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VOL. LI

2010

No. 3

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Lucius M. Lampton, MD EDITOR D. Stanley Hartness, MD Michael O’Dell, MD ASSOCIATE EDITORS Karen A. Evers MANAGING EDITOR PUBLICATIONS COMMITTEE Dwalia S. South, MD Chair Philip T. Merideth, MD, JD Martin M. Pomphrey, MD Leslie E. England, MD, Ex-Officio Myron W. Lockey, MD, Ex-Officio and the Editors THE ASSOCIATION Randy Easterling, MD President Tim J. Alford, MD President-Elect J. Clay Hays, Jr., MD Secretary-Treasurer Lee Giffin, MD Speaker Geri Lee Weiland, MD Vice Speaker Charmain Kanosky Executive Director 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 391582548. 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© 2010, Mississippi State Medical Association.

MARCH 2010

VOLUME 51

NUMBER 3

SCIENTIFIC ARTICLES Prevalence and Trends in Obesity among Mississippi Public School Students, 2005-2009

Elaine Fontenot Molaison, PhD, RD; Jerome R. Kolbo, PhD, ACSW; Lei Zhang, PhD, MBA; Bonnie Harbaugh, PhD, RN; Mary G. Armstrong, MD; Keith Rushing, PhD, RD; Lindsey C. Blom, EdD and Ashley Green, BS

Cardiovascular Disease in Rheumatoid Arthritis: Disease and Treatment Interactions and their Implications on Treatment Decisions

Clinical Problem-Solving: Pseudo Seizures Vs Pseudo Zebra

D. Mark Pogue, MD; Judith G. Gearhart, MD and George Moll, Jr., MD, PhD

PRESIDENT’S PAGE Pigs Have Already Flown

Randy Easterling, MD; MSMA President

EDITORIALS There is a Tide in the Affairs of Men

W. Lamar Weems, MD; MSMA Past President

The Great Myth

Dwalia S. South, MD; MSMA Past President, Chair, MSMA Committee on Publications

RELATED ORGANIZATIONS Information and Quality Healthcare University of Mississippi Medical Center

94 95

DEPARTMENTS Placement/Classified Una Voce

95 96

ABOUT THE COVER: “TRICYRTIS HIRTA (TOAD LILY)” - From the botanical family Liliaceae, this Toad lily flower head was photographed by Brett Tisdale, MD, a board certified emergency physician practicing in McComb. Toad lilies add summer and autumn bloom to shade gardens. Unique, its anthers look like the eyes on a slug, its stamens arch like showerheads, and its six differently shaded petals (actually tepals) alternate like men and women at a dinner table. Unless massed and displayed prominently up front and center where you're inclined to sit and gaze into its face, the blossom of T. hirta is easy to miss in the garden. Only one-inch small in loosely branched clusters or cymes, purple-spotted with yellow throats, they appear a cross between an orchid and a tiger-lily. This perennial’s subtlety has snob appeal (what you call your basic “connoisseur plant”). One close encounter with its amethystine reflection and you'll soon see why this selection, if not the entire genus, is an instant attention-getter.❒ March

VOL. LI

Official Publication of the MSMA Since 1959

Suzanne Sanders, MD and Stephen A. Geraci, MD

MARCH

2010

No. 3

2010 JOURNAL MSMA

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JOURNAL MSMA

MARCH

2010

• SCIENTIFIC ARTICLES •

Prevalence and Trends in Obesity among Mississippi Public School Students, 2005-2009

Elaine Fontenot Molaison, PhD, RD; Jerome R. Kolbo, PhD, ACSW; Lei Zhang, PhD, MBA; Bonnie Harbaugh, PhD, RN; Mary G. Armstrong, MD; Keith Rushing, PhD, RD; Lindsey C. Blom, EdD and Ashley Green, BS BSTRACT

The purpose of this research was to determine the prevalence of overweight and obesity in Mississippi children and youth in grades K - 12, and to assess any changes in the prevalence during 2005, 2007, and 2009. Body Mass Index was calculated using measured height and weight data for 3,703 public school students, and the prevalence of overweight and obesity was estimated. Additional analysis compared prevalence estimates by gender, race, and grade for the 2009 data, and comparisons were made between the 2005, 2007, and 2009 data. In 2009, the prevalence of obesity for all students in grades K - 12 was 23.9%, as compared to 23.5% in 2007 and 25.5% in 2005. However, no statistically significant differences were found over the three time periods. The disparity between races appears to be increasing over time with the prevalence remaining level for Nonwhite students while dropping each year for White students.

