurrent infections are age > 65 years, antibiotics, gastric suppressive agents, health care exposure, impaired immune response, history of CDI and underlying co-morbid conditions. 25% of the elderly may have recurrent CDI within 30 days of effective antibiotic treatment.7,9 Stool testing should only be performed only on unformed stools from at-risk patients with clinically significant diarrhea.* Immunocompromised patients with diarrhea should always be tested. Enzyme-linked immunosorbent assay (ELISA) toxin A/B is a fast and inexpensive test and is highly specific but has low sensitivity. Polymerase chain reaction (PCR) is sensitive and specific and may be used as a standard diagnostic test. Repeat testing or testing for cure should never be done for the same episode of diarrhea.10, ¥

Acid suppressant agents including proton pump inhibitors (PPI) and histamine 2 blockers have been associated with increased risk of CDI. The risk of CDI increases 1.4 to 2.75 times in patients who are exposed to PPI.10,11 Routine use of probiotics is uncertain. Avoid probiotics in immunocompromised patients, as there may be an increased risk for bacteremia.10,12 Discontinuation of the inciting antibiotic is key in the management of CDI. Failure to discontinue antibiotics can lead to prolong diarrhea and higher rate of recurrence. Antimotility drugs (e.g., loperamide) and opioids should be avoided as they may cause retention of toxins and cause complications such as ileus or toxic megacolon.10,13 See Table 1 for management of CDI.

* Checking formed stool for toxin decreases specificity of the diagnosis. If there is clinical suspicion for CDI in a patient with ileus: rectal swab for Clostridium difficile PCR should be done. Testing for asymptomatic patients should only be reserved for epidemiologic purposes. ¥ Therapeutic failure is not determined until treatment has been given for at least five days. If diarrhea persists, ensure inciting antibiotic has been discontinued and consider infectious diseases and surgical consultation.

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8

Patients with severe CDI should be closely monitored and TABLE 1: Treatment of Clostridium difficile Infection (CDI)10,12,16 receive early surgical consultation. Increased mortality has been associated with serum lactate > 5mmol/L and rising white blood cell count > 50,000 cells/microL. Fulminant colitis is a critical form of severe colitis [defined as more than 10 stools per day, elevated erythrocyte sedimentation rate (ESR) > 30 mm/h, fever > 99.5 F, tachycardia > 90/min, abdominal tenderness and distension, and colonic dilation on abdominal radiographs]. Resection of the entire colon should be considered in fulminant colitis.10,12

9

Hand hygiene with soap and water is essential as spores are not killed by alcohol based foams or gels.14 Clostridium difficile spores are spread via fecal-oral route. Spores ubiquitously remain on unanimated objects for months without losing viability. Gowns, gloves, dedicated thermometer, blood pressure cuff and stethoscope must be used. Contact precautions should be continued during the duration of diarrhea. Hydrogen peroxide sporicidal agent is efficacious in eradicating spores. Implementation of an antimicrobial stewardship program can help prevent the number of cases.10

10

Intestinal or fecal microbiota transplantation (IMT or FMT) may be an effective option for recurrent CDI in patients who have failed multiple courses of antibiotics. Stool is collected from a healthy donor, screened for transmittable diseases, filtered, and placed in a patient with CDI by colonoscopy to restore colonic microflora. It leads to 92% resolution of CDI.13 n

Corresponding Author: Saira Butt, MD; Assistant Professor, Clinical Infectious Diseases, University of Mississippi Medical Center, 2500 N. State St. # N502, Jackson, MS 39216. References 1. Korman TM; Diagnosis and management of Clostridium difficile infection. Semin Respir Crit Care Med. 2015;36: 31-43. 2. Brown KA, Khanafer N, Daneman N, et al. Meta-analysis of antibiotics and the risk of community-associated Clostridium difficile infection. Antimicrob Agents Chemother. 2013;572326-32. 3. http://www.cdc.gov/HAI/organisms/cdiff/Cdiff_infect.html 4. Wilcox MH, Mooney L, Bendall R, et al. A case-control study of communityassociated Clostridium difficile infection. J Antimicrob Chemother. 2008; 62:388–396. 5. Muto CA, Pokrywka M, Shutt K, et al. A large outbreak of Clostridium difficileassociated disease with an unexpected proportion of deaths and colectomies at a teaching hospital following increased fluoroquinolone use. Infect Control Hosp Epidemiol. 2005;26:273–280. 6. Pépin J, Valiquette L, Cossette B. Mortality attributable to nosocomial Clostridium difficile-associated disease during an epidemic caused by a hypervirulent strain in Quebec. CMAJ. 2005;173:1037–1042. 7. Loo VG, Bourgault AM, Poirier L, et al. Host and pathogen factors for Clostridium difficile infection and colonization. N Engl J Med. 2011; 365:1693. 8. Chitnis AS, Holzbauer SM, Belflower RM, et al. Epidemiology of communityassociated Clostridium difficile infection, 2009 through 2011. JAMA Intern Med 2013; 173:1359.

