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VOL. LVIII • NO. 5 • 2016

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VOL. LVIII • NO. 5 • MAY 2016

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


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

SCIENTIFIC ARTICLES Chikungunya in Mississippi: The Health Department Response 138 to Imported Cases Jerome Goddard, Wendy C. Varnado, Sheryl Hand, and Florencia Meyer Top 10 Facts You Should Know about Hearing Loss and Cognitive Decline Grace Gore Sturdivant, Au.D.



Top Abstracts from the 2015 American College of Physicians Mississippi Chapter Abstract Day at the University of Mississippi Medical Center S. Calvin Thigpen, MD

DEPARTMENTS From the Editor – Measles in Memphis Lucius M. Lampton, MD, Editor


MSMA Nominating Committee Seeks Candidates for Vacancies


MSMA Component Society Meeting Schedule


President’s Page – You are the Guardians at the Gate Daniel P. Edney, MD, MSMA President


MSMA Physicians Leadership Academy- Angela Wingfield, MD 170 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 © 2016 Mississippi State Medical Association.

Official Publication

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RELATED ORGANIZATIONS UMMC to Create New School of Population Health


ABOUT THE COVER “Wood Duckling Jump Day”– One of the most stunningly pretty of all waterfowl, wood ducks are special to North America because they are found nowhere else in the world. Males are iridescent chestnut and green, with ornate patterns on nearly every feather. The elegant females have a distinctive profile and delicate white pattern around the eye. These birds live in wooded swamps where they nest in holes in trees or in nest boxes put up around lake margins. They are one of the few duck species equipped with strong claws that can grip bark and perch on branches. The wood duck is the only North American duck that regularly produces two broods in one year. Average clutch size is 12 eggs, but more than one female may contribute to a clutch (dump nest), which can result in clutches of more than 60 eggs. These huge clutches are rarely incubated, but successful dump nests of less than 30 eggs are common in nest boxes. A wood duck clutch is incubated for an average of 30 days. Dr. Joe R. Bumgardner, a retired general surgeon in Starkville, was fortunate in photographing nine hatchlings (from 10 laid eggs) on ‘Jump Day’ as they emerged from their nest in a wood duck box to land on the ground. Dr. Bumgardner writes, “Just one day after hatching (or less), wood ducklings must take a leap of faith. One by one the ducklings jump from their nest which can be over 65 feet above the ground. They are so light that the fall doesn’t harm them. They make their way to water as their mother calls to them without any other help. There were a pair of bluebirds that were observing this whole event, and they too were captured in this documentary wood duckling jump. I captured this event from a Primos Double Bull camouflaged ground blind some 30 yards from the event using a 600mm focal length Nikon Telephoto lens and a Nikon dSLR camera, and this all occurred in a residential lake regional to Starkville."n VOL. LVIII • NO. 5 • 2016






Measles in Memphis “Measles is literally knocking at our back door,” said our State Epidemiologist Dr. Thomas Dobbs after health officials in Tennessee announced a measles outbreak in the Memphis area in April. Measles, a Class 1 reportable condition requiring an immediate report to MSDH within 24 hours, is a highly contagious airborne disease presenting with fever, a maculopapular rash, cough, coryza, conjunctivitis, and a pathognomonic enanthem. Once a feared childhood disease with significant morbidity and mortality (one in four cases are hospitalized, one in a thousand die), it is largely preventable through vaccination. Due to the success of the Measles vaccine (introduced in 1963), the virus was thought to have been eradicated in the United States by 2000, but the anti-vaccine movement has allowed the disease to return, with increasing numbers of outbreaks over the last decade. Although the index case in Memphis is unknown, six cases have been confirmed. (The route of introduction is usually importation by unimmunized travelers outside of the United States.) Measles spreads easily since patients are extremely contagious before symptoms

emerge. There is no specific treatment of the disease except supportive care, thus stopping exposure is the key. Most public health efforts are focused on tracking down contacts, quarantine (usually 21 days) of cases and of those exposed, and providing vaccinations. Here in Mississippi, four unimmunized Mississippi residents were placed under physician-supervised home quarantine after exposure in a pediatrician’s office in Memphis. (Thus, encourage possible exposures to telephone, not visit, your office if they develop a fever or rash!) These old diseases like measles are still out there, still deadly and threatening to our patients. This outbreak underscores that lofty percentages of vaccination of the population remain critical for the public’s health. Any attempt to soften our state’s immunization laws allowing increased exemptions will negatively impact the health of our patients. Physicians must use this outbreak to stress the science and importance of vaccinations to our patients and their families, who more and more hear only the ignorant voices of parents who scorn immunization for their children. 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

136 VOL. 57 • NO. 5 • 2016

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

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


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Chikungunya in Mississippi: The Health Department Response to Imported Cases JEROME GODDARD,1 WENDY C. VARNADO,1,2 SHERYL HAND2 AND FLORENCIA MEYER1

Abstract Chikungunya (CHIK), a newly recognized mosquito-borne disease in the Western Hemisphere, has resulted in well over a million cases since December 2013. Only about a dozen locally-acquired cases thus far have been reported in the U. S. (Florida), but approximately 1500 imported cases have been seen in returning travelers from the Caribbean and Central and South America. Public health officials are concerned that imported cases may lead to infection of local mosquitoes and, thus disease transmission. This paper documents 9 confirmed CHIK cases in Mississippi: 5 resulting from travel to the Dominican Republic, 2 from Haiti, 1 from Honduras, and 1 from Puerto Rico. In addition, the Mississippi State Department of Health response to those cases is presented and discussed. Key Words: C  hikungunya, Human cases, Mississippi, Control, Epidemiology Introduction Chikungunya (CHIK) is a mosquito-transmitted viral illness which is not usually fatal but can cause severe fevers (>39.00 C), headaches, fatigue, nausea, and muscle and joint pains.1 A maculopapular rash is often seen in patients two to five days after onset of fever. In contrast to other mosquito-borne diseases such as Zika, the vast majority of infected CHIK patients will become symptomatic. There is often excruciatingly painful swelling of the joints in the fingers, wrists, back, and ankles which is usually bilateral and symmetric, sometimes leading to long-term, post-infective rheumatisms such as rheumatoid arthritis and spodylarthropathy.2,3 Risk factors for hospitalization and severe disease include neonates exposed intrapartum, age >65 years, and persons with underlying medical conditions (e.g., diabetes, hypertension, or heart disease). While most acute symptoms will resolve within 7-10 days, some patients have persistent joint pains for months to years after acute infection. Since CHIK and dengue are very similar clinically, it is important to differentiate the two. CHIK virus was first isolated during a 1952 epidemic in Tanzania,4 and the word “chikungunya” derives from a word in the Kimakonde language, meaning “to become contorted,” or “that which bends up,” referring to the position patients assume when suffering severe joint pains.5 The geographic distribution of CHIK has historically included most of Sub-Saharan Africa, India, Southeast Asia, Indonesia, and 138 VOL. 57 • NO. 5 • 2016

the Philippines, although the disease is rapidly increasing both in incidence and geographic range. During 2004-2006 on several islands in the Indian Ocean there was a tremendous outbreak, which spread to India, ultimately sickening millions of people.6 In December 2013, chikungunya spread to the Western Hemisphere, appearing in Saint Martin, the French West Indies, and subsequently to other Caribbean islands, Central and South America, and the United States, where there have been at least 1,280,000 cases.5,7 About a dozen cases have been locally acquired in the U.S. so far and more are sure to follow. The virus and its pathophysiology. Chikungunya virus belongs to the genus Alphavirus within the Togaviridae family. It has a singlestranded RNA genome with positive polarity (ssRNA+) and an icosahedral nucleocapsid surrounded by a lipid membrane derived from its host. Like other ssRNA+ viruses, its genome is immediately infectious when delivered to the cytoplasm of susceptible cells. Other known viruses in this same genus include Semliki Forest virus, Ross River virus, Sindbis virus, Venezuelan Equine Encephalitis Virus, and O’nyong-nyong. CHIK transmission is almost exclusively by mosquitoes in the genus Aedes, in particular A. aegypti and A. albopictus (see next section for more discussion), which are both abundant in much of the world.8,9 In the Americas, currently the preferred vector seems to be A. aegypti.10,11 However, the broader worldwide distribution of A. albopictus is worrisome in the light of the 2005 outbreak in La Reunion Island in the Indian Ocean, where only one mutation in the envelope protein E1 protein of the CHIK virus led to increased infectivity of CHIK for A. albopictus and, thus the unprecedented explosion of that outbreak.12 The rapidly evolving envelope proteins of the virus, E1 and E2, seem to drive fast adaptation to new vectors. CHIK virus is inoculated into a human when an infected female mosquito takes a blood meal. Vertical transmission of CHIK virus from mother to child during near-term deliveries may also be possible;13 however, other avenues of person-to-person transmission have not been documented. A recent study shows that non-human primates can also be infected,14 so other vectors and transmission cycles may be involved in CHIK ecology.

The virus infects and replicates mainly in skin fibroblasts and to a lesser extent in myofibroblasts.15 Infected fibroblasts in the skin produce a robust local immune response mainly in the form of interferon type 1, which contains much of the infection.15,16 The virus readily replicates in a variety of epithelial adherent cells in the laboratory17 but has limited replication in blood containing circulating monocytes and lymphocytes.17,18 However, monocyte-derived macrophages are able to replicate the virus efficiently. Viral particles that make it to the bloodstream are able to replicate in monocytes and in lymphocytes to varying degrees.17 Virus is then transmitted via blood to the liver, where it replicates efficiently and finally spreads systemically to fibroblasts of the muscle, joints, and skin. In clinical samples, CHIK virus has been detected in blood and cerebrospinal fluid. Vector ecology. As mentioned, CHIK is primarily transmitted by the yellow fever mosquito, Aedes aegypti, and the Asian tiger mosquito, A. albopictus. Both species are very similar in appearance and habits. Aedes aegypti is cosmotropical in distribution, occurring worldwide within the 20°C isotherms. This is a small black species with prominent white bands on its legs and a silver-white lyre-shaped figure on the upper sides of its thorax (Figure 1). Aedes aegypti breeds in artificial containers around buildings such as tires, cans, jars, flowerpots, and gutters and usually bites during the morning or late afternoon. They may readily enter houses and prefer human blood meals, biting principally around the ankles or back of the neck. The reported flight range is from 100 ft to 100 yd. Interestingly, in many places in the U.S. where A. albopictus has been introduced, this species has virtually disappeared, apparently being displaced. FIGURE 1. Aedes aegypti, the yellow fever mosquito. Note lyreshaped marking on back (Photo courtesy the Centers for Disease Control, James Gathany photographer).

FIGURE 2. Aedes albopictus, the Asian tiger mosquito. Note single white line on back (Photo courtesy the Centers for Disease Control, James Gathany photographer).

Due to the potential introduction of CHIK into the Western Hemisphere and abundant presence of competent mosquito vectors, heightened surveillance has been underway for CHIK cases in the U.S. since at least 2011.21 This paper documents imported cases of CHIK in Mississippi and the state health department response to those cases. Methods Due to a confirmed case of CHIK reported in an Alabama resident, the Mississippi State Department of Health (MSDH) issued a health alert network (HAN) announcement on June 18, 2014, to all hospitals and healthcare providers statewide requesting heightened awareness of possible CHIK cases in Mississippi. Subsequently, 9 Mississippi cases of CHIK were identified, all cases confirmed by testing done at the CDC or Focus Diagnostics Laboratory. The case definition used for CHIK cases in Mississippi was: 1) acute onset of fever and arthralgias involving two or more joints, AND 2) recent travel within previous two weeks to an area with identified CHIK transmission, AND 3) absence of a more likely cause. Lastly, after case identification, followup, environmental surveys, and educational efforts were initiated to track the cases and prevent local transmission of the virus. Cases Identified

Aedes albopictus is widely distributed in the Asian region, the Hawaiian Islands, parts of Europe, and much of the Americas, including the southern U.S., where it was accidentally introduced in 1986.19,20 This species is similar in appearance to A. aegypti having a black body and silver-white markings, with the major difference between the two being that A. albopictus has a single, silver-white stripe down the center of the dorsum of the thorax (instead of the lyre-shaped marking) (Figure 2). They breed in artificial containers such as cans, gutters, jars, tires, and flowerpots, and seem especially fond of discarded tires. This is an aggressive mosquito, often landing and biting immediately. The reported flight range is generally less than a quarter mile.

To date, a total of 9 human CHIK cases have been identified from Mississippi, 8 in 2014 and 1 in 2015. Of the 8 cases occurring in 2014, 3 lived in Mississippi in the Jackson metropolitan area, 3 along the Gulf Coast, and 2 in south Mississippi (but not on the coast). Five of the patients had recently returned from the Dominican Republic, 2 from Haiti, and 1 from Puerto Rico. The single 2015 case lived in the Jackson metropolitan area as well and had just returned from Honduras. The age range for all Mississippi CHIK cases was 14 – 55 (avg 29; median 30). All patients reported typical CHIK signs and symptoms such as fever, joint swelling and painful arthralgias (Figure 3). The Health Department Response In each of the 9 CHIK cases reported so far, staff from the MSDH Office of Epidemiology verified facts related to each case (contact information, reporting clinician, etc.), determined if fellow travelers of each patient were also ill, coordinated on-site home inspection(s) and all communication efforts with the healthcare provider, patient, and the JOURNAL MSMA


FIGURE 3. Joint swelling and rash in a Mississippi Chikungunya case (Photo courtesy Mississippi Department of Health).

public, and lastly, initiated educational efforts concerning avoidance of mosquito exposure, especially within the first 10 days after onset of illness. In addition, the District Environmentalist (health inspector) from the location where each CHIK case occurred, along with an entomologist from the MSDH central office, coordinated an on-site environmental survey of the patient’s residence and neighborhood (see Table 1). TABLE 1. On-site environmental health and entomological responses to cases of CHIK in Mississippi, 2014-2015.

Evaluate location of the residence – whether dense urban site or rural sparsely populated area Search for and identify any mosquito breeding sites around residence and 200 yard radius Immediately remediate mosquito breeding sites (tip and toss, etc) Distribute CDC and Health Department Fact Sheets to persons at residence and any dwellings in a 300 yard radius Educate homeowners about mosquito breeding and personal protection Share findings with District and Central Office Health Department staff Contact local mosquito control agency to determine capabilities and offer advice/help Discuss options of spraying with a truck and/or hand-held fogging of premises

In the 3 cases occurring in coastal Jackson County, MS, personnel from the local county mosquito control contractor (Mississippi Mosquito Control, Inc.) performed on-site entomological inspections and hand-fogging of pesticides around (outside) each residence. Hand-fogging was conducted with a Colt ULV fogger using a pyrethroid insecticide according to label directions. The 3 cases occurring in the Jackson metro area (Hinds, Rankin, and Madison Counties) were investigated by the second author (WCV) and the premises were hand-fogged for mosquitoes using a Burgess thermal fogger® and pyrethroid insecticides according to label directions. The other 3 cases were investigated by entomology or environmental health personnel and application of pesticides deemed not needed.


As far as can be determined, there was no local transmission of CHIK in Mississippi resulting from these 9 imported cases. This could be due to the fact that genetic analysis of CHIK strains in the Caribbean suggest that they are not well adapted to Aedes albopictus, which is the predominant and widespread species in Mississippi.5,22 Epidemiologically, one of the most important concerns in imported CHIK cases is to prevent patients from spending time outdoors during the acute viremic (infective) stage of their illness. Both A. albopictus and A. aegypti are daytime biters which are readily found around homes around the patio, in the backyard, and may easily bite patients ill with CHIK. The fact that CHIK has not been locally transmitted in Mississippi thus far should not allay concerns of the medical community. There is a burgeoning epidemic in the Americas in a population not previously exposed to CHIK virus, so an explosive expansion of cases could still occur, such as what happened on La Reunion Island in the Indian Ocean, where hundreds of thousands of cases (if not millions) occurred in a short period of time. Compounding matters, the current outbreak of Zika virus occurring in the Western Hemisphere seems to indicate a succession of emerging arboviruses, primarily those transmitted by Aedes albopictus.23 Since Zika virus seems to be following the exact footsteps of CHIK and dengue,24 a coordinated effort is needed among epidemiology, environmental health, and entomology personnel to prevent and/or mitigate such epidemics in the U.S. n References

Conduct further enhanced mosquito source reduction activities as needed

140 VOL. 57 • NO. 5 • 2016

1. Weaver SC, Smith DW. Alphavirus infections. In: Guerrant RL, Walker DH, Weller PF, eds. Tropical Infectious Diseases. 3 ed. London: Saunders (Elsevier); 2011:519-524.

2. Foissac M, Javelle E, Ray SC, Guerin B, Simon F. Post-chikungunya rheumatoid athritis, Saint Martin. Emerg. Inf. Dis. 2015;21:530-532.