KEY WORDS:

OBESITY, CHILDHOOD, OVERWEIGHT

INTRODUCTION It is well established that the prevalence of childhood obesity had increased across the nation between 1980 and 2004.1 More recently, however, the National Health and Nutrition Examination Survey (NHANES) showed no significant changes in the percentage of obesity AUTHOR INFORMATION: Dr. Molaison is an Associate Professor in the Department of Nutrition & Food Systems at The University of Southern Mississippi. Dr. Kolbo is a Professor in the School of Social Work at The University of Southern Mississippi. Dr. Zhang is the Director of the Office of Health Data and Research in the Mississippi State Department of Health and an Associate Professor in the School of Nursing at the University of Mississippi Medical Center. Dr. Harbaugh is an Associate Professor in the School of Nursing at The University of Southern Mississippi. Dr. Armstrong is the Medical Director for Public Health District V, for the Mississippi State Department of Health. Dr. Rushing is an Assistant Professor in the Department of Nutrition & Food Systems at The University of Southern Mississippi. Dr. Blom is an Assistant Professor of Physical Education at Ball State University. Ms. Green is currently a graduate student in the Master of Public Health Program at The University of Southern Mississippi. CORRESPONDING AUTHOR: Elaine Fontenot Molaison, PhD, The University of Southern Mississippi, Department of Nutrition & Food Systems, 118 College Drive #5172, Hattiesburg, MS 39406, Phone: 601-266-6548, Fax: 601-266-6343, Elaine.molaison@usm.edu

among US children aged 2 to 19 years between 2003-2004 and 20052006.2 Similarly, the national Youth Risk Behavior Survey (YRBS) has reported no significant changes in the percentage of obesity among US students in grades 9-12 who attended public and private schools between 2005 and 2007.1 In contrast to national child obesity trends, analysis of Mississippi’s YRBS data revealed that self-reported prevalence of obesity among public high school students has continued to rise and has shown an upward linear trend between 2001 and 2007.1 It should be noted that the incremental rise in obesity between 2007 and 2009 (0.4%) was less than that between 2001 and 2003 (1.7%). Further, it is encouraging that the difference in obesity prevalence observed between 2007 and 2009 was not statistically significant. The YRBS, however, does not include elementary level children and, in 2005, the state did not obtain weighted YRBS data on high and middle school students. Consequently, it is difficult to determine, based only on high school self-reports, whether or not changes in childhood obesity are occurring in Mississippi. In Mississippi, a second source of obesity data is the Child and Youth Prevalence of Obesity Surveys (CAYPOS).3-5 Every other year since 2003, actual heights and weights have been collected on weighted, representative samples of public school students. Between 2003 and 2005, the CAYPOS indicated that the prevalence of obesity among children and youth in the public schools was increasing.3,5 In 2003, 24% of students in grades 1 – 8 were obese and 14.7% were overweight. By 2005, 25.5% of Mississippi students in grades K – 12 were obese and 18.4% were overweight. In the 2005 study, the highest prevalence was among middle school students (28.9%), followed by elementary students (25.0%), and then high school students (23.5%). In the 2007 CAYPOS, however, a modest decrease in the prevalence of obesity was reported. Between 2005 and 2007, the prevalence of obese children and youth declined from 25.5% to 23.5%. The prevalence dropped from 28.9% to 22.8% in the middle school and from 23.5% to 20.8% in the high school, yet was relatively unchanged among the elementary level (25.0% to 25.3%). While the prevalence rates were still very high, the decline in middle and high school sugMARCH