10. Cohen SH, Gerding DN, Johnson S, et al. Clinical practice guidelines for Clostridium difficile infection in adults: 2010 update by the Society for Healthcare Epidemiology of America (SHEA) and the Infectious Diseases Society of America (IDSA). Infect Control Hosp Epidemiol. 2010; 31:431-455. 11. Barletta JF, El-Ibiary SY, Davis LE, et al. Proton Pump Inhibitors and the Risk for Hospital-Acquired Clostridium difficile Infection. Mayo Clin Proc. 2013; 88:1085. 12. Massimo Sartelli, Mark A. Malangoni, Fikri M. Abu-Zidan. WSES guidelines for management of Clostridium difficile infection in surgical patients. World J Emerg Surg. 2015; 10: 38. 13.  Trudel JL, Deschênes M, Mayrand S, et al. Toxic megacolon complicating pseudomembranous enterocolitis. Dis Colon Rectum 1995;38:1033-8 14. Wullt M, Odenholt I, Walder M. Activity of three disinfectants and acid ified nitrite against Clostridium difficile spores. Infect Control Hosp Epidemiol. 2003;24:765–768 15. Aroniadis OC1, Brandt LJ, Greenberg A, et al. Long-term Follow-up Study of Fecal Microbiota Transplantation for Severe and/or Complicated Clostridium difficile Infection: A Multicenter Experience. J Clin Gastroenterol. 2015 (ahead of print) 16. Rokas KE1, Johnson JW1, Beardsley JR1, et al. The Addition of Intravenous Metronidazole to Oral Vancomycin is Associated With Improved Mortality in Critically Ill Patients With Clostridium difficile Infection. Clin Infect Dis. 2015;61(6):934-41.

9. Eyre DW1, Walker AS, Wyllie D, et al. Predictors of first recurrence of Clostridium difficile infection: implications for initial management. Clin Infect Dis. 2012;55:S7787. NOVEMBER 2015 • JOURNAL MSMA 349


C L I N I C A L

P R O B L E M - S O L V I N G

C A S E

A Rash Decision LAURA J. MILLER, MD A 57-year-old Caucasian female presented to clinic with a left palmar rash. She had a history of rheumatoid arthritis, osteoporosis, emphysema and depression. She had been evaluated in an emergency department multiple times for the same complaint of left hand rash. Two months prior to this clinic presentation, a three-view radiograph of her left hand showed no abnormality. She had been prescribed oral clindamycin, oral doxycycline, topical triamcinolone cream and topical mupirocin ointment. She had completed the oral antibiotics and reported diligent use of the topical drugs as well as over-the-counter moisturizers and emollient preparations but there was no improvement in the rash. She admitted to trying a home remedy that involved placing her hand in “bleach water.” She had been referred to dermatology by the emergency department but did not obtain an appointment. She was also taking daily aspirin, a calcium supplement, alendronate sodium (Fosamax) and bupropion hydrochloride (Wellbutrin SR). She had no prior hand or arm surgery and denied tobacco, alcohol and drug use. She reported a 5-6 year history of dry and scaly skin on her hand and also stated that she had injured her left palm with a knife several months ago. She stated that the lacerated area never properly healed and now caused her pain with constant redness and inflammation. On review of systems, she reported difficulty grasping items with her left hand secondary to pain, described a feeling of generalized weakness and fatigue but denied other issues. Physical examination revealed a normally developed, wellnourished female who was alert and in no distress. Her temperature was 97.6°F, weight 132 pounds, blood pressure 140/76 mmHg, heart rate 87 beats per minute and respiratory rate 16 breaths per minute. Her physical examination was unremarkable except for the palmar aspect of her left hand, which was erythematous with diffuse scaling. There was no apparent abscess formation or drainage, and the rash did not extend past the wrist. The patient was unable to tolerate palpation and manipulation of the hand secondary to pain. The differential at this point is quite broad. Due to her history of dry scaling skin on her hand for greater than 5 years, it would be reasonable to establish a differential diagnosis that included chronic prolonged skin conditions such as psoriasis, a chronic contact dermatitis, atopic dermatitis or xerotic eczema, a drug eruption or nonspecific dermatitis. Given her history, there could be a superimposed cellulitis or dermatitis due to hygiene or bleach exposure. Due to the patient’s reported history of rheumatoid arthritis and weakness, and possibility