16. Couderc T, Lecuit M. Chikungunya virus pathogenesis: From bedside to bench. Antiviral Res. 2015;121:120-131.

3. Javelle E, Gautret P, Simon F. Chikungunya, the emerging migratory rheumatism. Lancet Infect. Dis. 2015;15:509-510.

17. Sourisseau M, Schilte C, Casartelli N, et al. Characterization of reemerging chikungunya virus. PLoS Pathog. 2007;3(6):e89.

4. Robinson MC. An epidemic of virus disease in Southern Province, Tanganyika Territory, in 1952-53. I. Clinical features. Trans. R. Soc. Trop. Med. Hyg. 1955;49:28-32.

18. Her Z, Malleret B, Chan M, et al. Active infection of human blood monocytes by Chikungunya virus triggers an innate immune response. J. Immunol. May 15 2010;184(10):5903-5913.

5. Morens DM, Fauci AS. Chikungunya at the door -- deju vu all over again? N. Eng. J. Med. 2014;371:885-887. 6. Weaver SC, Lecuit M. Chikungunya virus and the global spread of a mosquito-borne disease. N. Engl. J. Med. 2015;372:1231-1239. 7. Sam I-C, Kummerer BM, Chan Y-F, Roques P, Drosten C, AbuBaker S. Updates on chikungunya epidemiology, clinical disease, and diagnostics. Vector Borne and Zoonotic Dis. 2015;15:223-230. 8. Delatte H, Paupy C, Dehecq JS, Thiria J, Failloux AB, Fontenille D. Aedes albopictus, vector of chikungunya and dengue viruses in Reunion Island: biology and control. Parasite. Mar 2008;15(1):3-13. 9. Gratz NG. Critical review of the vector status of Aedes albopictus. Med. Vet. Entomol. 2004;18(3):215-227. 10.

Johansson MA. Chikungunya on the move. Trends Parasitol. 2015;31:43-45.

19. Lambrechts L, Scott TW, Gubler DJ. Consequences of the expanding global distribution of Aedes albopictus for dengue virus transmission. PLoS Negl. Trop. Dis. 2010;4(5):e646. 20.

21. CDC. Preparedness and response for chikungunya virus: introduction in the Americas: Pan American Health organization/U.S. Centers for Disease Control, Washington, D.C. ISBN # 978-92-75-11632-6, 149 pages; 2011. 22. Weaver SC, Osorio JE, Livengood JA, Chen R, Stinchcomb DT. Chikungunya virus and prospects for a vaccine. Expert Rev. Vaccines. 2012;11:1087-1101. 23. Fauci AS, Morens DM. Zika virus in the Americas - yet another arbovirus threat. N. Engl. J. Med. 2016;374:601-604. 24.

11. Vega-Rua A, Zouache K, Girod R, Failloux AB, Lourenco-de-Oliveira R. High level of vector competence of Aedes albopictus and Aedes albopictus from ten American countries as a crucial factor in the spread of Chikungunya virus. J. Virol. 2014;88:6294-6306. 12. Tsetsarkin KA, Vanlandingham DL, McGee CE, Higgs S. A single mutation in chikungunya virus affects vector specificity and epidemic potential. PLoS Pathog. 2007;3(12):e201. 13. Gerardin P, Barau G, Michault A, et al. Multidisciplinary prospective study of motherto-child chikungunya virus infections on the island of La Reunion. PLoS Med. Mar 18 2008;5(3):e60. 14. Gardner J, Rudd PA, Prow NA, et al. Infectious chikungunya virus in the saliva of mice, monkeys and humans. PLoS ONE. 2015;10(10):e0139481. 15. Schilte C, Couderc T, Chretien F, et al. Type I IFN controls chikungunya virus via its action on nonhematopoietic cells. J. Exp. Med. Feb 15 2010;207(2):429-442.

Rai KS. Aedes albopictus in the Americas. Ann. Rev. Entomol. 1991;36:459-484.

Anonymous. Zika virus: a new global threat for 2016. Lancet. 2016;387:96.

Author Information: Department of Biochemistry, Molecular Biology, Entomology and Plant Pathology, 100 Twelve Lane, Clay Lyle Entomology, Mississippi State University, Mississippi State, MS 39762, U.S.A. E-mail: jgoddard@ entomology.msstate.edu.


Mississippi Department of Health, P.O. Box 1700, Jackson, MS 39215, U.S.A. E-mail: Wendy.Varnado@msdh.state.ms.gov and Sheryl.Hand@ msdh.state.ms.gov.


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Top 10 Facts You Should Know about Hearing Loss and Cognitive Decline Grace Gore Sturdivant, Au.D., CCC-A, F-AAA Introduction As an invisible handicap, hearing problems are often overlooked or rationalized. Many factors contribute to hearing problems, but the most common are noise exposure, ototoxic medications, and aging. Age-related hearing loss is not simply a matter of getting older but is rather a complex condition dependent on an individual’s health status, in particular cardiovascular and metabolic health, cumulative effects of noise and ototoxic medications, and genetics. In rare cases, specific disease and disorders can cause hearing difficulties. Agerelated hearing loss is usually gradual onset of bilateral, high frequency hearing loss. The common perception that sounds are “loud but unclear” results when the crisp, high frequency consonant sounds such as /s/, /t/, and /p/ are no longer audible relative to the low frequencies of sound which carry the perception of overall volume. With modern advances in hearing aid technology, mild to severe degrees of hearing loss can be treated with hearing aid devices. Noise reduction, directional microphones, and Bluetooth connectivity including smartphone app controls are making hearing aids more appealing than ever before to an ever-broadening patient base. I will outline what I believe to be the most compelling evidence to support incorporating hearing screenings and/or questions regarding hearing ability into general physical exams with the ultimate goal of improving the quality of life in seniors.


Hearing loss is a widespread chronic health condition. Following arthritis and hypertension, hearing loss is the third most prevalent chronic health condition facing older adults.1 An estimated 1/3 of Americans between ages 65 and 74 and nearly half of those over the age of 75 have hearing loss.2 While 26.7 million Americans 50 years or older have a clinically-significant hearing loss, fewer than 15% use hearing aids.3


Common Causes of Hearing Loss in Adults Cerumen Impacon Presbycusis, Age-Related Loss Noise Exposure Ototoxic Medicaons Otosclerosis Meniere’s Disease Autoimmune Inner Ear Disease Acousc Neuroma Head Trauma

Dementia is commonly overestimated due to hearing loss. Common dementia screening tools such as the Mini Mental State Examination (MMSE), the Sternberg Memory Scan, and the California Learning test are administered verbally to older adults. Each of these tests assumes normal hearing ability and normal central auditory processing ability.4 In a study of institutionalized patients diagnosed with senile dementia, 83% of the sample were found to have at least a mild degree of hearing loss, and 33% of the subjects were re-classified to a less severe category of dementia following amplification of the test administrator’s voice.5 Late onset Alzheimer’s Disease and untreated hearing loss often present with similar symptoms such as depression, anxiety, isolation, reduced communication ability, inappropriate psychosocial responses, defensiveness, and negativity.6

3 4

Cognitive load is increased when hearing loss is present. In speech understanding tasks, hearing loss causes increased effort, leaving less cognitive reserve for recalling information.7 For patients with dementia and, therefore, slower processing speeds, hearing loss further compromises cognitive ability. This leads to a negative synergistic effect for hearing loss and cognitive decline, with the comorbid result as worse than either disease in isolation.8,9

Cognitive impairment is positively correlated with hearing loss. A higher than expected prevalence of hearing loss occurs in individuals with cognitive deficits when compared to normal hearing cohorts.10 Studies suggest that individuals with hearing loss have a 24% increased risk of cognitive impairment over those with normal hearing, with a positive correlation between the degree of hearing loss and the risk of dementia. Individuals with mild hearing loss are twice as likely to develop dementia as those with normal hearing. Those with moderate hearing loss are three times more likely, and those with severe hearing loss have five times the risk of developing dementia.11,12

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Onset of cognitive decline may be earlier in those with hearing loss. Adults with untreated hearing loss develop cognitive impairment 3.2 years sooner than the normal hearing cohort.11 Rate of cognitive decline may be faster in patients with hearing loss. In individuals with hearing loss, the rate of cognitive decline is 30-40% faster than the rate of decline in normal hearing individuals. The rate of cognitive decline is positively associated with the severity of the individual’s baseline hearing loss.11

Cerumen often contributes to hearing loss. Though frequently overlooked, cerumen impaction is an easily reversible cause of conductive hearing loss. A study of residents of a skilled nursing facility found that 65% had cerumen impaction in at least one ear. Hearing was improved and scores on the Mini Mental State Examination (MMSE) showed statistically significant improvement following removal.15 There are social and emotional consequences of hearing loss. Individuals with untreated hearing loss more often report feeling sad or lonely, depressed, worried, paranoid, and more socially isolated than those who use amplification.13,14

There are major benefits of treatment with hearing aids. Those affected by hearing loss and their significant others report benefits from amplification use, including better relationships and more confidence.13,14 Hearing loss is associated with decreased social/emotional, communicative, and cognitive function for subjects with unaided hearing loss as compared to those using hearing aids.17 Most recently, the October 2015 Journal of the American Geriatrics Society published a 25 year study of 3,670 older adults which found that hearing aid use attenuated cognitive decline in older adults with hearing loss.18


Primary care physicians are an important factor for improved hearing. Only 23% of adults report undergoing a hearing screening during a physical exam. 20% of those without hearing aids reported that a positive recommendation from their doctor would motivate them to pursue amplification.16 Physicians can also recommend healthy behaviors that can reduce hearing loss risk. There is a significant association between hearing loss and age, but hearing loss can be prevented or reduced through health behavior change. Using hearing protection consistently around loud sounds, quitting smoking, eating a healthy diet and exercising, and taking up a musical instrument have all been shown to reduce risk of decline in peripheral and central auditory processing. Conclusion Hearing loss is not only a quality of life issue but also a serious health issue. Hearing loss is not an isolated problem but a potential contributing factor to other medical and psychological conditions. Individuals with even a mild degree of hearing loss can experience dramatic improvements in their quality of life, and, while we cannot definitively say that hearing aids postpone dementia, we can say that using hearing aids is associated with decreased statistical likelihood of developing cognitive decline. As individuals are inclined to view hearing loss as a medical issue, consumers often believe that their physicians should be the source of guidance for their hearing problems. By incorporating basic hearing screenings, otoscopy to rule out cerumen impactions, and questions about hearing ability into routine general physical exams, physicians can aid in earlier enjoyment of the positive health benefits of treatment with hearing aids and preventative strategies to reduce risk for further decline in hearing. If hearing loss or tinnitus is suspected, physicians should refer to an audiologist. There is a wide discrepancy in the expertise level of individuals licensed to dispense hearing aids. To ensure that your patients receive quality and appropriate care, refer to a masters or doctoral level audiologist who is credentialed by the American Speech and Hearing Association (CCC-A) or the American Academy of Audiology (ABA). n References 1. Collins JG. Prevalence of selected chronic conditions: United States, 1990–1992. Vital Health Stat Ser 10 Data Natl Health Surv. 1997; 194:1–89. 2. National Institute on Deafness and Other Communicative Disorders. (2010). Quick Statistics http://www.nidcd.nih.gov/health/statistics/pages/quick.aspx. 3. Chien W, Lin FR. Prevalence of hearing aid use among older adults in the United States. Arch Intern Med. 2012 Feb; 172(3):292–293.  4. Dumont R, Hagberg C. Kaufman Adolescent and Adult Intelligence Test (KAIT): Test Review. Journal of Psychoeducational Assessment. 1994; Vol. 12(2): 190-196. 5. Weinstein BE, & Amsel. Hearing loss and senile dementia in the institutionalized elderly. Clin Gerontologist, 1986; 4: 3-15. 6. Chartrand S. The absence of hearing healthcare in a so-called “tidal wave of Alzheimer’s cases.” Audiology Online. 2 July 2002. http://www.audiologyonline.com/articles/article_ detail.asp?article_id=352. 7. Allen NH, Burns A, Newton V, Hickson F, Ramsden R, Rogers J, Butler S, Thistlewaite G, Morris J. The effects of improving hearing in dementia. Age Aging. 2003; 32:189-193. 8. Palmer C. Managing hearing loss in a patient with Alzheimer disease:  A case report. Dementia Review Journal, 2000;2,14. 9. Schum DJ, and Beck DL. Negative Synergy – Hearing Loss and Aging. 2008. http://www.audiologyonline.com/articles/ar ticle_detailasp?article_id=2045. 10. Gold M, Lightfoot LA, Hnath-Chisolm T. Hearing loss in a memory disorders clinic. A specially vulnerable population. Archives of Neurology, 1996;53(9): 922-928.



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11. Lin FR, Yaffe K, Xia J, et al. Hearing Loss and Cognitive Decline in Older Adults. JAMA Intern Med. 2013; 173(4):293-299. doi:10.1001/jamainternmed.2013.1868. 12. Lin FR, Metter EJ, O’Brien RJ, Resnick SM, Zondervan AB, Ferrucci L. Hearing loss and incident dementia. Archives of Neurology, 2011;68, 214-220. 13. National Council on Aging (NCOA): The Impact of Untreated Hearing Loss in Older Americans. Conducted by the Seniors Research Group. Supported through a grant from the Hearing Industries Association. www.ncoa.org. 1999. 14. Kochkink S, and Rogin CMA. Quantifying the obvious: The impact of hearing instruments on quality of life. Hearing Review, 2000;7(1), 8-34. 15. Moore AM, Voytas J, Kowalski D, Maddens M. Cerumen, hearing, and cognition in the elderly. J Am Med Dir Assoc. 2002;3(3):136–9. 16. Abrams H, Kihm J. An Introduction to MarkeTrak IX—A New Baseline for the Hearing Aid Market. Hearing Review 2015 June. 17. Mulrow CD, Aguilar C, et al. Quality of life changes and hearing impairment, a randomized trial. Annals of Internal Medicine, 1990;113 (188-194). 18. Amieva H, Ouvrard C, et al. Self-Reported Hearing Loss, Hearing Aids, and Cognitive Decline in Elderly Adults: A 25-Year Study. J Am Geriatr Soc 63:2099–2104, 2015.

Author Information: Dr. Sturdivant is Assistant Professor and Vice Chief of the Audiology Division at UMMC, specializing in the diagnosis and rehabilitation of adults with hearing loss. She earned her Doctor of Audiology (Au.D.) from Vanderbilt University School of Medicine in 2011, prior to which, she received a Bachelor of Science in Communicative Disorders from the University of Mississippi. Mailing address: 2500 N. State Street, 5 East, Department of Otolaryngology and Communicative Sciences, Jackson, MS 39216.