2010 JOURNAL MSMA

gested that like data from the National YRBS and other national studies, the prevalence may be leveling off or beginning to drop in Mississippi.4 Whether or not the obesity rates are continuing to increase, leveling off, or declining may have a significant impact on the health and well-being among children, youth and adults. Evidence has been progressively accumulating that obese children do not necessarily have to wait until adulthood to suffer serious health consequences from their excess weight. Obese children are more likely to suffer complications from obesity related cardiovascular, pulmonary, and metabolic diseases, as well as depression and low self-esteem.6-11 Based on NHANES estimates of overweight and obesity through 2004, projection analysis predicts 86.3% of adults (> 20 years old) will be overweight or obese by 2030. In addition, health care costs associated with the rise in obesity are expected to reach one trillion dollars annually by 2030.12 Educational Initiatives With children spending the majority of their waking hours at school, across the nation many policy efforts have been geared toward changes in the school setting. These range from mandatory Body Mass Index (BMI) assessments in all schools to limiting the availability of competitive foods on school campuses to increasing physical activity in schools. However, limited research on the outcomes of these initiatives is currently available.13-18 Through a mix of state and federal legislation, Mississippi recently began implementing several state-wide school-based initiatives to address the problem of childhood obesity. In 2004, Congress enacted the Child Nutrition and WIC Reauthorization Act (Section 204 of Public Law 108-265) mandating any local education agency participating in a program authorized by the Richard B. Russell National School Lunch Act (NSLA) or the Child Nutrition Act of 1966 (CNA) to establish a school wellness policy no later than the first day of the school year beginning after June 30, 2006.19 The primary objective of the law was to prevent inactivity and obesity among children. The law established that, at a minimum, the local wellness policies shall contain: goals for nutrition education and physical activity; nutrition guidelines for foods available at each school; assurance that guidelines for the wellness policy are not less restrictive than those set forth by the NSLA or the CNA; plans for measuring implementation of the local wellness policy; and involvement of a representative group of community and school stakeholders in the development of the school wellness policy.20 In 2006, the Mississippi State Board of Education also approved Beverage Regulations for Mississippi Schools. This legislation established phased implementation of strict guidelines for the types of beverages that could be served at school campuses during the regular and extended school day. In Phase One, beginning in August 2007, sale of all full-calorie, sugared carbonated beverages was prohibited to students at Mississippi schools during the school day. In phase two, beverage vending was further restricted to include only bottled water, low-fat and non-fat milk, and 100% fruit juice in age-appropriate servings for elementary and middle schools. High schools are allowed bottled water, no- or low-calorie beverages and age-appropriate servings of low- or non-fat milk, 100% juice, light juice/light sports drinks, and at least 50% of beverages must be water or no-calorie options.21

JOURNAL MSMA

MARCH

2010

In 2007, the Mississippi Code of 1972 was amended (section 37-13-134, The Mississippi Healthy Students Act) and the Mississippi Public School Accountability Standards were revised by establishing stricter nutrition, physical activity, and physical education standards for Mississippi schools.22,23 Based on this legislation, the Mississippi Department of Education created two interpretive documents: 1) Nutrition Standards and, 2) Physical Education/Comprehensive Health Education Rules and Regulations.24,25 The Nutrition Standards established specific requirements for food choices offered in the cafeteria and on campus, how food is prepared at schools, marketing of healthy foods to students and staff, minimum and maximum time allotments for students' and staff meal periods, and methods for increasing participation in the child nutrition school breakfast and lunch programs. The Physical Education/ Comprehensive Health Education Rules and Regulations provided time requirements, sample curriculum, and schedules for physical education, physical activity, and activity-based instruction for students in grades K-8; fitness testing for fifth grade students; and guidelines for physical education, comprehensive health education, and fitness testing for students in grades 9-12.25 By the fall of 2008, all standards and requirements had been phased in by the public schools in Mississippi. In light of the recent educational initiatives in Mississippi, the purpose of this research was to once again determine the prevalence of overweight and obesity of children and youth in grades K - 12 and to assess any changes in the prevalence between 2005, 2007, and 2009.

METHODS The sampling frame consisted of 475,680 students in 894 public schools offering kindergarten or any combination of grades 1 through 12 in Mississippi. As with the 2003, 2005, and 2007 CAYPOS, the sample design was a two-stage stratified probability design. The first stage included the random selection of 96 schools. A systematic sample of schools was drawn with probability proportional to the enrollment in grades K - 12 of each school. In the second stage of sampling, classes were randomly selected within the sampled schools. Classes were selected using equal probability systematic sampling. All eligible students in the selected classes were asked to participate in the survey. The sample was designed to yield a self-weighting sample so that every eligible student had an equal chance of selection, thereby improving the precision of the estimates. As in each of the previous years, the weighting process was intended to develop sample weights so that the weighted sample estimates accurately represented the entire K -12 public school students in Mississippi. Every eligible student was assigned a base weight which was equal to the inverse of the probability of selection for the student. Adjustments were made to the initial weights to remove bias from the estimates and reduce the variability of the estimates. The CAYPOS was conducted in April 2009 in Mississippi. The study received continued institutional review board approval through the Human Subjects Committee at The University of Southern Mississippi, as the study protocol matched the 2003, 2005, and 2007 CAYPOS.3,4 As with the previous studies, once selected schools agreed to participate and classes were chosen, measuring equipment (i.e., digital scales and stadiometers) and passive consent forms were delivered to