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of an infectious process, laboratory investigation is warranted. We order a complete blood count to investigate for an infectious process or anemia as contributing causes to her rash and fatigue. We order a thyroid stimulating hormone to evaluate hypothyroidism as cause of her fatigue. Blood tests were performed to evaluate her weakness. Thyroid stimulating hormone and a basic metabolic profile were normal. A complete blood count was normal except for mean platelet volume 9.9 mcm3, (11.5-14.5) and mean corpuscular hemoglobin 31.4 pg (27-31). Given these laboratory findings, we do not have a clear cause for her weakness and will continue to focus on rash treatment. Since she has been treated with oral antibiotics previously with no improvement and did not have an abnormal white blood cell count or fever, we think the rash is likely due to a chronic condition. At this point, psoriasis and xerotic eczema are highest on our differential diagnosis. Psoriasis is a common disease in the United States, affecting 2 percent of the total population.9 It is characterized by red, scaly plaques and can range from localized areas of inflammation or wide-spread cutaneous involvement. There are several types of psoriasis, including plaquetype and pustular localized psoriasis.9 Plaque-type psoriasis usually presents with thick red scaly lesions and is often confused with atopic, irritant, and seborrheic dermatitis, cutaneous T-cell lymphoma or pityriasis rubra pilaris.6, 9 Pustular localized psoriasis usually presents with erythematous papules or plaques studded with pustules often on palms or soles and is often confused with drug eruption or dyshidrotic eczema.9 Both types of psoriasis are usually treated with topical corticosteroids, calcipotriene, coal tars, anthralin or tazarotene as well as phototherapy and systemic agents. 6, 9 Given her red scaly lesions, we thought the patient’s rash to be plaque-type as she did not have pustules. She was diagnosed with suspected psoriasis, continued on her topical treatments, and given an oral prednisone taper. She followed up in clinic 6 weeks later and had completed her prednisone taper with no improvement in her left hand pain or appearance. She denied fevers and, in the interim, had visited a wound care clinic where bandages were applied to her hand over her topical treatments. She reported worsening of the rash with migration onto the dorsal aspect of the left hand as well as worsening of the existing palmar rash. She had developed multiple open wounds on the palm and on the dorsal aspect of the fifth digit. She had improvement in her weakness in the interim. Photographs were taken with plans to send them to