Journal of the Mississippi State Medical Association Keith Robinson, Assoc HR-Service Partner UMMC Talent Acquisition University of Mississippi Medical Center 2500 North State Street Jackson, MS 39216-4505 KRobinson@umc.edu

Dear Mr. Robinson: EOE, M/F/D/V.   Contact Information Vikas Majithia, MD, MPH Division of Rheumatology Chief University of Mississippi Medical Center 2500 North State Street Jackson, MS 39216 144 VOL. 57 • NO. 5 • 2016

Thank you for your interest in the JOURNAL MSMA. Your ad is typeset for a 24 line b/w ad at the rate of $5.50 per line ($132) plus an additional typesetting charge of $25 for a rate of $157 for the current insertion; $132 should you wish to run again thereafter. This ad could run in the May 2016 issue. Please proof, sign off, fax back (FAX 601-853-6746) or call if you have questions, 601-853-6733, extension 323. We will mail an


Committee Seeks Candidates for Vacancies in MSMA Offices Delegates attending the 148th MSMA Annual Session August 12-13, 2016 in Jackson will cast ballots to fill new terms of office for a number of association posts. The Nominating Committee is seeking input from the membership as the committee prepares a slate of nominees. The list of nominees developed by the Nominating Committee will be published to the entire membership before June 12, 2016. Eligibility: All nominees must be active members of the association. No physician may be put forth on the ballot unless that physician has expressed a willingness to serve if elected. Nominations for Vacancies: A chart follows listing the vacancies that will be filled by election in 2016. The names of incumbents, the length of each term of office and the incumbent’s eligibility to be re-elected are indicated. Nominating Committee: The Nominating Committee is composed of the nine most recent Past Presidents of the association residing in Mississippi. The Immediate Past President is the chair. OFFICERS & TRUSTEES President-elect at large Secretary at large Trustee District 2 Trustee District. 4 Trustee District 5 Trustee Resident/Fellow Trustee Student

INCUMBENT Lee Voulters Michael Mansour Brett Lampton William Grantham Dwight Keady Nicole Lee Brock Banks

AMA DELEGATES & ALTERNATE DELEGATES Position 1 Delegate at large Position 2 Delegate at large Position 3 Delegate at large Position 4 Alternate at large Position 5 Alternate at large Position 6 Alternate at large Position 7 Work Team at large Position 8 Work Team at large Position 9 Work Team at large Position 10 Work Team at large Position 11 Work Team at large Position 12 Work Team at large JOURNAL MSMA Associate Editor

Sharon P. Douglas J. Clay Hays, Jr. Claude Brunson Randy Easterling Lucius Lampton James Rish R. Lee Giffin Lee Voulters Jennifer J. Bryan Thomas Joiner Geri Lee Weiland Hugh Gamble, II INCUMBENT Stanley Hartness

COUNCILS Accreditation at large Accreditation at large Budget & Finance at large Budget & Finance at large Constitution & Bylaws at large Constitution & Bylaws at large Constitution & Bylaws at large Constitution & Bylaws at large Ethical and Judicial Affairs Ethical and Judicial Affairs Ethical and Judicial Affairs Legislation District 1 Legislation District 2 Legislation District 3 Legislation Resident Legislation Student Medical Education District 2 Medical Education District 4 Medical Education District 5 Medical Service District 4 Medical Service District 5 Medical Service Resident Medical Service Student Public Information District 1 Public Information District 2 Public Information District 3

INCUMBENT Lori Marshall Crystal Tate Susan Chiarito Chip Holbrook John Cross J. Martin Tucker Crystal Tate Victor Pang S. Kenn Beeman Ryan McGaughey Kathleen Lyons Michael Mansour B. Pearson Windham J. Murray Estess James Wilkinson Neal Boone DeWayne Gammel Jonathan Jones John Voss J. Anthony Cloy Michael Shrock Jonathan Buchanan Daniel Hester Robert Suares Son G. Lam Charlotte Magnussen

Terms of Office: President-elect: 1 year 2016-2017; Officers, Trustees & Councils (physicians): 3 years 2016-2019; Delegates to the AMA: 3 years; Trustees & Councils (students & residents): 1 year 2016-2017. Journal Associate Editor: 2 years 2016-2018. Incumbents NOT eligible for re-election are noted as the color grey. Email Nominations to CKanosky@MSMAonline.com or contact any member of the Nominating Committee: Claude Brunson, MD: Jim Rish, MD; Steve Demetropoulos, MD; Tom Joiner, MD; Tim Alford, MD; Randy Easterling, MD; Pat Barrett, MD; Dwalia South, MD; Eric Lindstrom, MD.





Top Abstracts from the 2015 American College of Physicians Mississippi Chapter Abstract Day at the University of Mississippi Medical Center [Each year the Mississippi Chapter of the American College of Physicians (ACP) and the Department of Medicine at the University of Mississippi Medical Center host an abstract competition among the state’s internal medicine residents, subspecialty fellows, and medical students. The event serves as a celebration of scholarship and a recognition of high quality patient care, novel disease processes, and unusual presentations of common illnesses. This year’s competition included 102 abstracts total from the categories of basic science research, clinical research, quality improvement projects, and clinical vignettes. Faculty from the Department of Medicine serve as judges. The abstracts presented here represent the work that received the highest scores at the competition.] —S. Calvin Thigpen, MD, FACP Governor-Elect, Mississippi Chapter, ACP Associate Program Director, Internal Medicine Residency University of Mississippi Medical Center 1. Stilbene derivatives inhibit prostate cancer cell proliferation and expression of metastasis-associated protein 1 2. Simvastatin inhibits epithelial-to-mesenchymal transition through induction of HO-1 in cultured renal proximal tubule cells 3. 2003 to 2012 mortality-to-incidence ratios for breast, colorectal, and cervical cancer in core Delta counties compared to non-Delta Mississippi counties 4. Near instant bone density analysis of the spine for the abdominal radiologist using color enhanced CT images 5. Analysis of the current rapid response system using the National Early Warning Score (NEWS) 6. Evaluating perceptions of and barriers to successful inpatient glycemic control among resident physicians 7. The knock: Opening the door to improved hand hygiene in dermatology outpatient clinics 8. The kiss of sudden cardiac death 9. Lessons learned in the treatment of Stronglyoides hyperinfection in a patient with acquired immunodeficiency syndrome 10. Management of Metformin-Associated Lactic Acidosis with SLED 11. Don’t forget about latent autoimmune diabetes of the adult 12. Refractory hypoglycemia: A rare initial manifestation of advanced hepatocellular carcinoma 13. Babesia in the southeast United States 14. Hyperemesis gravidarum precipitating thyroid storm resulting in Wernicke’s encephalopathy 15. A fever from Africa: An unusual presentation of hemophagocytic lymphohistiocytosis 16. They say his heart grew three sizes that day: An unusual case of esophageal dysphagia 17. Chronic eosinophilic pneumonia mimicking COPD exacerbation 18. Hyperpigmentation: A rarely recognized manifestation of vitamin B12 deficiency 19. Systemic loxoscelism: A rare cause of Coombs positive hemolytic anemia 20. A rare case of microvascular pulmonary arteriovenous malformations in a young female presenting with hypoxemic respiratory failure 21. Severe hypocalcemia following administration of zoledronic acid in an osteoporotic patient with a history of roux-en-y gastric bypass 22. Death by diarrhea 23. Paroxysmal nocturnal hemoglobinuria: Rare disease with expensive but effective treatment 24. A case of pulmonary mucormycosis in a patient with granulomatosis with polyangiitis 146 VOL. 57 • NO. 5 • 2016

1. S tilbene derivatives inhibit prostate cancer cell proliferation and expression of metastasisassociated protein 1 Benjamin A. Bates; Diva Whalen, PhD; Avinash Kumar, MD; Jian-Quan Weng, PhD; Agnes M. Rimando, PhD; Anait S. Levenson, MD University of Mississippi School of Medicine (Mr. Bates); Cancer Institute, University of Mississippi Medical Center (Dr. Whalen and Dr. Kumar); USDA, Agriculture Research Service, Natural Products Utilization Research Unit, Oxford, MS (Dr. Weng and Dr. Rimando); Department of Pathology, University of Mississippi Medical Center (Dr. Levenson) - Corresponding author: Benjamin A. Bates (babates@umc.edu) Introduction Evidence has emerged on the link between diet and cancer progression. Research has shown that dietary stilbenes, which can be found in grapes, berries, and peanuts, target metastasis-associated protein 1 (MTA1), which mediates chromatin remodeling and gene silencing. Pterostilbene exerts its anticancer and anti-metastatic effects through several key mechanisms, including down-regulation of MTA1. Our goal is to synthesize pterostilbene derivatives that exhibit increased potency and specificity against prostate cancer (PCa) cells, lengthened bioavailability, and pharmacologic safety. Methods We synthesized eighteen pterostilbene derivatives with the objective of improving its potency in inhibiting MTA1 and PCa cell proliferation. We treated DU145 and PC3M PCa cell lines with various concentrations (1, 5, 25, 50 µM) of different derivatives and analyzed cell proliferation by MTT assay and MTA1 expression by western blot. MTT assay was used to compare the potency of pterostilbene derivatives to pterostilbene. Western blot analysis of MTA1 provided information about the ability of pterostilbene derivatives to down-regulate MTA1 in comparison to pterostilbene. Discussion We found that treatment of DU145 cells with all compounds resulted in inhibition of cell proliferation albeit with different efficacy. We also found diverse degrees of the MTA1 expression inhibition by the different derivatives in PC3M cells. Quantitative analysis is underway to identify the most potent compound(s) for consideration as new chemopreventive strategy for the management of PCa. References Dhar S, Kumar A, Li K, Tzivion G, Levenson TS. Resveratrol regulates PTEN/Akt pathway through inhibition of MTA1/HDAC unit of the NuRD complex in prostate cancer. Biochimica et Biophysica Acta. 2015;1853(2):265-75.

2. S imvastatin inhibits epithelial-to-mesenchymal transition through induction of HO-1 in cultured renal proximal tubule cells Jeb S Clark, MD; Anthony Carter, MS; Mehul Dixit, MD; Istvan Arany, PhD Internal Medicine Residency Program, Department of Medicine, University of Mississippi Medical Center (Dr. Clark); University of Mississippi School of Medicine (Mr. Carter); Division of Nephrology, Department of Pediatrics, University of Mississippi Medical Center (Dr. Dixit and Dr. Arany) - Corresponding author: Jeb S. Clark, MD (jsclark@umc.edu) Introduction While benefits of statins in lipid lowering are well documented, much less is known about their antioxidant, anti-fibrotic, etc… effects that are independent of cholesterol reduction. Studies have shown that simvastatin (SIM) inhibits epithelial-to-mesenchymal transition (EMT) –a key step in fibrogenesis- in renal epithelial cells. The mechanism of this inhibition, however, has yet to be completely determined. Our laboratory recently demonstrated that SIM transcriptionally activates the heme oxygenase-1 (HO-1) gene in cultured renal proximal tubule cells. Others showed that HO-1 inhibits transforming growth factor beta-1 (TGFβ1)-mediated EMT that may involve suppression of production of reactive oxygen species (ROS). Accordingly, we tested the hypothesis that SIM inhibits TGFβ1-dependent ROS production and consequent EMT via induction of HO-1 in cultured renal proximal tubule cells. Methods Porcine renal proximal tubule cells (LLC-PK1) were treated with either 10 µM SIM or 10 ng/ml TGFβ1 or with their combination for 24 hours in the presence or absence of 20 µM tin-protoporphyrin [(SnPP) to inhibit HO-1 activity] or the ROS scavenger N-acetyl-cysteine (NAC; 10 µM) and promoter activity of the alpha-smooth muscle actin (αSMA) gene (marker of EMT) was determined in a reporter luciferase assay. Changes in the actin cytoskeleton were also determined by fluorescence microscopy in phalloidin-stained cells following 2-day-exposure to TGFβ1, SIM or their combination. Impact of SIM and HO-1 induction [by overexpression or stimulation by cobalt-protoporphyrin (CoPP)] on TGFβ1dependent ROS production was also assessed using the oxidant-sensitive 2’,7’-dichlorofluorescein-diacetate (DCFDA). JOURNAL MSMA


Expected Results TGFβ1 treatment significantly increased activity of the αSMA promoter, which was attenuated by SIM or NAC. Importantly, pre-treatment with SnPP reversed beneficial effects of SIM. Furthermore, cells exposed to TGFβ1 exhibited increased formation of stress fibers consistent with the onset of EMT, which was also attenuated by SIM. In addition, SIM treatment as well as endogenous induction or exogenous overexpression of HO-1 attenuated TGFβ1-dependent ROS production. Discussion Our results suggest that SIM –via induction of HO-1- suppresses TGFβ1-dependent ROS production and, hence EMT. Further evaluation of the underlying mechanism of this anti-fibrotic nature of SIM in the kidney is needed, which may be useful in treatment of chronic kidney disease.

3. 2 003 to 2012 mortality-to-incidence ratios for breast, colorectal, and cervical cancer in core Delta counties compared to non-Delta Mississippi counties John Clark Henegan, Jr, MD Division of Hematology and Oncology, Department of Medicine, University of Mississippi Medical Center - Corresponding author: John Clark Henegan, MD (jhenegan@umc.edu) Objectives To compare, as a surrogate for health care disparities, the mortality-to-incidence ratio (MIR) for three screenable malignancies – breast, colorectal, and cervical cancer –in core Mississippi Delta counties to non-Delta counties in the state. Methods Data were obtained from the online Mississippi Cancer Registry for the age-adjusted rates of incidence and mortality for breast, colorectal, and cervical cancer by Mississippi county from 2003-2012. Cancer-specific MIR was calculated by dividing each county’s age-adjusted mortality rate by its age-adjusted incidence rate. Core Delta and non-Delta counties (excluding buffer counties as defined by the Mississippi Cancer Registry) were compared. To determine if any detected difference could be confounded by rurality, the MIR of Delta counties was also compared to Mississippi non-Delta counties classified as “Rural” by the Mississippi Cancer Registry. All comparisons involved a two-sided student T-test and assumed unequal variance between the two samples. Results

Per 100,000 Cancer Age-Adjusted Mortality Rates Age-Adjusted Incidence Rates

Cervical 6.59 (5.238.20) 13.40 (11.3815.67)

Delta Breast 32.18 (29.1335.48) 104.86 (99.21110.74)

Colorectal 30.04 (27.8132.41) 65.98 (62.6469.44)

Cervical 3.31 (3.003.64) 9.13 (8.609.69)

Non-Delta Breast Colorectal 23.83 19.00 (23.02(18.4624.67) 19.55) 113.75 88.50 (111.94(87.33115.58) 89.68)

Delta vs. Non-Delta Counties, pvalues of t-test Mortality-to-Incidence Ratio

Cervical Cancer 0.24

Breast Cancer 0.03

Colorectal Cancer 0.01

Delta vs. Rural Counties, p-values of t-test Mortality-to-Incidence Ratio

Cervical Cancer 0.33

Breast Cancer 0.09

Colorectal Cancer 0.02

Conclusion In Mississippi from 2003 to 2012, the MIR was statistically different for breast and colorectal cancer between Delta and non-Delta counties. When comparing counties in the core Delta to Rural counties in the state, only the colorectal cancer MIR remained statistically different. New and specific methods of colorectal cancer management are needed in the Delta.

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4. N  ear instant bone density analysis of the spine for the abdominal radiologist using color enhanced CT images Boshen Liu, MS; Andrew D. Smith, MD, PhD; Danny Hankins, MD; Manohar Roda, MD; David Joyner, MD; Majid Khan, MD; Chris Reed, DO; Nisha Swaminathan, MD; Jason Bryan, MS; Amit Vasanji, PhD; Michael Griswold, PhD; Xu Zhang, PhD; Thomas Mosley, PhD Department of Radiology, University of Mississippi Medical Center (Mr. Liu, Dr. Smith, Dr. Hankins, Dr. Roda, Dr. Joyner, Dr. Khan, Dr. Reed, Dr. Swaminathan); Image IQ, Cleveland Clinic (Mr. Bryan, Dr. Vasanji); Department of Biostatistic, University of Mississippi School of Medicine (Dr. Griswold and Dr. Zhang); The MIND Center, University of Mississippi School of Medicine (Dr. Mosley) - Corresponding author: Andrew Smith, MD, PhD (asmith4@ umc.edu) Purpose To establish CT colorization techniques for rapid bone density screening of the spine.   Methods Nonenhanced CT images of the mid lumbar spine were obtained in 660 participants of the GENOA study with a quantitative CT (QCT) imaging phantom in place. Attenuation at L3/L4 was associated with measured bone mineral density (BMD) to derive optimal cut points for colorizing osteoporosis as red, low BMD as blue, and normal BMD as green. In a random sample (N=120), five radiologist independently categorized BMD using visual assessment of sagittal grayscale images, visual assessment of sagittal colorized images, and QCT BMD measurements of axial grayscale images (mean BMD = gold standard).   Results Mean CT attenuation coefficients were highly correlated with BMD at L3/L4 (R=0.960/0.961). Optimal cut point for osteoporosis / low BMD was 96HU and for low BMD / normal BMD was 120HU. Mean sens/spec/ppv/npv at L3/L4 across 5 readers for classifying BMD was 51/55/37/81 for grayscale image interpretation, 88/81/78/94 for colorized image interpretation, and 94/91/86/95 when using QCT BMD software. Average interpretation time per case was significantly longer for QCT imaging (49 seconds) compared to visual interpretation of grayscale (8.4 seconds, p<0.001) or colorized images (8.5 seconds, p<0.001). The mean Youden index for correctly categorizing disease was 32 for grayscale, 77 for colorized images, and 86 for QCT imaging.   Conclusion Visual interpretation of colorized sagittal CT images of the spine to differentiate osteoporosis, low BMD, and normal BMD can be accomplished in <10 seconds per study with high sensitivity and specificity.

5. A  nalysis of the current rapid response system using the National Early Warning Score (NEWS) Jeffrey J Grondin, MD and Andrew M. Wilhelm, DO Internal Medicine Residency Program, Department of Medicine, University of Mississippi Medical Center (Dr. Grondin); Division of Pulmonology, Department of Medicine, University of Mississippi Medical Center (Dr. Wilhelm) - Corresponding author: Jeffrey J Grondin, MD (jgrondin@umc.edu) Introduction The function of a rapid response team is early intervention to prevent adverse outcomes. Clinical deterioration is often detectable hours before an adverse event. We sought to compare our current rapid response criteria versus a validated early warning score. Utilization of a more sensitive system in our population could result in earlier detection of clinical deterioration when compared to the existing protocol. Methods We conducted a quality improvement study at a teaching hospital in Jackson Mississippi. We retrospectively analyzed all rapid response events from a medical ward (2 North) during the time frame 7/1/2013-6/30/2014. Patient alertness and vital signs were evaluated 24 hours before the rapid response using the current rapid response activation and the National Early Warning Score (NEWS). The trigger for physician notification using the NEWS was set at a cumulative score of 5 or a single category score of 3. Results There was a total of 63 rapid response events on 2 North within the designated time frame. All but 4 of these events met NEWS criteria; these events also did not meet the current rapid response criteria and were, therefore, discarded from analysis. Forty-four of the remaining 59 events would have caused an earlier activation using the NEWS scoring system, with a mean time difference of 15.2 hours.