the schools. Each school designated a school nurse who was responsible for collecting data and had been trained on the use of equipment. Two or three days before data collection began, students in the selected classes were read a prepared paragraph containing information about the study. Each student was then given a passive parental consent form to take home to parents or guardians. If a parent did not want his or her child to participate in the study, the parent was instructed to indicate such on the form, sign it, and have the child return it to the teacher. Prior to the collection of heights and weights, the nurse would check with the teacher to determine if any students returned a signed form. Students who returned a signed form did not participate in the study. There were neither consequences for nonparticipation nor rewards for participation. As with the previous studies, the protocol for making measurements required that the weight scale be placed on a hard, smooth surface; carpeted areas were not to be used. The scale was calibrated to zero before use and recalibrated after every 10th student. All students were weighed and measured in a location where the information gathered would be confidential. Other students were not able to read the scale or height measurement or hear a weight or height given. Nurses reported the height and weight, rounded to the nearest whole inch or pound, respectively, along with age, sex, date of birth, racial or ethnic background, and the school code number. No allowance was made for weight of clothing; however, students were asked to remove belts, heavy jewelry, jackets, and shoes. No student names were written on the data collection forms. In previous years, nurses recorded all data on Optiscan forms and mailed them to the study authors. In the 2009 CAYPOS, nurses were sent an email with a link to a secure website developed and maintained by Qualtrics, Inc.26 to record and submit their data. These data were compiled in aggregate form by the Qualtrics software and made available in excel format to the study authors for analysis.

DATA ANALYSIS Body Mass Index was computed for each responding student based on height (in meters) and weight (in kilograms). The height in feet and inches was first converted to meters. The weight in pounds was then converted to kilograms. BMI was calculated using the SAS program, gc-calculate-BIV.sas as follows: BMI = Weight (in kg)/ [Height (in m)].2 BMI values were checked to ensure that the results were biologically plausible, using the limits developed by the CDC. BMI percentiles were computed using the SAS program, gc-calculateBIV.sas. Children and adolescents are classified into four categories: (1) underweight (BMI is less than the 5th percentile); (2) normal weight (BMI is equal to or greater than the 5th but less than the 85th percentile); (3) overweight (BMI is greater than the 85th but less than the 95th percentile); and (4) obese (BMI is greater than or equal to the 95th percentile).27 SUDAAN 10.028 was used to calculate weighted estimates and standard errors, and Proc Crosstab procedure was used to compare prevalence of child overweight among different subgroups. As in previous years, differences between summary statistics were considered statistically significant if the p-value from Chi-square test was less than 0.05. For comparisons between 2009, 2007, and 2005, differences be-

tween summary statistics were considered statistically significant if their associated 95% confidence intervals did not overlap.

RESULTS Characteristics of Participants from the 2009 CAYPOS Eighty-two of the 96 schools sampled participated in the study (85%). The student response rate was 87% (3,703 usable records/4,266 eligible sampled students). Thus, the overall response rate was 74% (product of school response rate and student response rate), which was above the threshold of 60% required to obtain weighted estimates. The final sample consisted of 3,703 students in grades K - 12, including 1,839 males (49.8%), 1,864 females (50.2%), 2,053 Nonwhites (56.3%) and 1,648 Whites (43.7%) (Table 1). For this report, the category Nonwhite is considered a close measure for African American because 93% of Nonwhite students were African American. The number of students in other race categories was too small for separate analysis. TABLE 1: CHARACTERISTIC OF PARTICIPANTS, CAYPOS, GRADES K-12, MISSISSIPPI, 2009 Characteristic Gender Male Female Race White a Nonwhite Missing Grade Elementary K 1st 2nd 3rd 4th 5th Middle school 6th 7th 8th High school 9th 10th 11th 12th Total a

Unweighted count

Weighted percent

1,839 1,864

49.8 50.2

1,648 2,053 2

43.7 56.3 0.0

163 274 338 271 447 163

4.2 7.9 8.5 7.3 11.7 4.5

143 344 501

3.7 8.9 13.6

435 263 153 208 3,703

12.3 7.6 4.1 5.7 100

Ninety-three percent of Nonwhite Students were African American.

Results of 2009 CAYPOS Based on Subgroups of Participants As a group, 23.9% of the children and youth in grades K - 12 were classified as obese, and another 18.5% of the children were classified as overweight giving a combined total of 42.4% of the children and youth at or above the 85th percentile for BMI for age and gender. A more detailed analysis of the data by gender, race, and grade level is discussed below. Gender In 2009, 23.0% of females were classified as obese, with another 18.8% as overweight. Among males, 24.8% were obese and another 18.2% were overweight (Table 2). Race In terms of race, 19.5% of the White students were classified as obese with another 17.9% as overweight. Among the Non-white students, 27.4% were obese and 19% were overweight. There is a statisMARCH

2010 JOURNAL MSMA

TABLE 2: PREVALENCE OF OVERWEIGHT AND OBESITY BY GRADE LEVEL, GENDER, AND RACE, CAYPOS, , 2005, 2007, AND 2009 Elementary (K-5) (%, 95% CI)