dermatology for review. She was prescribed clobetasol cream to apply topically to the rash. Biopsy was discussed with the patient who vehemently refused secondary to fear of pain and complications from the procedure. Our greatest concern at this point due to the patient’s lack of improvement is that the rash may be a malignant process. We think that it may be a skin cancer or cutaneous lymphoma and would like pathologic analysis of a skin biopsy. Due to its unilateral presentation on one extremity and gradual worsening, we want to obtain a diagnosis quickly so that we may adjust our treatment regimen to target the correct pathophysiology. Given the patient’s staunch refusal to pursue biopsy for a more definitive diagnosis and her inability to see a dermatologist, we think that it is prudent to schedule her for frequent follow up visits to monitor the rash as well as take photographs to document evolution of the rash. One month later, she reported that her rash was worsening in appearance, size and pain. She stopped wound care in the interim but reported compliance with her topical medications. She denied swelling of the hand and denied weakness in the hand but admitted not grasping things with her left hand secondary to pain. She was continued on her current treatment and was again referred to dermatology. She agreed to schedule a biopsy in the future. Due to her enlarging rash with worsening cracking of the skin, as well as continued diffuse erythema and serous yellow drainage, she was admitted to the hospital for treatment with intravenous antifungals and antibiotics for suspected cellulitis superimposed on a psoriatic rash. While hospitalized, we believe that the patient will benefit from a dermatology consult given that the rash has not approved with appropriate treatment. We review our treatment plan with a dermatologist who recommends continuation of our current plan and agrees to see her as an outpatient. We continue to think that the patient would most benefit from biopsy due to the extensive treatments that have not improved her symptoms. We make another effort to convince the patient that a biopsy would give us the best chance to have a definitive diagnosis of the cause of the rash, which would direct our treatment course. During her inpatient hospital stay, she was given intravenous clindamycin and oral terbinafine (Lamisil). She had minimal improvement of her left hand rash and pain. A complete blood count revealed all values within reference ranges, and an erythrocyte sedimentation rate was elevated at 17 mm/hr (ref range 1-9 mm/hr) and C-reactive protein of 0.1 mg/dL (reference range 0-1.0 mg/dL). Wound cultures showed light growth of coagulase-negative staphylococcus and a fungal culture grew penicillium species. She completed a course of IV medication and was discharged home with an additional week of oral clindamycin and terbinafine. She was to follow up in one week at the outpatient clinic for her biopsy.

Given the clinical appearance of acute infection, she was started on empiric antibiotics. Despite hospital wound cultures showing a superimposed infection with penicillium and fungus, the patient’s white blood cell count remains normal. Coagulase-negative staphylococcus is typically a contaminant in superficial wound cultures but we chose to continue clindamycin to prevent possible worsening. She does have an elevated ESR, and we think this is possibly related to her history of osteoarthritis and rheumatoid arthritis, as well as a suspected inflammatory skin condition with a superimposed infectious process. We chose not to biopsy the rash while she is inpatient and prefer to get a tissue sample after she completes her antibiotic and antifungal medications. Given the lack of improvement during her inpatient stay, our suspicions are heightened that a rarer process is the cause of this rash. Since we diagnosed and treated suspected psoriasis and she has had no improvement, a diagnostic biopsy is indicated. Biopsy can differentiate psoriasis from similar conditions. 4 Over one month later, she presented to clinic for follow up. She continued to have no improvement of the rash, and the rash had continued to spread, now involving the entire palmar and dorsal aspects of her left hand and wrist. During the interim between hospital discharge and her clinic follow up, she had been evaluated by another hospital’s emergency department and wound care clinic and had received IV vancomycin. At this clinic visit, the physician consulted with a dermatologist who recommended griseofulvin (Grifulvin V) twice daily and scheduled the patient for an outpatient appointment. She was also given oral clindamycin and sulfamethoxazole/ trimethoprim (Bactrim DS) and rescheduled for a biopsy. At this point, we are more concerned that the patient has a more aggressive or serious condition such as a skin cancer or other malignant process. We also will want a definitive diagnosis of psoriasis prior to starting systemic treatment. We think this patient has very poor insight into her condition and the benefits of biopsy. She also expresses continual concern and fear for painful procedures and financial burdens of specialty appointments. As the patient’s rash is continuing to worsen, we again discuss with her that we recommend a biopsy and explain that it may give a definitive diagnosis, which will then lead to appropriate treatment. One week later, she received a punch biopsy of the lesion. She was admitted to the hospital one week later for cellulitis of her left hand and the punch biopsy was still pending. Lab work at time of admission to the hospital showed complete blood count components within normal limits, a basic metabolic panel that was normal except for a potassium concentration of 2.7 mEq/L (reference range 3.5-5.0). Erythrocyte sedimentation rate was again 17 mm/hr and C-reactive protein of 0.5 mg/dL. She was given vancomycin intravenously and was discharged home with oral clindamycin and oral griseofulvin with plan to be seen in clinic or be notified regarding the biopsy pathology.