NEWS Current

Present at time of RR

Present in 24 hours before RR

15 45

44 14

When all 59 independent samples meeting NEWS activation were compared using a two-tailed t-test, use of the early warning score resulted in a mean time of 11.3 (p<0.001) for earlier identification of deteriorating patients. Comparing the mean time intervals of activation (mean current system- mean NEWS) showed 7.56 hours earlier activation using the NEWS system (95% CI +/- 3.4). Conclusion The implementation of the standardized NEWS scoring system would result in earlier detection of deteriorating patients for earlier intervention, an average of 11.3 hours earlier. Fourteen events which met current criteria in the 24 hours leading up to the event did not result in a rapid response activation, indicating poor utilization of the current system. Further education and automation of the triggers would result in optimal utilization of the rapid response system, ideally preventing adverse patient outcomes and allowing for earlier medical intervention.

6. E valuating perceptions of and barriers to successful inpatient glycemic control among resident physicians William B. Horton, MD; S. Calvin Thigpen, MD Internal Medicine Residency Program, Department of Medicine, University of Mississippi Medical Center (Dr. Horton); Division of General Internal Medicine & Hypertension, Department of Medicine, University of Mississippi Medical Center (Dr. Thigpen) - Corresponding author: William B. Horton, MD (wbhorton@umc.edu) Introduction The link between uncontrolled hyperglycemia and increased patient morbidity, mortality, and length of hospital stay is well-established.1 Before educational interventions and policies aimed at improving inpatient glycemic control can be established, institutions should gain a better understanding of how practitioners view inpatient glycemic control. We developed a questionnaire and surveyed resident physicians to examine their perceptions of and barriers to successful inpatient glycemic control. Methods We designed a questionnaire, and Institutional Review Board (IRB) approval was granted. We then administered the questionnaire to Internal Medicine and Medicine-Pediatric resident physicians at the University of Mississippi Medical Center to determine their viewpoints regarding the importance of inpatient glycemic control, knowledge of inpatient glycemic target values, and problems encountered when trying to manage hyperglycemia in hospitalized patients. Results Of 87 eligible resident physicians, 73 (83.9%) completed the questionnaire (84.9% Internal Medicine residents; 34.2% first-year residents; 28.8% second-year residents; 28.8% third-year residents; 8.2% fourth-year residents). Most residents (72.2%) agreed that they felt comfortable treating and managing inpatient hyperglycemia, and most (56.2%) also agreed that they had received adequate education and preparation. However, only a slim majority (51.4%) could identify appropriate inpatient random glucose target values in non-critically ill patients. Only 50% could correctly identify glycemic targets in critically ill patients, and only 41.7% of respondents knew appropriate preprandial glucose targets in non-critically ill patients. Lack of knowledge of basal plus bolus insulin regimens and lack of discussion about glucose management on teaching rounds were both barriers to successful inpatient glycemic control for 51.4% of respondents. When asked to identify the single greatest barrier to successful inpatient glycemic control, lack of education (25.4%), nursing issues such as withholding insulin (22.4%), and system issues such as dietary components and fingerstick glucose/insulin timing (22.4%) were the most commonly cited answers. Fear of hypoglycemia was only the sixth most common response (4.5%). Discussion Most residents reported feeling comfortable managing inpatient hyperglycemia but had trouble identifying appropriate inpatient glycemic targets from the most recent consensus guidelines.1 Lack of education and nursing/system issues were the most commonly cited barriers to ideal inpatient glycemic management. Limitations of this study include the wording of the questions and Likert scale answers both being subject to interpretation of the respondent and respondents being from one academic medical center. Future interventions should focus on resident education along with improving system environments to aid in successful inpatient glycemic control.

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References 1. Moghissi ES, Korytkowski MT, DiNardo M, et al. American Association of Clinical Endocrinologists and American Diabetes Association consensus statement on inpatient glycemic control. Endocr Pract. 2009; 15(4): 353-369.

7. The knock: Opening the door to improved hand hygiene in dermatology outpatient clinics Jess L. Rush; Richard H. Flowers; Kathleen M. Casamiquela, MD; Stephanie K. Jacks, MD; Jamil Ibrahim, PhD; Robert T. Brodell, MD University of Mississippi School of Medicine (Mr. Rush, Mr. Flowers); Department of Pathology, University of Mississippi Medical Center (Dr. Casamiquela, Dr. Jacks, and Dr. Brodell); School of Health Related Professions, University of Mississippi Medical Center (Dr. Ibrhaim) - Corresponding author: Jess L. Rush (jlrush@umc.edu) Background Despite overwhelming evidence supporting its benefits, hand hygiene adherence remains low among medical professionals1. Residents at University of Mississippi Medical Center (UMMC) recognized that faculty members often failed to use recommended hand hygiene in outpatient clinics. This study assessed the extent of this problem and enacted a replicable, time-efficient method of monitoring and feedback designed to improve hand hygiene in the office setting. Methods All seven dermatology faculty members at UMMC participated in this observational prospective quality assessment/quality improvement (QA/ QI) study. Adherence was defined as using alcohol based hand rub (ABHR) or hand-washing upon entering the examination room. Faculty members were observed by one resident during three separate weeklong periods in May 2014 (pre-intervention), October 2014, and July 2015 (post-intervention). Faculty members were not informed about the study during the initial pre-intervention phase. Two interventions were planned: Educational Intervention Following the initial observational phase, a resident presented evidence in support of hand hygiene and the data demonstrating an unsatisfactory initial adherence rate at a faculty meeting. The faculty members were informed they would be observed again at an unspecified time in the future. Feedback Intervention Faculty, residents, nurses, and students were instructed to knock on a counter if they witnessed any team member enter a patient’s room without using hand hygiene. This subtle reminder was intended to stimulate immediate use of hand hygiene without drawing undue attention or embarrassment to non-adhering team member. Results The first phase involved 69 patients, second phase involved 101 patients, and the third phase involved 94 patients. The first phase was preintervention, and the second and third phases were post-intervention. The proportion of those who used appropriate hand hygiene prior to the intervention was 55.1%. After the intervention, the proportion was 81.2%. After eight more months, the adherence rate remained high at 89.4%. A chi-square analysis demonstrated these proportions are significantly different χ2 (2,N=264) = 28.068, p<0.0001. Conclusion Although the study design did not permit a determination of the relative importance of the educational intervention versus “the” knock, we believe the persistent use of “the” knock was responsible for the long-term improvement in hand-hygiene. “The knock” is easy to sustain and replicable. It is effective and time-efficient, and the medical team enjoyed “catching” each other in lapses of hand hygiene. Thus, “the” knock is a critical systemic change that opens the door to prolonged improvement in hand hygiene. References Centers for Disease Control and Prevention (CDC). Guideline for Hand Hygiene in Health-Care Settings- Recommendations of the Healthcare Infection Control Practices Advisory Committee and the HICPAC/SHEA/APIC/IDSA Hand Hygiene Task Force, 2002. MMWR Morb Mortal Wkly Rep. 2002; 51(No. RR-16):1-56.

8. The kiss of sudden cardiac death L. Wesley Aldred, MD; Erica Turse, DO; R. Dane Ballard, MD; J. Barr Biglane, MD; Bryan Barksdale, MD Internal Medicine Residency Program, Department of Medicine, University of Mississippi Medical Center (Dr. Aldred and Dr. Turse); Cardiology Fellowship Program, Division of Cardiology, Department of Medicine, University of Mississippi Medical Center (Dr. Ballard and Dr. Biglane); Division of Cardiology, Department of Medicine, University of Mississippi Medical Center (Dr. Barkdale) - Corresponding author: L. Wesley Aldred, MD (laldred@umc.edu)



Introduction Although coronary heart disease and heart failure are the major causes of sudden cardiac arrest, myocarditis has also been shown to be a common cause. Myocarditis, defined as an inflammatory infiltration of the myocardium with associated necrosis or degeneration, has many forms and even more causes. Herein, we report a case of sudden cardiac arrest secondary to myocarditis. Case Discussion A 21-year-old male was found unresponsive and pulseless in his car. First responders began cardiopulmonary resuscitation. Shortly after emergency medical services arrived, he was successfully defibrillated for ventricular fibrillation. Return of spontaneous circulation was obtained, and he was transferred to our facility. Patient was negative for drugs or ethanol with normal electrolytes. However, initial lab work showed an elevated troponin T of 2.19 ng/mL with an electrocardiogram (ECG) showing mild ST segment elevations in leads V1 and V2. We then took him for urgent coronary angiography, which showed normal coronaries. However, his left ventriculogram revealed an ejection fraction of 35 percent, with anterolateral dyskinesis and posterobasal akinesis. Subsequently, we admitted him to the cardiac intensive care unit with presumed atypical Takotsubo cardiomyopathy. His initial ECG was also concerning for Brugada syndrome. This finding, in addition to an elevation of his C-reactive protein to 8.6 mg/dL, prompted cardiac magnetic resonance imaging (CMR) that showed findings consistent with myocarditis. Further history revealed that the patient had been diagnosed with infectious mononucleosis two weeks prior to admission. Lab work confirmed IgG and IgM antibodies to the viral capsid antigen of the Epstein-Barr virus (EBV). The patient’s condition improved, and prior to discharge we placed an implantable cardiac defibrillator in the patient. Conclusion The incidence and prevalence of myocarditis are unclear due to the large number of patients that manifest asymptomatically. When symptomatic, patients can present with a myriad of symptoms including chest pain, arrhythmias, heart failure, sudden cardiac arrest, and sudden cardiac death. Myocarditis is estimated to have an incidence of 0-6% in infectious mononucleosis.3,4 6% of those with mononucleosis have ST-T abnormalities; however, death from EBV is extremely rare.5,6 The CMR combined with positive serologic testing helped to confirm this mercurial disease, which is challenging to diagnose and treat. There is still much to be learned about myocarditis and the role viruses play in the disease. However, early recognition and treatment with heart failure therapy remain the standard for managing these sick patients with several studies also suggesting that steroids may play some role.4,7 References: 1. 2006 American College of Cardiology/American Heart Association/Heart Rhythm Society. 2. Drory, Turetz, Hiss, et al. Sudden Unexpected Death in Persons <40 Years of Age. Am J Cardiol 1991;68;1388-1392. 3. Sabbatani, Manfredi, Ortolani et el. Myopericarditis During a Primary Epstein-Barr Virus Infection in an Otherwise Healthy Young Adult. An Unusual and Insidious Complication. Case report and a 60-Year Literature Review. Le Inferzioni in Medicina 2012; 2; 75-81. 4. Baykurt, Caglar, Ceviz et al. Successful treatment of Epstein-Barr virus infection associated with myocarditis. Pediatrics International 1999; 41;389-391. 5. Johannsen E, Schooley R, Kaye K. Epstein-Barr virus (Infectious Mononucelosis). In: Principles and Practices of Infectious Diseases 8th ed. Bennett JE, Dolin R, Blaser MJ, Eds. Elsevier Inc., 2015: 1754-1771.e6. 6. Hoagland RJ. Mononucleosis and Heart Disease. Am J Med Sci 1964; 248: 1-6. 7. Ghosal R, Lewis KE, Chandramouli S. Infectious mononucleosis complicated by acute hepatitis and myocarditis: a response to corticosteroids. BMJ Case Reports; 2009. DOI: 10.1136/bcr.10.2008.1083.

9. L essons learned in the treatment of stronglyoides stercoralis hyperinfection in a patient with acquired immunodeficiency syndrome Roberto G. Aru; L. Campbell Behlen, MD; Catherine E. Lowe, MD; Frederick H. Asher, MD; Richard D. deShazo, MD University of Mississippi School of Medicine (Mr. Aru); Internal Medicine Residency Program, Department of Medicine, University of Mississippi Medical Center (Dr. Behlen and Dr. Lowe); Division of Hospital Medicine, University of Mississippi Medical Center (Dr. Asher); Division of Allergy & Immunology, Department of Medicine, University of Mississippi Medical Center (Dr. deShazo) - Corresponding author: Roberto G. Aru (raru@umc.edu) Introduction Human Immunodeficiency Virus (HIV) infection has been associated with 21-fold increased prevalence in Strongyloides stercoralis infection.1 S. stercoralis is a parasite that has been associated with diarrhea and gastrointestinal bleeding, especially with gastritis, duodenitis, or jejunitis.1,2,3 Here, we report a case of refractory bleeding secondary to S. stercoralis infection in a patient with Acquired Immunodeficiency Syndrome (AIDS). Case Description This patient is a 44-year-old African-American male with a history of AIDS (CD4 count 1) who presented with diffuse abdominal pain. He had been admitted three weeks prior with vomiting, diarrhea, and abdominal pain. He had jejunitis on computed tomography (CT) scan, and

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stool studies were collected which resulted S. stercoralis. He underwent esophagogastroduodenoscopy (EGD) with biopsies for confirmation. He was treated with Ivermectin and discharged in stable condition. Patient returned to the emergency department with similar complaints, in addition to melena. Physical exam was significant for oral thrush, tachypnea, 3/6 holosystolic murmur, abdominal guarding and tenderness, decreased but symmetric dorsalis pedis pulses, and diffuse muscle wasting. Upon admission, hemoglobin and hematocrit were 5.6 and 18.3, respectively. CT abdomen showed small bowel obstruction in right lower quadrant of the abdomen with hyperdense material in the lumen of the duodenum and jejunum. The patient received multiple packed red blood cell transfusions, and he underwent repeat EGD, which showed innumerable oozing ulcers in the duodenum and a large clot. Duodenal biopsies were taken, which yielded parasites compatible with S. stercoralis infestation. He required emergent interventional radiology embolization of the gastroduodenal artery and a branch of the superior mesenteric artery supplying the jejunum. Patient was started on Albendazole and Ivermectin. He improved clinically, and at time of discharge, stool ova and parasite (O&P) denoted no S. stercoralis infection. Additionally, he had resolution of his diarrhea with no signs or symptoms of bleeding. He was continued on Albendazole and Ivermectin treatment for 14 additional days and was discharged from the hospital without further events. Discussion This example of a S. stercoralis superinfection limited to the GI tract failed standard Ivermectin treatment likely because of the autoinfective capability of S. stercoralis and immunocompromised state secondary to HIV infection. Patient could have received confirmatory stool O&P at discharge of previous admission to denote if there was resolution of the infection. Therapy in the immunocompromised, as well as those with poor intestinal absorption secondary to inflammation, should be more extensive than standard, 3-day Ivermectin therapy. References

1. Assefa S, Erko B, Medhin G, Assefa Z, Shimelis T. Intestinal parasitic infections in relation to HIV/AIDS status, diarrhea and CD4 T-cell count. BMC Infect Dis. 2009 Sep 18; 9:155. 2. Keiser P, Nutman T.B. Strongyloides stercoralis in the Immunocompromised Population. Clin. Microbiol. Rev. 2004 Jan vol. 17 no. 1 208-217. 3. Grove D.I. Strongyloides: a conundrum for gastroenterologists. Gut. 1994 Apr; 35(4): 437â&#x20AC;&#x201C;440.