Male Overweight 2005 18.6 (16.8-20.4) 18.7 (16.3-21.2) 2007 17.5 (15.5-19.7) 16.3 (13.9-19.0) 2009 18.2 (16.5-20.0) 18.0 (15.5-20.8) Obesity 2005 25.2 (23.0-27.4) 24.2 (21.6-27.0) 2007 24.2 (22.0-26.6) 25.7 (22.3-29.4) 2009 24.8 (22.5-27.4) 24.2 (20.9-27.7) Female Overweight 2005 18.1(15.7-20.5) 17.5 (14.5-20.9) 2007 19.7 (17.3-22.3) 20.5 (18.1-23.2) 2009 18.8 (17.2-20.5) 17.4 (14.8-20.3) Obesity 2005 25.9 (22.6-29.2) 25.9 (21.8-30.6) 2007 22.9 (20.4-25.5) 24.8 (20.9-29.2) 2009 23.0 (20.8-25.3) 24.0 (20.2-28.2) White male Overweight 2005 17.9 (15.3-20.9) 17.7 (14.1-22.0) 2007 17.5 (14.7-20.6) 17.3 (14.2-20.8) 2009 17.8 (15.4-20.6) 18.1 (13.7-23.6) Obesity 2005 23.6 (21.1-26.4) 21.3 (19.0-23.7) 2007 23.6 (20.3-27.2) 23.0 (18.7-27.9) 2009 22.5 (19.1-26.4) 18.7 (13.3-25.6) Nonwhite male Overweight 2005 19.2 (16.8-21.9) 19.6 (17.8-21.6) 2007 17.7 (14.8-20.9) 15.3 (11.1-20.7) 2009 18.4 (16.0-21.1) 17.9 (14.1-22.5) Obesity 2005 26.4 (22.8-30.4) 26.7 (23.3-30.4) 2007 25.0 (21.9-28.5) 28.3 (23.2-34.0) 2009 26.6 (23.8-29.6) 27.9 (23.6-32.7) White female Overweight 2005 17.6 (14.3-21.6) 18.1 (14.9-21.9) 2007 19.1 (15.7-22.9) 18.3 (15.1-22.1) 2009 17.9 (15.7-20.3) 18.4 (14.5-23.1) Obesity 2005 22.3 (18.5-26.7) 22.8 (20.1-25.8) 2007 18.4 (14.9-22.6) 20.7 (15.5-27.2) 2009 16.4 (13.8-19.5) 16.8 (12.3-22.4) Nonwhite female Overweight 2005 18.4 (15.8-21.4) 17.0 (14.8-19.4) 2007 20.1 (17.2-23.4) 22.6 (18.9-26.8) 2009 19.6 (17.6-21.8) 16.8 (13.9-20.2) Obesity 2005 28.4 (24.1-33.1) 28.0 (22.6-34.2) 2007 26.4 (23.2-29.8) 28.5 (23.8-33.8) 2009 28.1 (25.2-31.2) 28.4 (23.2-34.2) * Sample size is less than 50. The estimates may not be reliable.

Middle school (6-8) (%, 95% CI)

19.3 (15.3-24.0) 18.5 (13.1-25.5) 17.1 (14.0-20.6) 28.4 (23.9-33.3) 20.1 (16.3-24.5) 27.1 (22.9-31.8)

18.1 (15.0-21.7) 19.3 (15.6-23.6) 19.5 (16.3-23.3)

Overweight

24.4 (19.3-30.3) 24.4 (20.0-29.4) 23.7 (19.0-29.1)

19.6 (15.6-24.2) 19.7 (15.5-24.6) 18.9 (15.3-23.1)

18.2 (14.4-22.9) 18.1 (12.4-25.5) 20.5 (18.4-22.9)

29.4 (23.9-35.6) 24.9 (20.9-29.4) 23.7 (20.0-27.8)

22.8 (18.7-27.5) 17.1 (13.4-21.6) 21.1 (17.6-25.2)

Middle school (6-8)

High school (9-12)

(%, 95% CI)

18.3 (13.4-24.5)* 17.4 (9.9-28.7)* 15.8 (10.8-22.6)*

18.2 (16.4-20.2)* 17.8 (12.0-25.5)* 19.4 (13.9-26.5)*

31.5 (29.5-33.5) 18.9 (12.1-28.3)* 25.4 (18.4-34.0)

22.3 (18.2-26.9)* 28.8 (21.8-37.0) 25.2 (18.3-33.5)

2005

18.4 (17.0-19.8)

2007

18.6 (17.1-20.1)

18.3 (16.6-20.1)

19.2 (17.4-21.1)

18.7 (14.4-23.9)

2009

18.5 (17.3-19.7)

17.7 (15.7-19.9)

18.0 (15.4-20.8)