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She returned to clinic to review her biopsy pathology that revealed atypical lymphoproliferative infiltrate concerning for mycosis fungoides (cutaneous T-cell lymphoma), in transformation to CD-30 positive T-cell lymphoma. The pathology report indicated that the neoplastic cells were relatively small and uniform and did not express ALK-1 protein, favoring a primary cutaneous lymphoma. Two months later, because of delays in insurance authorization, the patient had a lymph node biopsy taken from her left axillary region that was suspicious for involvement by T-cell lymphoma. Cutaneous T-cell lymphoma, also known as mycosis fungoides, is a malignancy that involves CD4+ T-helper cells.10 It often imitates benign skin conditions, and it can be very difficult to definitively diagnose early in the disease process without a biopsy.10 It can manifest as patch, plaque or tumor. It can also diminish in intensity with topical corticosteroids or phototherapy.10 It should be considered in the differential diagnosis if a chronic psoriatic-type lesion or eczema has not responded appropriately to treatment. One of the reasons cutaneous T-cell lymphoma was not immediately high on our differential diagnosis is that it is a rare condition. United States data from 1992 through 2001showed an annual incidence of 4.5 cases per million, with palmoplantar keratoderma observed in only 11.5% of mycosis fungoides cases.5,8 Palmoplantar involvement is generally a secondary presentation in people who have skin involvement of their trunk or extremities.8 Only in 0.6% of cases is the prevalent presentation on the palms or soles, forming what has been designated “mycosis fungoides palmaris et plantaris.”7,8 The patient had a computed tomography scan of the chest, abdomen and pelvis, which showed an enhancing fluid-filled cystic structure in the left axilla with inflammation and stranding at the site of the prior lymph node biopsy. It also revealed an increased number of small left-sided lower cervical and supraclavicular lymph nodes, and no lymphadenopathy or metastatic disease in the abdomen or pelvis was seen. The patient was referred to hematology where she began undergoing chemotherapy treatments before moving out of state and transferring her care. Cutaneous T-cell lymphoma is often diagnosed in people in their 50s or 60s.1 It often presents as pruritic, inflammatory patches that can be present for years without severe worsening.1,10 We think that this patient had scaly lesions for multiple years before these worsened and caused concern that led her to present for treatment. The prognosis of patients with cutaneous T-cell lymphoma is based upon the presence or absence of extracutaneous disease and type and amount of skin involvement.1 n Key words: c utaneous T-cell lymphoma, mycosis fungoides, rash, palmar rash

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Corresponding Author: Laura J. Miller, MD, Family Medical Clinic of Crystal Springs, 104 West Railroad Avenue South, Crystal Springs, MS 39059. (laurajacksonmiller@gmail.com) References 1. Duhovic C, Child F, Wain EM. Management of cutaneous T-cell lymphoma. Clin Med. 2012; 12(2):160-164. 2. Elmer KB, George RM. Cutaneous T-cell lymphoma presenting as benign dermatoses. Am Fam Physician. 1999; 59(10):2809-2813. 3. Femiano F, Buonaiuto C, Heulfe I. What news are on mycosis fungoides. J Stomatological Investigation. 2008; 2:57-65. 4. Luba KM, Stulburg DL. Chronic plaque psoriasis. Am Fam Physician. 2006; 73(4):636-644. 5. Morton LM, Wang SS, Devesa SS, Hartge P, Weisenburger DD, Linet MS. Lymphoma incidence patterns by WHO subtype in the United States, 19922001. Blood. 2006; 107(1): 265–276. 6. Pardasani AG, Feldman SR, Clark AR. Treatment of psoriasis: an algorithmbased approach for primary care physicians. Am Fam Physician. 2000; 61(3):725733. 7. Smoller BR. Mycosis fungoides palmaris et plantaris [Letter to the Editor]. Arch Derm.1996;132:468. 8. Topf S, Luftl M, Neisius U, et al. Mycosis fungoides palmaris et plantaris- an unusual variant of cutaneous T-cell lymphoma. Eur J Derm. 2006; 16(1):84-86. 9.

Weigle N, McBane S. Psoriasis. Am Fam Physician. 2013; 87(9):626-633.

10. Zackheim HS, McCalmont TH. Mycosis fungoides: the great imitator. J Am Acad Derm. 2002; 47(6):914-918.


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