10. Management of metformin-associated lactic acidosis with SLED G.A. Bader, MD; J.M. Tate, MD; S. Degen, MD; W. Latack, MD Department of Medicine Keesler AFB, Keesler Medical Center - Corresponding author: Joshua M. Tate, MD (Joshua.tate.2@us.af.mil) Introduction: Metformin is widely considered a first-line medication for the management of Type 2 Diabetes Mellitus (T2DM), with clinical efficacy for reducing cardiovascular and total mortality rates.1 Metformin-associated lactic acidosis (MALA) remains a rare but potentially fatal condition. Metformin toxicity is driven by suppression of hepatic gluconeogenesis, and interference with oxidative phosphorylation, resulting in the formation of lactate from pyruvate.2 Metformin toxicity is typically noted at serum levels >5mcg/mL, with normal therapeutic range being 1-2mcg/mL. Standard of care for this condition is rapidly evolving with recent evidence recommending prolonged hemodialysis or CVHDF to remove metformin serum levels in patients with hemodynamic instability.3-5 The following case series describes the management of two MALA cases managed with Sustained Low Efficiency Dialysis (SLED). Case Descriptions A 72-year-old female with a history of RCC s/p nephrectomy, CKD, and T2DM. Patient sought treatment after five days of anorexia, vomiting, and diarrhea. Patient continued taking metformin and lisinopril. She was somnolent, blood pressure 90/60 with otherwise normal exam. Labs notable for: Na 130, K 6.8, HCO3 7.2, Cr 9.2 (baseline 1.2), lactate 10.3, and pH 7.07. There was no clinical or imaging evidence to support sepsis, ischemic bowel, or other acute process. After initial hyperkalemia treatment, she was admitted to the ICU and 8 hour SLED treatment was completed due to marginal blood pressures. Metabolic acidosis and hypotension rapidly corrected, along with correction of her altered mentation. A 67-year-old male with a history of CAD and T2DM. Patient sought treatment after 3 days of vomiting, malaise, anorexia, and oliguria. Patient continued metformin, lisinopril, hydrochlorothiazide, and furosemide. Blood pressure was 180/77 with otherwise unremarkable exam. Labs at presentation included: Na 123, K 6.2, HCO3 15, Cr 9.8 (baseline of 0.8), lactate 6.6, and pH 7.244. The patient was admitted to the ICU and SLED was initiated with rapid correction in lactic acidosis. SLED was used due to significant hyponatremia. Metformin level was 8mcg/mL prior to initiation of SLED and 3mcg/mL following 16 hour SLED treatment, showing resolution of metformin toxicity. Discussion SLED is becoming a commonly utilized dialysis modality for critically ill patients with acute renal failure, given its perceived safety, efficacy and convenience in patients.6 To date, there are very few case reports utilizing SLED in the treatment of MALA.7 These cases highlight an evolving role of SLED in the management of MALA in critically ill patients, as displayed in the above cases.



References 1. UK Prospective Diabetes Study (UKPDS) Group. Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS). Lancet 1998;352:854-865. 2. Kraut, J.A., and Madias, N.E. Lactic Acidosis. NEJM 2014;371:2309-19. 3. Baro-Serra, A., et al. The importance of early haemodiafiltration in the treatment of lactic acidosis associated with the administration of metformin. Nefrologia 2012;32(5):665-9. 4. Peters, N. et al. Metformin-associated lactic acidosis in an intensive care unit. Crit Care. 2008;12:R149. 5. Fitzgerald, E. Mathieu, S., Ball, A. Metformin associated lactic acidosis. BMJ 2009;339:b3660. 6. Marshall, M.R., et al. Sustained low-efficiency dialysis for critically ill patients requiring renal replacement therapy. Kidney International 2001;60:77785. 7. Teutonico, A., et al. Treatment of metformin-associated lactic acidosis with sustained low-efficiency daily dialysis. Clin Kidney J. 2008;1(5):380-1.

11. Don’t forget about latent autoimmune diabetes of the adult H. Baker Boler; L. Wesley Aldred, MD; Sarah Kerut, MD; Jerry Sheppard, MD University of Mississippi School of Medicine (Mr. Boler); Internal Medicine Residency Program, Department of Medicine, University of Mississippi Medical Center (Dr. Aldred and Dr. Kerut); Division of Hospitalist Medicine, University of Mississippi Medical Center (Dr. Sheppard) - Corresponding author: H. Baker Boler (hboler@umc.edu) Introduction Latent autoimmune diabetes in adults (LADA) describes patients with a phenotype for type 2 diabetes combined with islet antibodies and slowly progressive b-cell failure. It is an important entity to recognize, as it can alter management strategies in diabetes. Herein we report a case of diabetic ketoacidosis (DKA) in a patient who was found to have LADA. Case Description A 35-year-old morbidly obese black male with untreated hypertension presented to the Emergency Department (ED) complaining of shortness of breath, nausea, and vomiting for two days. He also reported weight loss, polyuria, and polydipsia. He had a family history of non-insulin dependent diabetes mellitus in his maternal grandmother and multiple cousins. In the ED he was noted to have severe metabolic acidosis with an anion gap of 38 mmol/L, a bicarbonate level of 4.0 mmol/L, a pH of 7.15, a glucose elevated to 504 mg/dL, and ketones in his urine, which is diagnostic of DKA. We started the patient on an insulin infusion and admitted him to the MICU. He had no evidence of infection, had no recent trauma, and had not undergone any recent surgeries. His hemoglobin A1c was found to be elevated above 18.9%. His DKA resolved with an insulin infusion and he was transitioned to subcutaneous insulin. Given the severity of his DKA, and the lack of precipitating factors, we ordered glutamic acid decarboxylase antibody levels, which were found to be elevated at 0.16 nmol/L. Discussion DKA is much more common in patients with autoimmune type 1 diabetes mellitus. However it can occur in patients with type 2 diabetes mellitus if provoked by times of catabolic stress, such as trauma, surgery, and infections. Our patient, who was 35 years old and morbidly obese, fits the phenotype for type 2 diabetes mellitus. However, he lacked a precipitating factor for DKA. In this type of clinical scenario, LADA needs to be considered. It is important to uncover this diagnosis, as these patients will likely require lifelong insulin. References 1. 2.

Stenstrom G, Gottsater A, et al. Latent Autoimmune Diabetes in Adults. Diabetes 54:S68-S72, 2005. Kitabchi AE, Umpierrez GE, Miles JM, and Fisher JN. Hyperglycemic Crises in Adult Patients with Diabetes. Diabetes Care. 2009;32(7):1335-43.

12. Refractory hypoglycemia: A rare initial manifestation of advanced hepatocellular carcinoma Christa Bowes, MD; Rebecca Pace, MD; Jose Subauste, MD2 Internal Medicine Residency Program, Department of Medicine, University of Mississippi Medical Center (Dr. Bowes); Division of Endocrinology, Department of Medicine, University of Mississippi Medical Center (Dr. Pace and Dr. Subauste) - Corresponding author: Christa Bowes, MD (cbowes@umc.edu) Introduction Hepatocellular carcinoma (HCC) with a paraneoplastic manifestation has a prevalence of 4-27%.1 Although hypoglycemia as a paraneoplastic syndrome is not an uncommon presentation with advanced HCC, hypoglycemia as initial presentation is rare. Here we report a case of refractory hypoglycemia as an initial manifestation of HCC.

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Case Description A 33-year-old Hispanic male presented to the Emergency Department after being found confused by co-workers. He complained of weakness, fatigue and headaches over the last month and a 20lb weight loss in the last year. He had no previous medical problems. On physical examination he was lethargic and slow to respond to questions. Examination of his abdomen revealed hepatomegaly with a palpable mass in the left lobe. No bruit or rub heard over the mass, and no other stigmata of chronic liver disease present or acromegaly. Pulmonary and cardiovascular systems were unremarkable. Glucose on admission was 29mg/dL, which prompted further hypoglycemia evaluation. Laboratory tests revealed Insulin <1uU/ mL, C-Peptide 0.04ng/mL, Insulin Antibody negative, Proinsulin 2.3pmol/L and sulfonylurea screen negative. Serum testing confirmed Chronic Hepatitis B, AFP-Tumor Marker was >50000IU/mL, Insulin-Like Growth Factor 1 (IGF1) 22ng/mL, and Insulin-Like Growth Factor II (IGF2) 506ng/mL, IGF2/IGF1 molar ration of 23. Growth Hormone < 0.01ng/mL. Computed tomography of the abdomen confirmed a 21cm mass concerning for HCC. Lesions in both hepatic lobes and a 1cm nodule in the right upper lobe of the lung were noted concerning for metastases. Despite intravenous dextrose infusion he continued to have episodes of fasting hypoglycemia. He was started on Prednisone, chewable dextrose tablets, and high protein-carbohydrate meals. He was weaned off intravenous dextrose with no further episodes of hypoglycemia. Discussion Two types of hypoglycemia have been described with HCC. Type A hypoglycemia occurs with advanced HCC. As the liver is replaced by tumor it is no longer able to meet the glucose demands of the body.2 Type B hypoglycemia occurs due to defective processing of the precursor to IGF2 (pro-IGF2) by the hepatocytes and causes increased glucose uptake. Molar ratio of IGF2:IGF1 was 10:1 which supports our suspicion of a nonislet cell mediated hypoglycemia. Steroids and high carbohydrate meals have been described as options for management of hypoglycemia in HCC. Steroids aid with stimulating gluconeogenesis, and prednisolone, the active metabolite in prednisone, has been described to decrease pro-IGF2 levels.1 It is important to consider the diagnosis of HCC in patients who present with chronic liver disease and hypoglycemia as paraneoplastic syndromes play a significant role in management and are associated with a poor prognosis.3 References 1. Sharma M, Reddy D, Kiat T. Refractory hypoglycemia presenting as first manifestation of advanced hepatocellular carcinoma. ACG Case Rep J. 2014; 2(1):50-52. 2. Tsai C, Chou S, Liu H, Lin J, Lin Y. Persistent hypoglycemia as an early, atypical presentation of hepatocellular carcinoma: A case report and systemic review of the literature. Oncology Letters. 2014; 8(4):1810-1814. 3. Qu Q, Wang S, Chen S, Zhou L, Rui J. Prognostic role and significance of paraneoplastic syndromes in hepatocellular carcinoma. The American Surgeon. 2014; 80(2); 191-196.

13. Babesia in the Southeast United States Savannah Duckworth, MD; Megan Edwards, DO; John Clark Henegan, MD; James Benjamin Brock, MD. Internal Medicine Residency Program, Department of Medicine, University of Mississippi Medical Center (Dr. Duckworth); Department of Neurology, University of Mississippi Medical Center (Dr. Edwards); Division of Hematology & Oncology, Department of Medicine, University of Mississippi Medical Center (Dr. Henegan); Division of Infectious Diseases, Department of Medicine, University of Mississippi Medical Center (Dr. Brock) - Corresponding author: Savannah Duckworth, MD (seduckworth@umc.edu) Introduction In the United States, human babesiosis is caused by infection with protozoan Babesia microti. B. microti is transmitted to humans by  Ixodes scapularis tick, (via) blood transfusion, or transplacental. Presentations range from asymptomatic to life threatening conditions. Complications are more common in immunocompromised and elderly patients. Babesiosis generally occurs in the Northeast where I. scapularis is endemic. We report a case of human babesiosis without exposure to an endemic region. Description An 85-year-old man was found weak and unresponsive at home in southwest Mississippi. History included cerebral vascular accident; pulmonary embolism; deep vein thrombosis on warfarin; splenectomy; and IgG4-related disease treated with rituximab and prednisone. Patient indicated right-sided back/hip pain, headaches, hematuria, chills, fatigue, and generalized weakness. He reported travel to Texas but none to Babesiaendemic areas. He received red blood cell transfusions in Texas for IgG4-related disease. On exam, temperature 102.8 F with heart rate of 95 bpm. Respiratory rate normal and blood pressure 149/80 mm Hg. No rashes noted. Labwork revealed normal white blood cell count, elevated lactate dehydrogenase (450 U/L), and elevated serum creatinine (2.59 mg/dL). Thrombocytopenic on admission (80,000/cmm)- this value decreased further (57,000/cmm). Fragmented red blood cells negative, haptoglobin was < 5.83 mg/dL, and HIV antibody screen negative. Peripheral smear showed inclusions, burr cells, spurr cells, and rouleaux formation. Inclusions encompassed ~10% total red blood cells. Smears submitted to Centers for Disease Control and Prevention (CDC) parasitology division confirmed Babesia. CDC parasitology lab reported B. microti indirect flourescent antibody titer of 1:256 and positive B. microti PCR. Clindamycin and quinine were begun. Patient underwent red blood cell exchange transfusion. Peripheral blood smear following exchange was without Babesia. Platelets recovered. He was discharged with quinine and clindamycin, then azithromycin and atovaquone. Peripheral blood smear reviewed since discharge contnued negative for intraerythrocytic parasites. JOURNAL MSMA


Discussion Transmission of Babesia species by blood transfusion is well-described in medical literature. Average incubation period is 37 days, which would be consistent with our patient’s history. However, epidemiologic investigation did not reveal contamination of Texas blood supply nor was the donor infected. The cause of our patient’s infection remains unclear. Risks for severe babesiosis include advanced age, asplenia, rituximab administration, and acquisition by transfusion. Despite high-grade parasitemia, our patient achieved clinical remission. Recognition of Babesia infection, institution of antimicrobial therapy, and red blood cell exchange are essential for treatment. Our patient reaffirms that an index of suspicion for uncommon infections should be present when clinical evidence is consistent, despite no epidemiologic risk factors. References

1.  Vannier EG, Diuk-Wasser MA, Ben Mamoun C, Krause PJ. Babesiosis. Infect Dis Clin North Am. 2015 Jun;29(2):357-70. doi: 10.1016/j. idc.2015.02.008. 2. Centers For Disease Control and Prevention. Parasites- Babesiosis. Page last reviewed: February 4, 2014. Page last updated: February 4, 2014. 3.  Tanyel E, Guler N, Hokelek M, Ulger F, Sunbul M. A case of severe babesiosis treated successfully with exchange transfusion. Int J Infect Dis. 2015 Jul 29. pii: S1201-9712(15)00186-1. doi: 10.1016/j.ijid.2015.07.019. 4. Leiby D. Transfusion-transmitted Babesia spp: Bull’s eye on Babesia microti. American Society for Microbiology in January 2011, Vol 24: 14-28. 5. Vannier E, Krause P. Human Babesiosis. NEJM 2012, Vol 366: 2397-2407. 6.  W hite, et al. Human Babesiosis in New York State: Review of 139 Hospitalized Cases and Analysis of Prognostic Factors. Journal of American Medical Association Internal Medicine, October 1998, Vol 158 No. 19.

14. Hyperemesis Gravidarum precipitating Thyroid storm resulting in Wernicke’s encephalopathy Jeffrey J. Grondin, MD; Christina Glover, MD; Shema Ahmad, MD Internal Medicine Residency Program, Department of Medicine, University of Mississippi Medical Center (Dr. Grondin); Division of Endocrinology, Department of Medicine, University of Mississippi Medical Center (Dr. Glover and Dr. Ahmad) - Corresponding author: Jeffrey J. Grondin, MD (jgrondin@ umc.edu) Introduction Beta human chorionic gonadotropin (HCG) is known to stimulate thyroid stimulating hormone (TSH) receptors directly leading to increased free thyroxine (f T4), in extreme cases resulting in thyroid storm. Consumption of substrates for metabolic reactions, like thiamine, is increased in both pregnancy and thyrotoxicosis due to increased metabolic demands. Case Description A 34 year old black female, G3P0202 at 7 weeks 2 days gestation was admitted for recurrent nausea and vomiting, a 30 pound weight loss and altered mental status. She had been admitted a month prior and found to have abnormal thyroid function tests; she was lost to follow-up until this presentation. Upon admission, she was dehydrated and tachycardic to 147; fluid resuscitation was initiated with D5LR. Various lab abnormalities were present including acute kidney injury, elevated liver enzymes, hyperbilirubinemia, leukocytosis, anion gap metabolic acidosis, multiple electrolyte derangements, and hyperglycemia. Thyroid function tests on presentation TSH <0.01 (0.27-4.2mcIU/mL), f T4 7.77 (0.93-1.7 ng/ dL), Beta HCG elevated at 240529, all significantly worse from prior admission. She was admitted to medical intensive care unit for thyroid storm. Treatment was initiated with Methimazole, Hydrocortisone and Propranolol. Obstetrics evaluated patient and assessed a normal intrauterine pregnancy. Her mental status continued to worsen despite therapy and improvement in thyroid function markers: f T4 2.79 (hospital day 4); f T4 1.6 (hospital day 7). Thyroid peroxidase antibody, thyroid stimulating immunoglobulin, and thyrotropin receptor antibody were all negative, and thyroid ultrasound was normal. Lumbar puncture with cerebrospinal fluid studies was unremarkable. CT head found no acute intracranial abnormality. A working diagnosis of Wernicke’s encephalopathy was made and high dose thiamine replacement was initiated on hospital day 4. Thiamine (vitamin B1) levels drawn on hospital day 4 returned low at 25 nmol/L (70-180). MRI brain findings were compatible with this diagnosis. Thiamine levels improved to 235 nmol/L, with replacement. Mental status was slow to improve. She remained unable to communicate verbally and suffered with severe agitation. On hospital day 10, patient was noted to have dramatic improvement in mental status, being able to verbally communicate and answer some questions appropriately. Discussion: The pathophysiology surrounding this case involves gestational thyrotoxicosis associated with Wernicke’s encephalopathy due to direct stimulation of TSH receptor by beta HCG. The hypermetabolic state of pregnancy and thyrotoxicosis requires increased metabolic substrates and cofactors including vitamin B1. Wernicke’s encephalopathy should be suspected and treatment initiated as soon as possible for best prognosis. References 1. Shinha, D., Singla, M., Bajracharya, B., & Winer, N. (2014). A case of gestational thyrotoxicosis associated with Wernicke’s encephalopathy. Endocrine Practice, 20(12), 237-240. 2. Anaforoglu, I., Yildiz, B., Incecayir, O., & Algun, E. (2012). A woman with thyrotoxicosis- and hyperemesis gravidarum- associated Wernicke’s encephalopathy. Neuro Endocrinology Letters, 33(3), 285-289. 156 VOL. 57 • NO. 5 • 2016

3. Millson, C., Harding, K., & Hillson, R. (1995). Wernike-Korjakoff syndrome due to hyperemesis gravidarum precipitated by thyrotoxicosis. Postgraduate Medical Journal, 71(834), 249-250.