20.1 (18.8-21.5)

25.0 (22.3-27.7)

28.9 (24.8-33.0)

23.5 (20.6-26.4)

Obesity

18.0 (16.2-19.8)

19.4 (16.5-22.3)

18.1(15.9-20.3)

2005

25.5 (23.3-27.7)

2007

23.5 (21.6-25.7)

25.3 (22.1-28.7)

22.8 (19.8-26.1)

20.8 (17.6-24.5)

2009

23.9 (22.0-25.9)

24.1 (21.2-27.2)

25.4 (22.0-29.2)

22.3 (19.1-25.9)

17.9 (14.4-22.0)

18.2 (13.8-23.7)

16.9 (14.6-19.6)

White Overweight 2005

17.7 (15.5-19.9)

2007

18.3 (16.5-20.2)

17.8 (15.8-19.9)

20.1 (15.7-25.2)

17.5 (13.2-22.7)

2009

17.9 (16.3-19.5)

18.3 (15.2-21.8)

16.7 (13.9-19.9)

18.4 (15.9-21.3)

Obesity 2005

22.9 (20.4-25.4)

22.9 (20.5-25.6)

28.4 (23.6-33.8)

19.9 (16.6-23.7)

2007

21.0 (18.5-23.7)

21.9 (18.4-25.9)

19.5 (13.8-27.0)

20.1 (16.2-24.8)

2009

19.5 (17.1-22.1)

17.8 (14.0-22.3)

21.6 (17.6-26.2)

19.6 (15.7-24.1)

20.1 (16.9-23.7)

18.9 (15.8-22.6)

Nonwhite

Overweight 2005

18.8 (17.2 20.4)

18.2 (16.2-20.5)

2007

18.9 (16.7-21.3)

18.9 (15.9-22.2)

18.3 (15.7-21.3)

19.6 (14.4-26.0)

2009

19.0 (17.3-20.9)

17.4 (14.8-20.3)

19.2 (15.0-24.2)

21.6 (18.7-24.7)

Obesity 19.8 (14.8-25.9)* 19.8 (15.2-25.5)* 18.2 (13.1-24.7)*

18.0 (13.2-24.2)* 20.5 (15.0-27.3) 19.7 (15.5-24.6)

25.8 (18.5-34.9)* 20.9 (16.2-26.6)* 28.5 (22.7-35.1)

25.8 (11.4-48.5)* 22.3 (16.1-30.0) 22.4 (17.2-28.5)

2005

18.1 (12.4-25.7)* 22.0 (13.9-33.2)* 17.6 (12.1-24.7)

16.0 (14.7-17.5)* 17.2 (9.8-28.3)* 17.6 (14.1-21.6)*

25.5 (20.9-30.8)* 20.0 (13.2-29.2)* 17.9 (12.9-24.4)*

18.0 (13.0-24.4)* 10.9 (7.7-15.3)* 14.8 (10.0-21.3)*

20.4 (18.3-22.6)* 17.1 (14.4-20.2)* 20.3 (13.5-29.4)*

19.7 (17.0-22.7)* 18.7 (12.4-27.2)* 23.1 (19.2-27.6)

32.0 (23.5-41.9) 29.0 (23.4-35.3) 29.5 (22.9-37.1)

26.0 (18.7-34.9) 20.5 (14.8-27.7) 26.6 (22.2-31.5)

Gender and Grade Level Among females, the highest rates were at the elementary level followed by the middle school and high school. For males, the highest rates were at the middle school followed by the elementary school and high school. Specifically, at the elementary level, 24.0% of females were obese and 17.4% were overweight. For males, 24.2% were obese and 18.0% were overweight. Among middle school students, 23.7% of girls were obese and 18.9% were overweight. For males, 27.1% were obese and 17.1% were overweight. At the high school

2010

27.4 (24.5-30.3)

27.4 (24.4-30.6)

29.3 (23.4-36.0)

25.9 (21.8-30.5)

2007

25.7 (22.9-28.7)

28.4 (23.8-33.5)

25.4 (21.2-30.0)

21.4 (16.5-27.3)

2009

27.4 (25.1-29.8)

28.1 (24.7-31.9)

29.0 (24.9-33.5)

24.7 (21.0-28.8)

Body mass index (BMI) > 85th percentile and < 95th percentile for age and gender.

Body mass index (BMI) > 95th percentile for age and gender.

Grade Level Among elementary level students (grades K â&#x20AC;&#x201C; 5), 24.1% were classified as obese with 17.7% classified as overweight. Among the middle school students (grades 6 â&#x20AC;&#x201C; 8), 25.4% were obese and 18.0% were overweight. Among the high school students (grades 9 -12), 22.3% were obese and 20.1% were overweight. (Table 2)

MARCH

Elementary (K-5) c

Gender and Race As for gender and race, Nonwhite females had significantly higher prevalence rates than White females (28.1% vs. 16.4%). Among males, 26.6%of Nonwhite males and 22.5% of White males were obese (Table 2).