15. A fever from Africa: An unusual presentation of hemophagocytic lymphohistiocytosis Nancy Harrison, MD; Johann Hsu, MD; Nikki Cager, MD; Wesley Aldred, MD; Zeb Henson MD Internal Medicine Residency Program, Department of Medicine, University of Mississippi Medical Center (Dr. Harrison, Dr. Cager, and Dr. Aldred); Division of Hematology & Oncology, Department of Medicine, University of Mississippi Medical Center (Dr. Hsu); Division of General Internal Medicine & Hypertension, Department of Medicine, University of Mississippi Medical Center (Dr. Henson) - Corresponding author: Nancy Harrison, MD (nsharrison@umc.edu) Introduction A patient with fever of unknown origin is a diagnostic and therapeutic challenge, especially when confounded by a clinical syndrome suggestive of an African illness. We present a complicated presentation of a case of hemophagocytic lymphohistiocytosis (HLH). Case Description A 41-year-old male with no past medical history presented with fever, chills, arthralgia and macular rash on his trunk and distal extremities. His symptoms began while working off shore in Equatorial Guinea. Physical exam showed severe synovitis of his ankles, wrists and proximal interphalangeal joints bilaterally. Laboratory work revealed leukocytosis, microcytic anemia, elevated lactate dehydrogenase, elevated creatinine, elevated transaminases, and signs of significant inflammatory response including elevated erythrocyte sedimentation rate, C-reactive protein and a ferritin >100,000 mg/L. Antinuclear antibody, rheumatoid factor, hepatitis and HIV was negative. We treated empirically with doxycycline and quinine for malaria and vancomycin and meropenem for sepsis. Bone marrow biopsy revealed prominent clear inclusions within erythroid precursors. No hemophagocytes were noted. Serologic testing returned negative for Chikungunya virus, malaria, Parvovirus, Epstein Barr, dengue, Cytomegalovirus, and Arbovirus. After admission the patient’s symptoms severely worsened. Antibiotics were discontinued, and he was started on stress-dose methylprednisolone to suppress immune response. Initially symptoms improved but then returned. Bone marrow specimens were sent to the Center of Disease Control for additional viral testing including an “African Viral Panel.” These results were also negative. Occult infection and malignancy were ruled out via computed tomography; however mild splenomegaly was discovered. Interleukin 2 returned elevated (4720) and his natural cell activity resulted low to absent, thus meeting 5 of 8 criteria of HLH. HLH was presumed to be virally induced, likely from an unknown African virus. We started him on dexamethasone and etoposide per the HLH 2014 protocol. Subsequently, his fevers resolved and his ferritin trended down. Discussion Initially, this patient’s clinical picture suggested severe sepsis secondary to viral illness such as Chikungunya, malaria or another African viral illness given his recent travel history. However, with fever of unknown origin and ferritin > 3,000 μg/L, HLH should also be considered. HLH is a rare and often fatal disease that is difficult to diagnose. In adults, HLH is most commonly secondary to infection, hematologic disorders, malignancy or rheumatologic diseases. This patient likely had virally-induced HLH that we were unable to identify. No reports of African viral illness have been associated with HLH. References 1. Andrew J Wormsbecker, David D Sweet, Shawna L Mann, et al. Conditions associated with extreme hyperferritinemia (> 3000 μg/L) in adults. Intern Med J. 2015 Aug:45(8):828-33. Doi: 10.1111/imj.12768 2. Jan-Inge Henter, Anna Carin Horne, Maurizio Arico, et al. HLH-2004 Diagnostic and Therapuetic Guidelines for Hemophagocytic Lymphohistiocytosis. Pediatric Blood Cancer 2007, 48:124-131 3.  Nadine Rouphael Maakaroun, Abeer Moanna, et al. Viral infections associated with hemophagocytic syndrome. Rev. Med. Virol. 2010; 20: 93–105. 4. Neda Hashemi-Sadraei, Pimprapa Vejpongsa, Muhamed Baljevic, et al. Epstein-Barr Virus-Related Hemophagocytic Lymphohistiocytosis: Hematologic Emergency in the Critical Care Setting. Case Reports in Hematology Volume 2015, Article ID 491567, 6 pages.

16. They say his heart grew three sizes that day: An unusual cause of esophageal dysphagia Jason S. Henry, MD, MSC; James J. Hogg; S. Calvin Thigpen, MD Internal Medicine Residency Program, Department of Medicine, University of Mississippi Medical Center (Dr. Henry); University of Mississippi School of Medicine (Mr. Hogg); Division of General Internal Medicine & Hypertension, Department of Medicine; University of Mississippi Medical Center (Dr. Thigpen) - Corresponding author: Jason S. Henry, MD (jshenry@umc.edu)



Introduction Cardiac dysphagia is an uncommon diagnosis in clinical practice, although generally accepted in the setting of severe left atrial enlargement. Case Description A 59-year-old African American man presented with a chief complaints of dysphagia to solids, unrelenting hiccups, and the sensation of food becoming stuck at the base of the neck. His symptoms had progressively worsened over the past fifteen months and were associated with 40-pound weight loss. His past medical history was remarkable for cocaine abuse, alcoholism, 40+ pack years of cigarette smoking and candida esophagitis. Aside from the identification of a buccal lipoma, the physical exam was benign. Upper endoscopy was performed and revealed evidence of mild esophagitis and a small hiatal hernia; however, there were no findings that could adequately explain the patient’s symptoms. A computed tomography scan of the neck, chest and abdomen failed to reveal any concerning lesions but demonstrated instead a significantly enlarged heart, which appeared to be compressing posterior the mediastinal structures. A transthoracic echocardiogram revealed moderate to severe dilation of all four chambers with an estimated ejection fraction (EF) of 10-15%. A barium swallow confirmed the suspicion that esophageal compression by the enlarged left atrium was the underlying etiology. Despite his significantly reduced EF, the patient’s heart failure symptoms were minimal at the time of presentation and his electrocardiogram did not show evidence of conduction abnormality. The patient was started on optimal medical therapy for his heart failure and given counseling regarding his cocaine abuse. Discussion Dysphagia is a worrisome symptom and always merits further investigation. A careful history and physical exam can help to elucidate the cause in the majority of patients. External compression of the esophagus by a dilated left atrium has been well described in the literature but is rarely seen in practice. Manometric studies performed in patients with severe left atrial enlargement have suggested that the dysphagia may be related to localized zones of high-pressure oscillations which correspond to the heart rate. Local mucosal and nerve plexus ischemia secondary to external compression may also contribute in some cases. Treatment of the underlying cause of atrial enlargement is required to improve symptoms, which in this case consisted of medical management of his heart failure and life-long abstinence from cocaine. The patient continued to abuse cocaine and passed away from complications of his cardiomyopathy approximately two months after his initial presentation. References 1.  Cappell MS Manometric findings in dysphagia secondary to left atrial dilatation. Giant, cyclic midesophageal pressure waves occurring with every heart beat. Dig Dis Sci. 1991;36(5):693. 2. Gotsman I, Mogle P, Shapira MY An unusual cause of dysphagia. Postgrad Med J. 1999;75(888):629.

17. Chronic eosinophilic pneumonia mimicking COPD exacerbation Tara C. Lewis; William B. Horton, MD; Celso Gomez-Sanchez, MD University of Mississippi School of Medicine (Ms. Lewis); Internal Medicine Residency Program, Department of Medicine, University of Mississippi Medical Center (Dr. Horton); Division of Endocrinology, Department of Medicine, University of Mississippi Medical Center (Dr. Gomez-Sanchez) - Corresponding author: Tara C. Lewis (tclewis@umc.edu) Introduction Chronic eosinophilic pneumonia (CEP) is a rare disorder with incidence estimated at 0.23 cases/100,000 population per year in a recent study.1 CEP is characterized by marked accumulation of eosinophils in the interstitial and alveolar spaces of the lungs.2 Typical symptoms include productive cough, fever, breathlessness, weight loss, and night sweats.3 Case Presentation A 70-year-old white male veteran with chronic obstructive pulmonary disease (COPD) and lung adenocarcinoma successfully treated with right upper lobectomy in 2004 presented with a three-week history of shortness of breath, nonproductive cough, and increasing home oxygen requirement. The patient was chronically on two liters home oxygen therapy but had recently required four liters home oxygen prior to admission. He also reported being a former smoker with 200 pack-year smoking history and noted recurrent episodes of pneumonia since childhood. He was afebrile with stable vitals on initial presentation. Physical examination demonstrated lung fields that were clear to auscultation bilaterally with expiratory wheezes in the left lower posterior lobe, and no rales or rhonchi. Laboratory studies were notable for elevated white blood cell count at 11.7 K/cmm with 49.8% eosinophils on differential. Absolute eosinophil count was elevated at 4.9 K/cmm. Chest radiography showed evidence of lung scarring and patchy bilateral infiltrates. Computed tomography (CT) of the chest without contrast demonstrated chronic postsurgical changes and interval development of bilateral patchy infiltrates throughout the lungs. He was started on levofloxacin and ipratropium/albuterol for suspected COPD exacerbation and bacterial pneumonia. Pulmonology was consulted and performed bronchoalveolar lavage (BAL) with bronchoscopy. BAL differential results showed 77% eosinophils. Pulmonology believed this to be CEP and recommended treatment with prednisone 40 mg PO daily. Steroid therapy was initiated and the following day he reported symptomatic resolution. At that time, his WBC was within normal limits and differential now showed 2.3% eosinophils. Absolute eosinophil count had also returned to normal limits at 0.2. Blood, 158 VOL. 57 • NO. 5 • 2016

urine, and BAL cultures returned no growth. Streptococcus pneumoniae and legionella urinary antigens were also negative. He was discharged home to complete a steroid taper. At most recent follow-up, he was asymptomatic and reported resolution of nearly all of his pulmonary complaints. Discussion This case demonstrates why CEP should be considered in the differential diagnosis of any patient who presents with pulmonary complaints and considerable peripheral eosinophilia. BAL showing ≥ 25% eosinophilia nearly clinches the diagnosis.4 Prompt recognition and diagnosis can lead to appropriate therapy, with most patients seeing dramatic resolution of symptoms one or two days after corticosteroid administration.4 References 1. Sveinsson OA, Isaksson HJ, Gudmundsson G. Chronic eosinophilic pneumonia in Iceland: clinical features, epidemiology, and review. Laeknabladid 2007; 93(2): 111-116. 2. Allen JN, Davis WB. Eosinophilic lung diseases. Am J Respir Crit Care Med 1994; 150(5): 1423-1438. 3. Jederlinic PJ, Sicilian L, Gaensler EA. Chronic eosinophilic pneumonia. A report of 19 cases and a review of the literature. Medicine (Baltimore) 1988; 67(3): 154-162. 4. Marchand E, Reynaud-Gaubert M, Lauque D, et al. Idiopathic chronic eosinophilic pneumonia. A clinical and follow-up study of 62 cases. The Groupe d’Etudes et de Recherche sur les Maladies “Orphelines” Pulmonaires (GERM”O”P). Medicine (Baltimore) 1998; 77(5): 299-312.

18. Hyperpigmentation: a rarely recognized manifestation of vitamin B12 deficiency Lance T. Majors; Jimmy Wolfe, MD; Douglas A. Wolfe, MD University of Mississippi School of Medicine (Mr. Majors); Department of Neurology, University of Mississippi Medical Center (Dr. Jimmy Wolfe); Division of Cardiology, Department of Medicine, University of Mississippi Medical Center (Dr. Douglas Wolfe) - Corresponding author: Lance T. Majors (lmajors@ umc.edu) Introduction Vitamin B12 is a cofactor in DNA metabolism and is especially important in the maintenance of the neuronal myelin sheath. A deficiency of this water soluble vitamin manifests as a megaloblastic anemia and polyneuropathy. A less recognized yet documented presentation of B12 deficiency is cutaneous hyperpigmentation seen in 19% of patients in some study groups. This report describes a case of B12 deficiency in a patient presenting with marked hyper-pigmented lesions of the hands and feet. Case Description A 57 year-old black female presented to cardiology clinic for evaluation of arm pain. The patient reported pinprick chest pains, tingling in her fingers and toes, and hyperpigmentation of palmar and dorsal aspects of both hands and feet. Pertinent history included recent polyneuropathy and back pain for which she was prescribed gabapentin, cyclobenzaprine, and tramadol. Cardiac causes of chest pain were ruled out and the patient was referred for rheumatologic evaluation of suspected vasculitis. CMP, ANA, TSH, ESR, CRP, and CK were within normal limits. CBC showed mild normocytic anemia including hemoglobin 11.8 and hematocrit of 35.3 with an MCV of 87. Physical examination was positive for gait instability and hyperpigmentation. Neurological evaluation demonstrated a normal electromyogram. A B12 level of 38 pg/mL (ref: 240-900pg/mL) was obtained, indicating severe deficiency. Replacement therapy commenced with monthly 1000 mcg injections. Paresthesia and hyperpigmentation persisted through a two-month follow-up period. Five months from initiating therapy, the patient reported markedly decreased paresthesia and demonstrated significantly reduced cutaneous hyperpigmentation. Due to lingering gait instability, MRI of the spine was obtained showing spinal cord degeneration consistent with severe B12 deficiency. Discussion Vitamin B12 deficiency may result in both neurological and hematological sequelae. However, there have been a subset of well documented case reports as early as 1944 in which B12 deficiency is linked to cutaneous hyperpigmentation. Gilliam et al describe the underlying mechanism of this hyperpigmentation as the oxidation of glutathione leading indirectly to decreased melanin anabolism and subsequent increased tissue deposition. Although treatment often results in resolution of disease, neurological manifestations in severe disease such as spinal cord degeneration tend to persevere. From this we can conclude: (1) The literature proposes that hyperpigmentation is much more common in B12 deficiency than is often recognized; (2) earlier diagnosis of B12 deficiency may be made if included in the differential diagnosis of unexplained pigmentation disorders; and (3) earlier treatment of B12 deficiency may prevent permanent neurological damage. References 1. Agrawala RK, Sahoo SK, Choudhury AK, Mohanty BK, Baliarsinha AK. Pigmentation in vitamin B12 deficiency masquerading Addison’s pigmentation: A rare presentation. Indian Journal of Endocrinology and Metabolism. 2013;17(Suppl1):S254-S256. doi:10.4103/2230-8210.119591. 2. Kannan R, Ng MJM. Cutaneous lesions and vitamin B12 deficiency: An often-forgotten link. Canadian Family Physician. 2008;54(4):529-532. 3. Baker SJ, Ignatius M, Johnson S, Vaish SK. Pigmentation and Vitamin-B12 Deficiency. British Medical Journal. 1963;2(5366):1205. 4. Gilliam JN, Cox AJ. Epidermal Changes in Vitamin B12 Deficiency. Arch dermatol. 1973; 107(2): 231-236. 



19. Systemic loxoscelism: A rare cause of Coombs positive hemolytic anemia Keith W. Murdock, MD; Jeffery J. Grondin, MD; Scott M. Letellier, MD; Jericho L. Bell, MD Internal Medicine Residency Program, Department of Medicine, University of Mississippi Medical Center (Dr. Murdock and Dr. Grondin); Division of Hematology & Oncology, Department of Medicine, University of Mississippi Medical Center (Dr. Letellier); Division of General Internal Medicine & Hypertension, Department of Medicine, University of Mississippi Medical Center (Dr. Bell) - Corresponding author: Keith W. Murdock, MD (kmurdock@ umc.edu) Introduction Loxoscelism is a term used to described systemic illness caused by the envenomation by recluse spiders. Although it commonly presents with small necrotic lesions, it has been known to rarely cause multi-organ failure, DIC and hemolytic anemia (1). Here we report a case of systemic loxoscelism as a rare cause of autoimmune hemolytic anemia (AIHA). Case report 47-year-old African American female presented to the emergency room with a 1-week history of non-radiating back pain between her shoulder blades. Prior to her back pain, she noted a small area of redness and swelling on her back. She worked at a nursing home, which she reported had a brown recluse spider infestation and believed she had a spider bite. She sought outpatient medical care when she began having intermittent fevers and was treated with clindamycin. The lesion did not improve and developed into larger eschar. She returned to medical attention for nausea, fatigue, muscle weakness, and generalized abdominal pain. Physical exam was remarkable for a 1cm x 1cm dry eschar overlying the right scapular region with 2mm area of erythema surrounding it and sublingual jaundice. Labs on admission demonstrated an elevated bilirubin (primarily indirect), leukocyte count of 32 x 10 9 /L (5% blast, 6% bands, many nucleated RBC’s), hematocrit of 19.3%, lactate dehydrogenase of 1126units/L and haptoglobin <10mg/dL. Her direct Coombs was positive. Initial differential diagnoses included autoimmune hemolytic anemia, chronic myeloid leukemia, and drug induced hemolytic anemia. Upon admission to the hospital, the patient received blood transfusions. Peripheral smear was without schistocytes, had multiple nucleated RBC’s and left shifted population of neutrophils. She continued to be anemic despite transfusion and was started on 1 mg/kg prednisone for AIHA associated with a brown recluse spider bite. Her leukocytosis, anemia, eschar and symptoms normalized after completion of a steroid course. Discussion Systemic loxoscelism is a rare cause of Coombs positive hemolytic anemia. When confronted by a hemolytic anemia in a patient with a spider bite or who develops a suspicious eschar, a clinician should consider systemic loxoscelism as a cause. Additionally, with signs of systemic illness, the patient should be hospitalized for treatment and supportive care (2). In our case, the patient was able to achieve a full recovery after treatment with prednisone and close observation. References 1.  Lane DR, Youse JS. Coombs-positive hemolytic anemia secondary to brown recluse spider bite: a review of the literature and discussion of treatment. Cutis. 2004;74(6):341-7. 2. Thomas P. Forks, DO, PhD. Brown Recluse Spider Bites. J Am Board Fam Pract 2000;13:415-23.