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All (K-12) (%, 95% CI ) All

tically significant difference between the prevalence of obesity among the White and Nonwhite students (Table 2).

RACE, CAYPOS, MISSISSIPPI 2005, 2007, AND 2009

High school (9-12) (%, 95% CI)

95% confidence interval.

In 2009, 2007, and 2005, about 93%, 94%, and 95% of Nonwhite students were African American,

respectively.

level, 21.1% of females were obese, with 20.5% overweight. For males, 23.7% were obese and 19.5% were overweight. (Table 3) Race and Grade Level Among both White and Nonwhite students, the highest rates were at the middle school level followed by the elementary school and high school. Specifically, at the elementary level, 17.8% of White students were obese and 18.3% were overweight. For Nonwhite students, 28.1% were obese and 17.4% were overweight. At the elementary level difference in the prevalence of obesity between White and Nonwhite students was statistically significant (p = 0.006; Figure 1).

FIGURE 1: OBESITY PREVALENCE BY RACE AMONG MISSISSIPPI ELEMENTARY SCHOOL STUDENTS

Percent

All (K-12) (%, 95% CI)

TABLE 3: PREVALENCE OF OVERWEIGHT AND OBESITY BY GRADE LEVEL AND

40 35 30 25 20 15 10 5 0

p = 0.077 27.4 22.9

p = 0.020 28.4

p = 0.006 28.1

21.9 17.8

White

Nonwhite

2005

2007

2009

Year

Among middle school students, 21.6% of White students were obese and 16.7% were overweight. For Nonwhite students, 29.0% were obese and 19.2% were overweight. The difference in the prevalence of obesity between white and nonwhite students was not statistically significant (p = 0.069; Figure 2). At the high school level, 19.6% of White students were obese with 18.4% overweight. For Nonwhite

FIGURE 2: OBESITY PREVALENCE BY RACE AMONG MISSISSIPPI MIDDLE

Percent

SCHOOL STUDENTS 40 35 30 25 20 15 10 5 0

p = 0.825 29.3 28.4

p = 0.469

p = 0.069 29.0

25.4 21.6

19.5

White

Nonwhite

2005

2007

2009

Year

FIGURE 3: OBESITY PREVALENCE BY RACE AMONG MISSISSIPPI HIGH

Percent

SCHOOL STUDENTS 40 35 30 25 20 15 10 5 0

p = 0.178

p = 0.755

p = 0.071

25.9

19.9

24.7 20.1

21.4

19.6

DISCUSSION White

Nonwhite

2005

2007

as compared to 23.5% in 2007 and 25.5% in 2005. The prevalence of overweight was 18.2% in 2009 as compared to 18.6% in 2007 and 18.4% in 2005. The prevalence of obesity among males in 2009 was 24.8%, compared to 24.2% in 2007 and 25.2% in 2005. Among females, 23.0% were obese in 2009 compared to 22.9% in 2007 and 25.9% in 2005. As for race, 19.5% of White students were obese in 2009, compared to 21.0% in 2007 and 22.9% in 2005. Among Nonwhite students, 27.4% were obese in 2009 compared to 25.7% in 2007 and 27.4% in 2005. The prevalence among elementary students in 2009 was 24.1% compared to 25.3% in 2007 and 25.0% in 2005. Among middle school students, 25.4% were obese in 2009 compared to 22.8% in 2007 and 28.9% in 2005. Among high school students, 22.3% were obese in 2009 compared to 20.8% in 2007 and 23.5% in 2005 (Table 3).

2009

Year

students, 24.7% were obese and 21.6% were overweight. The difference in the prevalence of obesity between white and nonwhite students was not statistically significant (p = 0.071; Figure 3). Gender, Race, and Grade Level When race and gender were combined at the elementary level, 16.8% of White females were obese and 18.4% were overweight. Among Nonwhite females, 28.4% were obese and 16.8% were overweight. At the elementary level, these differences between rates of obesity between White and Nonwhite females were statistically significant. Among males, 18.7% of White males were obese, with 18.1% overweight. Among the Nonwhite males, 27.9% were obese and 17.9% were overweight. At the middle school level, 17.9% of White females were obese and 17.6% were overweight. Among Nonwhite females, 29.5% were obese and 20.3% were overweight. Among males, 25.4% of White males were obese, with 15.8% overweight. Among the Nonwhite males, 28.5% were obese and 18.2% were overweight. At the high school level, 14.8% of White females were obese and 17.6% were overweight. Among Nonwhite females, 26.6% were obese and 23.1% were overweight. Among males, 25.2% of White males were obese, with 19.4% overweight. Among the Nonwhite males, 22.4% were obese and 19.7% were overweight (Table 2). Comparison of 2005, 2007 and 2009 CAYPOS While no statistically significant differences were found over the three time periods (2005, 2007, 2009) for overall rates or by gender, race, or educational level, the data are described here. In 2009, the prevalence of obesity for all students in grades K - 12 was 23.9%