20. A  rare case of microvascular pulmonary arteriovenous malformations in a young female presenting with hypoxemic respiratory failure Meghan Poole, MD; Kenneth Ball, MD Medicine-Pediatrics Residency Program, Department of Medicine, University of Mississippi Medical Center (Dr. Poole); Division of Hospitalist Medicine, University of Mississippi Medical Center (Dr. Ball) - Corresponding author: Meghan Poole, MD (mppoole@umc.edu) Introduction Hypoxemia and shortness of breath are common problems faced by the internist. Pulmonary arteriovenous malformations (AVMs) are an uncommon cause of these symptoms. Here we present the case of a young female with hypoxemia who underwent a thorough work-up and was found to have a very rare cause of microvascular pulmonary AVMs, diffuse pulmonary hemangiomatosis. Case Report   A 20-year-old black female presented to clinic with generalized weakness, dizziness with ambulation, dyspnea on exertion, and platypnea.  Physical examination was notable for perioral cyanosis, hypoxemia, and orthodeoxia. Arterial blood gas showed a significantly elevated alveolar-arterial gradient, suggesting ventilation-perfusion mismatch. Chest x-ray was normal, ruling out major parenchymal and pleural disease. Computed 160 VOL. 57 • NO. 5 • 2016

tomography angiography showed no evidence of pulmonary embolism or AVM involving the large vessels. Bronchoscopy with transbronchial biopsies was performed and showed no evidence of interstitial lung disease. Transthoracic echocardiography showed no evidence of pulmonary hypertension. However, bubble study showed delayed entry of numerous bubbles into the left atrium, indicating a large right-to-left shunt most likely of pulmonary origin. Nuclear medicine lung perfusion scan confirmed this finding. Right heart catheterization with pulmonary angiography did not identify a discrete fistula but did demonstrate entry of agitated saline into the left atrium when injected into multiple bilateral subsegmental pulmonary arteries, leading to suspicion for diffuse microvascular AVMs. Open lung biopsy was performed and pathology returned as diffuse pulmonary hemangiomatosis.  She was discharged with home oxygen and plans for an 18-month trial of doxycycline based on a case report describing improvement in a patient with a similar condition, pulmonary capillary hemangiomatosis.  The efficacy of doxycycline is thought to be related to properties that inhibit angiogenesis.  Her symptoms improved with this treatment but she continued to require oxygen. Discussion This case emphasizes the importance of maintaining a broad differential and a systematic approach in the work-up of hypoxemia. A careful physical exam is also indispensable. In this patient, platypnea and orthodeoxia were important clues suggestive of shunt physiology.  AVMs are relatively rare causes of hypoxemia but should be considered when more common etiologies have been ruled out. Multiple or diffuse microvascular AVMs should be considered in a patient with evidence of pulmonary right-to-left shunt and no localization of fistula on imaging studies.  Pulmonary angiography supports the diagnosis when no discrete lesion is identified and shunting from multiple vascular territories is demonstrated.  Lung biopsy may be required for definitive diagnosis.   References: 1. Cartin-Ceba, Rodrigo. “Pulmonary Arteriovenous Malformations.” Chest 144 (2013): 1033-44. 2. Fuhlbrigge, Anne and Augustine Choi. “Diagnostic Procedures in Respiratory Disease.” Harrison’s Principles of Internal Medicine. Ed. Dennis Kasper. 19th ed. 2 vols. McGraw-Hill, 2015. 3. Ginns, Leo, et al. “Pulmonary Capillary Hemangiomatosis With Atypical Endotheliomatosis: Successful Antiangiogenic Therapy With Doxycycline.” Chest 124 (2003): 2017-22. 4. Schwartzstein, Richard. “Dyspnea.” Harrison’s Principles of Internal Medicine. Ed. Dennis Kasper. 19th ed. 2 vols. McGraw-Hill, 2015.

21. S evere hypocalcemia following administration of zoledronic acid in an osteoporotic patient with a history of roux-en-y gastric bypass Joshua M. Tate, MD; Blake E. Elkins, MD Department of Medicine, Keesler AFB, MS, Keesler Medical Center - Corresponding author: Joshua M. Tate, MD (Joshua.tate.2@us.af.mil) Introduction Bisphosphonates, including zoledronic acid, are extensively used in the treatment of osteoporosis. Hypocalcemia is a known potential adverse event with the use of bisphosphonates, although rarely observed. We are reporting the first described case of severe hypocalcemia in a post RouxEn-Y gastric bypass patient after receiving zoledronic acid therapy for osteoporosis. Case Description We present a 63-year-old female with a history of renal impairment, osteoporosis, secondary hyperparathyroidism, and Roux-En-Y gastric bypass with multiple micronutrient deficiencies. Patient was prescribed zoledronic acid infusion for treatment of osteoporosis. Two days following infusion of zoledronic acid, the patient developed peri-oral tingling and bilateral upper and lower extremity paresthesias. Labs completed ten days following zoledronic acid infusion showed severe hypocalcemia with calcium value of 5.4mg/dL and parathyroid hormone level of 1,058pg/ mL. The patient was sent to the emergency department and was found to have a positive Chvostek’s sign and electrocardiogram with prolonged QT interval (468msec). Patient was admitted to the intensive care unit, treated with intravenous calcium gluconate, and discharged with a calcium level of 9.34mg/dL. Patient was discharged with 4.8 grams calcium citrate, 0.25mcg of calcitriol, and 400mg of magnesium oxide daily to maintain calcium homeostasis. Discussion Zoledronic acid therapy is used in the treatment of osteoporosis. Bisphosphonates, including zoledronic acid, are known to cause hypocalcemia in 5-10% of individuals. The risk of hypocalcemia has been shown to be higher in individuals with preexisting vitamin D and calcium deficiencies, as can occur following bariatric surgery. Bisphosphonates work by inhibiting osteoclasts in favor of osteoblastic activity to help restore bone mass. In our calcium deficient post gastric bypass patient, she relied on osteoclast-induced repletion of calcium from bone to maintain calcium homeostasis. Following bisphosphonate therapy, our patient could no longer restore calcium levels through bone resorption as osteoclast activity was blocked, leading to severe hypocalcemia. To our knowledge, this is the first reported case of severe hypocalcemia following the use of bisphosphonates in a post gastric bypass patient. Given the increased prevalence of gastric bypass, increased awareness of this adverse reaction with bisphosphonates in this patient population is needed to avoid further morbidity. JOURNAL MSMA



1. Rakel A et al. Role of zoledronic acid in the prevention and treatment of osteoporosis. Clin Interv Again. 2011; 6:89-99. 2. Li EC et al. Zoledronic acid: a new parenteral bisphosphonate. Clin Ther. 2003; 25(11): 2669-2708. 3. Coxon FP et al. Protein geranylgeranylation is required for osteoclast formation, function, and survival: inhibition by bisphosphonates and GGTI298. J Bone Miner Res. 2000; 15(8): 1467-1476. 4. Black DM et al. Once yearly zoledronic acid for treatment of postmenopausal osteoporosis. N Engl J Med. 2007; 356(18):1809-1822. 5. Lyles KW et al. Zoledronic acid and clinical fractures and mortality after hip fracture. N Engl J Med. 2007; 357(18):1799-1809. 6. Chesnut CH et al. Short-tern effect of alendronate on bone mass and bone remodeling in postmenopausal women. Osteoporos Int 3 Suppl. 1993; 3:S17-19. 7. Papapetrou PD. Bisphosphonate-associated adverse events. Hormones. 2009; 8(2): 96-110. 8. Gasteyger C et al. Nutritional deficiencies after Roux-en-Y gastric bypass for morbid obesity aftern cannot be prevented by standard multivitamin supplementation. Am J Clin Nutr. 2008; 87(5): 1128-1133. 9. Elq AH. Symptomatic hypocalcemia associated with zoledronic acid treatment for osteoporosis: a case report. Oman Medical Journal. 2013; 28 (2). 10. Rosen CJ et al. Severe hypocalcemia after intravenous bisphosphonate therapy in occult vitamin D deficiency. N Engl J Med. 2003; 348(15): 15031504. 11. Chennuru S et al. Risk factors for symptomatic hypocalcemia complicating treatment with zoledronic acid. Intern Med J. 2008; 38(8): 635-637. 12. Kreutle V et al. Bisphosphonate induced hypocalcemia- report of six cases and review of the literature. Swiss Med Wkly. 2014;144:w13979. 13. Maalouf NM et al. Bisphosphonate-induced hypocalcemia: report of 3 cases and review of literature. Endocr Pract. 2006; 12(1): 48-53. 14. Kmetec A et al. Evaluation of safety and analgesic consumption in patients with advanced cancer treated with zoledronic acid. Radiol Oncol. 2013 Sep; 47(3):289-295. 15. Breen TL et al. Prolonged hypocalcemia after treatment with zoledronic acid in a patient with prostate cancer and vitamin D deficieny. JCO. 2004; 99:289. 16. Hananura M. Risk factors contributing to the development of hypocalcemia after zoledronic acid administration in patient with bone metastases of solid tumor. Biol Pharm Bull. 2010; 33 (4):721-724. 17. The Endocrine Society. Endocrine and Nutritional Management of the Post-Bariatric Surgery Patient: An Endocrine Society Clinical Practice Guideline. Nov 2010.

22. Death by diarrhea Erica Turse, DO, MPH; Indu Srinivasan, MD; Kumar Pallav, MD; Charu Subramony, MD; Luminita Rezeanu, MD; John Sheehan, MD; Shou-jiang Tang, MD; S. Calvin Thigpen, MD Internal Medicine Residency Program, Department of Medicine, University of Mississippi Medical Center (Dr. Turse); Division of Gastroenterology, Department of Medicine, University of Mississippi Medical Center (Dr. Srinivasan, Dr. Pallav, Dr. Sheehan, and Dr. Tang); Department of Pathology, University of Mississippi Medical Center (Dr. Subramony and Dr. Rezeanu); Division of General Internal Medicine & Hypertension, Department of Medicine, University of Mississippi Medical Center (Dr. Thigpen) - Corresponding author: Erica Turse, DO, MPH (eturse@umc.edu) Introduction Celiac disease is a well-known enteropathy affecting about 1% of the US population. What is less understood is refractory celiac disease (RCD) as its incidence is extremely rare. Here we present a case of RCD to highlight the severity of the pathophysiology of the disease and to alert clinicians of the diagnosis. Case Report A 74-year-old man with a 14 year history of biopsy-proven celiac disease presented with complaints of 13 months of ongoing diarrhea despite a continued gluten free diet (GFD). The patient’s complaints included steatorrhea with nocturnal stools 8-12 times daily with no melena or hematochezia. He denied associated symptoms of flushing, diaphoresis, hypotension, headaches, palpitations, or skin rashes. Prior to admission he had a colonoscopy revealing questionable microscopic colitis which was treated with Pepto-Bismol and oral steroids with no resolution of symptoms. He then underwent magnetic resonance enterography and small bowel capsule endoscopy revealing ulcerations and duodenal polyps. On admission, an endoscopy and colonoscopy showed severe villous blunting, increased lymphocytes, apoptosis, and crypt distortion throughout the entire small intestine and colonic mucosa. Biopsies were negative for Enteropathy-Associated T-cell Lymphoma (EATL). A Computed Tomography abdomen/pelvis showed no evidence of malignancy. He was found to have microcytic anemia and hypoalbuminemia. Additionally, all stool cultures were negative. Other labs drawn and non-revealing included HIV, lipase, C-reactive protein, erythrocyte sedimentation rate, thyroid-stimulating hormone, calcitonin, serum gastrin, 5-HIAA, fecal fat, reducing substances and anti-enterocyte antibody. Tissue transglutaminase antibodies were <1.2 and HLDQ2 was positive. He was started on budesonide daily with no improvement. Follow up disclosed elevated alkaline phosphatase (522 U/L), and he underwent liver biopsy and repeat EGD and colonoscopy which showed periportal type 2 non-alcoholic fatty liver disease consistent with his severe malnutrition and RCD negative for EATL. At this time he was started on TPN. The patient was sent for clinical trials but unfortunately prior to enrollment died from severe malnourishment.

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Discussion RCD is a diagnosis of exclusion and is defined when diarrhea continues despite 12 months of GFD.1,3 Two types of RCD exist.1,2 Type 2 RCD illustrates abnormal intraepithelial lymphocytes and an extremely poor prognosis.2,3 Five-year mortality is up to 50% with hypoalbuminemia and anemia as the main prognostic markers.1,3 Unfortunately, novel treatment agents do not exist and most patients are refractory to steroid therapy. Many individuals will require TPN and 33-67% progress to EATL within five years. 1,3 Current evidence suggests that cladribine and stem cell transplantation may be promising.3 References

1. 2. 3.

Rubio-Tapia A, Murray JA. Classification and Management of Refractory Celiac Disease. Gut 2010; 59(4) 547-557. Svajdler M, Daum O, Rychly B. Diagnosing Celiac Disease: Role of Pathologists. Int J of Celiac Disease 2014; 2(2) 70-75. Woodward J. The management of refractory coeliac disease. Ther Adv Chronic Dis 2013; 4(2) 77-90.

23. Paroxysmal nocturnal hemoglobinuria: rare disease with expensive but effective treatment Jared A. White; William B. Horton, MD; Jessica S. Lavender, MD; Frank Criddle, MD University of Mississippi School of Medicine (Mr. White); Internal Medicine Residency Program, Department of Medicine, University of Mississippi Medical Center (Dr. Horton and Dr. Lavender); Division of Hospitalist Medicine, University of Mississippi Medical Center (Dr. Criddle) - Corresponding author: Jared A. White (jawhite2@umc.edu) Introduction Paroxysmal nocturnal hemoglobinuria (PNH) is caused by a somatic mutation in the phosphatidylinositol glycan anchor gene. This mutation results in uncontrolled complement-mediated hemolysis and platelet activation due to the absence of CD55 and CD59 proteins.1 PNH is a rare acquired disorder, with an incidence of 1.5-2 cases per million annually, characterized by thrombosis in atypical locations (hepatic, abdominal, and cerebral veins), chronic persistent hemolysis, and bone marrow failure.2 The median age of onset is approximately 42 years.3 Here we present the case of a 58-year-old female who presented with hepatic vein thrombosis and was found to have PNH. Case Presentation A 58-year-old white female with history of breast cancer in remission (treated with lumpectomy, radiation, and chemotherapy) presented with a one-week history of leg and abdominal swelling. On initial presentation, she was hypotensive and disoriented. Laboratory studies revealed white blood cell count 5.9 TH/cmm, hemoglobin 11.5 g/dL, hematocrit 35.5%, platelet count 63 TH/cmm, alanine aminotransferase (ALT) 905 U/L, aspartate aminotransferase (AST) 609 U/L, and negative acetaminophen level. A non-contrast head computed tomography (CT) scan was unremarkable. Abdominal CT and liver ultrasound showed an enlarged liver, hepatic congestion, and hepatic vein thrombosis. She denied any risk factors for thrombosis or family history of clotting disorders. The following morning she underwent image-guided inferior vena cava venoplasty with placement of intrahepatic infusion catheter (IIC). Heparin infusion was started and alteplase was delivered via IIC. She required multiple blood product transfusions over the next 2-3 days, so Hematology was consulted and recommended obtaining CD 55/59 flow cytometry; results demonstrated PNH clones with deficiencies of CD 55 and 59. Eculizumab therapy was felt to be appropriate, so meningococcal vaccine was administered. Eculizumab was initiated and the patientâ&#x20AC;&#x2122;s quality of life has improved since that time. No other thrombotic events were observed and the patient has not required further blood product transfusions. Discussion This case highlights the need for increased awareness of PNH among healthcare professionals. Prompt recognition and diagnosis can lead to appropriate therapy which can decrease transfusion requirements and improve quality of life. Eculizumab is a humanized monoclonal antibody that reduces intravascular hemolysis by binding C5 and reducing formation of the membrane attack complex.4 Indications for eculizumab include thrombosis, transfusion-dependence, renal insufficiency, or other end-organ damage. The manufacturerâ&#x20AC;&#x2122;s recommended dosing for PNH totals approximately $102,665 in drug costs alone for the first seven weeks of therapy, making it an expensive therapeutic option.5 References:

1. Sahin F, Yilmaz AF, Ozkan MC, et al. PNH is a debilitating, fatal but treatable disease: same disease, different clinical presentations. Am J Blood Res 2015; 5(1): 30-33. 2. Sahin F, Ozkan MC, Mete NG, et al. Multidisciplinary clinical management of paroxysmal nocturnal hemoglobinuria. Am J Blood Res 2015; 5(1):1-9. 3. Schrezenmeier H, Muus P, Socie G, et al. Baseline characteristics and disease burden in patients in the International Paroxysmal Nocturnal Hemoglobinuria Registry. Haemotologica 2014; 99(5): 922-929. 4. Parker C. Eculizumab for paroxysmal nocturnal haemoglobinuria. Lancet 2009;373(9665):759-767. 6. Available at: http://www.uptodate.com/contents/eculizumab-patient-drug-information. Accessed September 24, 2015.



24. A case of pulmonary mucormycosis in a patient with granulomatosis with polyangiitis Ryan A. Williams, MD; Jennie K. Ellis; Swathi Gonnalagadda, MD; S. Calvin Thigpen, MD Internal Medicine Residency Program, Department of Medicine, University of Mississippi Medical Center (Dr. Williams); University of Mississippi School of Medicine (Ms. Ellis); Division of Rheumatology, Department of Medicine, University of Mississippi School of Medicine (Dr. Gonnalagadda); Division of General Internal Medicine & Hypertension, Department of Medicine, University of Mississippi Medical Center (Dr. Thigpen) - Corresponding author: Ryan A. Williams, MD (rawilliams@umc.edu) Introduction Mucormycosis is rare with estimated incidence of 1 in 1,000,000. It is a frequently devastating necrotizing fungal infection acquired through inhalation of spores that can spread to the brain or lungs.  Mortality rates for pulmonary mucormycosis have been reported as high as 76%.  We present a case of pulmonary mucormycosis in a patient with possible Anti-Nuclear Cytoplasmic Antibody (ANCA)-associated vasculitis. Case Description A 53-year-old black male with a history of Cryptogenic Organizing Pneumonia and hyperglycemia presented with a chief complaint of two months of progressive shortness of breath.  Associated symptoms included occasional hemoptysis, fevers, and a 20 pound weight loss.  Prior workup revealed positive p-ANCA, and the patient had been treated with prednisone and cyclophosphamide for suspected Granulomatosis With Polyangitis (GPA).  On admission, the patient was febrile with rhonchi in the bilateral lung bases.  Labs revealed a white blood cell count of 32,000 TH/cmm, creatinine of 4.38 mg/dL, and urinalysis with microscopic hematuria.  Computed tomography (CT) scan of the chest showed large thick-walled cavitary lesions in both lungs.  We treated him with prednisone for suspected GPA flare and broad spectrum antibiotics for possible pneumonia.  His oxygen requirement began to increase, so we initiated high dose solumedrol.  Given his lack of improvement, pulmonary performed bronchoscopy with fine needle aspiration which was interpreted as aspergillus.  We added Voriconazole, but he continued to decline.  He was intubated for hypoxic respiratory failure and expired two days later.  Endobrochial biopsy results later revealed acute necrotizing inflammation and mucormycosis with soft tissue invasion.  Discussion Hyperglycemia, treatment with glucocorticoids, and immunosuppression are major risk factors for mucormycosis.  Symptoms of mucormycosis may mimic a flare of ANCA Associated Vasculitis, such as GPA, with fever, hemoptysis, and dyspnea.  In addition, GPA treatments are risk factors for zygomycete infections.  Voriconazole has no activity against zygomycetes and may contribute to breakthrough zygomycosis.  Amphotericin and surgical management are key to survival. References 1. Petrikkos, G, Skiada A, et al. (2012) Epidemiology and Clinical Manifestations of Mucormycosis. Clin Infect Dis. 54 (suppl 1): S23-S34. 2. Pak J, Tucci VT, et. (2008) Mucormycosis in immunochallenged patients. J Emerg Trauma Shock. 1:106-113. 3. Nogueira EL, Ind PW, et al. (2010) Mucormycosis may mimic disease relapse in Wegener’s granulomatosis. J Rheumatol. 37(6): 1364-1365. 4. Abtahi SM, Omrani M, et al. (2012) Wegener’s granulomatosis and mucormycosis: A case study and review of literature. Adv Biomed Res. 1:23.

School of Medicine Reunions August 26 & 27, 2016

Honoring Classes of

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Registration will be available in June. Hotel information and event updates are available now on umc.edu/alumni. Questions? Concerns? Please contact us at 601-984-1115 / 800-844-5800 or alumni@umc.edu

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2016 Component Society Meetings



5 Coast Counties Medical Society at Oyster

2 Northeast Mississippi Medical Society

Reef Club

10 West Mississippi Medical Society at Anchuca B&B

18 Amite-Wilkinson Medical Society at Field Memorial Hospital

at Tupelo Country Club

JULY 12 North MIssissippi Medical Society

(location TBA)

6 Prairie Medical Society at Old Waverly 28 South Central Medical Society at Fernwood Country Club




4 South Mississippi Medical Society at

4 Central Medical Society at River Hills

Cotton Blues

8 Northeast Mississippi Medical Society

at Tupelo Country Club

12-13 Annual Session at the Hilton

13 Prairie Medical Society at Old Waverly 13 South Central Medical Society at

12 Delta Medical Society (location TBA)

Hotel in Jackson

Country Club

Fernwood Country Club

Dates and locations to be announced: Coast Counties Medical Society

Clarksdale & 6 Counties Medical Society

East Mississippi Medical Society

Singing River Medical Society

North Central Medical Society

Homochitto Valley Medical Society

Please check www.MSMAonline.com for updates on meeting dates and times. 166 VOL. 57 â&#x20AC;˘ NO. 5 â&#x20AC;˘ 2016


P R E S I D E N T ’ S


You are the Guardians at the Gate Serving as your president, I’ve been introduced to various groups more times than I can recount. Each time I’m introduced, there is one statement that brings me clarity as to why I’m doing this job and it is “He has a passion for organized medicine.” Why would anyone have a passion for organized medicine? For me, it is quite simple. I have a passion for medicine in general and being a physician in particular. I have learned from my mentors in MSMA over the past 25 years not to take anything in our profession for granted. Although the Hippocratic tradition is over 2,500 years old and the profession predates that, there is no guarantee that it will exist in a recognizable form a century from now. We all understand that our profession is under constant attack from all sides. Whether it’s from other providers who want to practice medicine without going to medical school or from corporations who want to force changes in how we practice in order to increase share value, we all feel the pressure for us to give in. We are pressured to give in on autonomy, on authority of the medical team, on reimbursement, and on scope of practice issues. We are pressured to allow others to invade the sacred nature of the doctor-patient relationship. The federal government, state government, local government, third party payers, employers, consumer groups, and everyone who wants to play doctor pressure us. We all recognize these issues and are experts at complaining in our doctor lounges to each other but what good does that do? What good does griping and complaining about the loss of the “good ole days” accomplish? In my opinion, it accomplishes absolutely nothing. However, there is a solution to our problems. Organized medicine such as embodied in our state by MSMA is the answer. Our MSMA is the one organization that empowers me to make a difference for the profession. I belong to several professional organizations all of which add value to my practice but only one is able to protect the overall ability for me to serve as a physician in Mississippi and that is MSMA. I am a faithful member of the American College of Physicians (ACP) and no other organization could have advocated for me to correct the burdensome issues with maintenance of certification for my specialty, and no other organization is able to promote my professional development as an Internist as does the ACP. However, as much as I respect and appreciate the ACP in my professional life, my specialty society could not stop the scope of practice attacks we faced in the legislature this year nor could it have rallied the coalition needed to defeat attacks on all doctors and our patients with telemedicine or the vaccine battle. MSMA has the ability to pull together the House of Medicine when the coalition of specialty societies is needed to push back the vandals at the gate. So, how do we as “physicians who care for Mississippi” serve as guardians at the gate for our profession? The single most important way is to remain members of MSMA as the political and advocacy arm of organized medicine, and then to be a member of the Mississippi Medical Political Action Committee (MMPAC) as the fundraising arm for our political efforts. Just being “a part of ” without ever serving on a council or leadership position is doing your part for the profession. When doctors stand together and band together with our patients we are a force to reckon with. Therefore, I urge you to maintain your membership in your specialty society but also invest in the future of medicine by staying a member of MSMA and contributing to our MMPAC. Be that guardian at the gate because the vandals will be back next year. Daniel P. Edney, MD, Vicksburg MSMA President 2015-16








UMMC Announces New School of Population Health The University of Mississippi Medical Center is advancing its mission to create a healthier Mississippi by forming the new University of Mississippi School of Population Health. UMMC received permission to plan the school from the Mississippi Institutes of Higher Learning on April 21. Planned to open in 2017, it will be the third school of its kind in the United States, says Dr. Bettina Beech, associate vice chancellor for population health. “Population health considers the whole continuum of factors that contributes to health outcomes,” Beech said. “In addition to biological factors, social, environmental, and behavioral factors are all important determinants of health.” This field of science focuses on how these factors interrelate and influence the distribution and determinants of disease and health in defined groups. It has a broader focus than public health, Beech says. The mission of the school is to create leaders prepared to transform health care delivery and the health of Mississippians. These leaders will include population scientists, clinicians, and administrators. The school will begin with three departments: preventive medicine, data science, and population health science. The first two are already in place within the School of Medicine and as part of the Center of Biostatistics and Bioinformatics, respectfully. Dr. Joshua Mann, professor and chair of the Department of Preventive Medicine, says that his department will be a bridge between the School of Medicine, the Medical Center’s clinical enterprise, and the School of Population Health.


The department will develop an accredited residency program in general preventive medicine. “In preventive medicine, we have our feet in two worlds: patient care and population-level health,” Mann said. Beech says that in the traditional health care delivery model, providers “take care of the patients at their doorstep” – those that visit clinics and hospitals for treatment. In population health and preventive medicine, Mann says, the emphasis is more on outpatient care and collaborations with communities and community groups to address the range of factors that influence health. Population health has begun to transform health care by addressing the “triple aim”: improving patient outcomes and enhancing the patient experience while simultaneously reducing costs. “With recent changes in health care funding, there is a greater emphasis on patient outcomes and not the volume of services provided,” Mann said. The United States has the world’s highest health expenditures, but the nation does not have the best health outcomes. Greater focus on disease prevention may tighten the gap, Beech says. “UMMC is taking a proactive approach and leading the nation in preparing for 21st century health care,” Beech said. “We are developing a creative, innovative model to address health and health care.” Mann 168 VOL. 57 • NO. 5 • 2016

Dr. Michael Griswold, professor and director of the Center of Biostatistics and Bioinformatics, says that the new department will help prepare the next generation of health care providers transition to value-based care, population health precision medicine.

Data science bridges the disciplines of statistics, computer science, and predictive analytics to turn large amounts of data into usable evidence. The department will offer M.S. and Ph.D. degrees in biostatistics and data science. “Our vision is to become a leading department of data science by providing cutting-edge expertise in research and education for translating data into evidence, answers, and actions,” Griswold said. “In population health, data is used to predict and prevent disease and to determine who is at risk,” Beech said. “This can provide a set of solutions to improve patient and community health outcomes.” UMMC will conduct national searches for a Department of Population Health Science chair and faculty members. The department will offer research-oriented M.S. and Ph.D. degrees in population health. Eventually, the school intends to add a Department of Health Care Economics. Dr. Ralph Didlake, associate vice chancellor for academic affairs, said, “The delivery model of population health fits well with the needs of Mississippi, and it is clear that this is the direction that we need to head as an institution.”


According to the proposal submitted to the IHL, Beech will serve as the school’s first dean. Beech is “an extremely strong candidate and a national authority on population health and well suited to be dean,” Didlake said. The school intends to hire faculty, recruit students, create coursework in 2016, and admit its first students in January 2017. The School of Population Health will be located in the Translational Research Center, scheduled for completion in 2017. Basic, applied and population scientists sharing the same physical space will promote collaboration, Beech says. However, the school will not be confined to that space. “We are going to look beyond the borders of the Medical Center to conduct work that is pragmatic and applied to improve health outcomes throughout the state,” Beech said. “In fifteen to twenty years, we hope to see noticeable results in the community.” The School of Population Health will be the seventh school on the UMMC campus. The others are medicine, nursing, dentistry, health related professions and graduate studies. The School of Pharmacy is located in Oxford with clinical programs at UMMC. “To start a new school is a major undertaking and an exciting development,” said Dr. LouAnn Woodward, vice chancellor for health affairs and dean of the School of Medicine. “Population health and the concept of disease prevention are the future of health care and health-care delivery.” n Construction of the new Translational Research Building


This is part of a spotlight series on the MSMA Physician Leadership Academy class of 2016.


Wingfield is a dermatologist at The Dermatology Clinic in Gulfport, Mississippi, which she established in September 2003. During her undergraduate career at Millsaps College, she realized that “bench research” was not a fit for her personality and that she preferred being around people and seeing the results of her work more quickly. That realization led her to attend medical school at Louisiana State University Health Sciences Center in New Orleans after graduating Millsaps with a B.A. in English and a B.S. in biology. Her decision to specialize in dermatology was also informed by her people-person ways: “I enjoy getting to know patients; this is difficult when they are very ill or in pain. Dermatology patients are stable and generally happy. I like seeing all age groups of people and enjoy the variety in diagnoses,” she explains. “It’s never boring.”

Angela Wingfield, MD


Internal Medicine Residency Employer: Southeast Alabama Medical Center (SAMC) Deadline: 6/1/2016 or open til filled Exciting opportunity for the right leader to shape SAMC’s educational environment, developing a new Internal Medicine Residency Program at this valuesfocused, not-for-profit community health system. SAMC improves the health and quality of life of people in southeast Alabama, southwest Georgia and the F Florida Panhandle, using advanced treatment and technology. Excellent salary, benefits. Tobacco-free, drug-free campus. REQUIREMENTS:   5 yrs active faculty ACGME residency;  3 yrs GME admin experience;  MD/DO, board/specialty certified; To apply: Send CV to tomw@dcallc.com Full job description: www.dcallc.com 170 VOL. 57 • NO. 5 • 2016

Dr. Wingfield is hard-working and conscientious about her work and her commitments. Her proudest accomplishment has been starting her own practice and growing it into a thriving, successful business that helps thousands of people every year. Dr. Wingfield was the first dermatologist on the coast to offer both PUVA and narrow-band UVB phototherapy treatments for psoriasis and vitiligo, and today the Dermatology Clinic PLLC is a referral center for other dermatologists to send their patients for light therapy. In October 2008, she moved her clinic to its present site, a state of the art beautiful 10,000 square foot building which also houses Vivify Spa. Vivify Spa is the only medical spa on the Mississippi gulf coast under the direction of a board certified dermatologist. Being active in MSMA is important to Dr. Wingfield because it allows physicians’ voices to be heard by individuals who make decisions that affect the practice of medicine. One of the frustrations she has faced as a dermatologist is the influence insurance companies have over patient care. “Insurance companies dictate the care even if it is not what is best for the patient. It’s frustrating. I hope to see the power shift back towards doctors and patients having more choices.” Through the Physician Leadership Academy, Dr. Wingfield hopes to become a more effective leader in her practice, her community and in the state. n

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148TH ANNUAL SESSION OF THE HOUSE OF DELEGATES Featuring: • The inauguration of President-Elect Lee Voulters, MD • Guest speaker Andrew W. Gurman, MD, President-Elect of the American Medical Association • CME sessions both mornings

August 12−13, 2016 The Hilton Hotel

1001 East County Line Road in Jackson


Profile for Journal MSMA

VOL. LVII • NO. 5 • 2016  

"the voice, the face, and the spirit of medicine in Mississippi"

VOL. LVII • NO. 5 • 2016  

"the voice, the face, and the spirit of medicine in Mississippi"