Like prevalence rates reported nationally, the prevalence of obesity among children and youth assessed through actual measures of height and weight no longer appears to be increasing. Since 2005, the 2007 and 2009 CAYPOS suggest that the prevalence of obesity has leveled off among children and youth in the public school system. While the leveling off of obesity is good news, the bad news is what appears to be an increasing disparity between White and Nonwhite students, especially for those in elementary and middle schools. The prevalence of obesity is again significantly lower among White students than the Nonwhite students. Further, while the prevalence has remained nearly the same for Nonwhite students over the three time periods (2005, 2007, 2009), it has dropped for the White students in the same period (22.9%, 21.0%, 19.5%, respectively). As for race, the differences between White and Nonwhite students continue to be statistically significant. Further, for both 2005 and 2007, significant differences between the White and Nonwhite students are found at the elementary level, suggesting the disparity is emerging among the younger children. Although the differences are not statistically significant, it is worth noting that in 2005 females had higher rates than boys in all three grade levels. In 2007, females had higher rates in only middle school. In 2009, boys had higher rates in all three educational levels. As in previous years, in 2009 the middle school again had the highest prevalence rates. However, there was no significant difference in grade levels nor was there a difference in grade levels over time. While the highest prevalence rates in the study were among Nonwhite females in middle school, these rates were not significantly higher than White females nor significantly different than in previous years. However, among the elementary level students, significant differences were found between Nonwhite and White students as well as among Nonwhite females and White females. Also, although the differences were not statistically significant, it is worth noting that the prevalence rates dropped for each of the three survey years among the White females in the elementary schools (22.8%, 20.7%, and 16.8%, respectively). It is encouraging to see signs of changes among females, particularly among young White females. Why is it that we are not MARCH

2010 JOURNAL MSMA

seeing similar signs of changes among males and Nonwhite students? What do these findings suggest in light of recent educational initiatives? Given that most of the initiatives have been fully implemented only during the same year (2008-2009) of the CAYPOS, it would be difficult at this time to associate changes, or the lack thereof, in prevalence rates to the recent policies, programs, and activities being implemented across the state. It is clear that continued monitoring of the prevalence rates is critical, especially as educational initiatives continue to be implemented. While there have been recent pediatric obesity-focused initiatives from the American Academy of Pediatrics along with the American Medical Association related to childhood obesity, there have not been any formal statewide medical initiatives instituted in Mississippi.29-31 However, a recent development provides a new opportunity for the Mississippi State Medical Association to lead a statewide initiative to screen school-aged children for obesity. Recent recommendations from the US Preventive Services Task Force issued January 18, 2010, by the American Academy of Pediatrics specifically recommends that clinicians screen children aged 6 years and older for elevated BMIs and offer them or refer them to intensive counseling and behavioral interventions to promote improvements in weight status.30 These recommendations differ from 2005 Task Force recommendations, as there is now stronger evidence that obese and overweight school aged children, once identified, can improve weight status with moderate to high intensity interventions.

11.

12.

13.

14.

15.

16.

17. 18.

19.

20.

21.

Acknowledgements: Funding for this study was through a grant from the Bower Foundation. The authors wish to thank Westat, Inc., for their assistance in the sampling and weighting of the data and to thank the Mississippi Schools and school nurses and personnel who were so instrumental in collecting the data.

22.

23.

REFERENCES 1.

Morbidity and Mortality Weekly Report. Youth Risk Behavior Surveillanceâ&#x20AC;&#x201D;United States, 2007. Centers for Disease Control Web site. www.cdc.gov/mmwr. Accessed December 1, 2009. 2. Ogden CL, Carroll MD, Flegal KM. High body mass index for age among US children and adolescents, 2003-2006. JAMA. 2008;299(20):2401-2405. 3. Kolbo JR, Penman AD, Meyer MK, Speed NM, Molaison EF, Zhang L. Prevalence of overweight among elementary and middle school students in Mississippi compared with prevalence data from the Youth Risk Behavior Surveillance System. Prev Chronic Dis. 2006;3:A84. 4. Kolbo JR, Armstrong MG, Blom L, Bounds W, Molaison E, Dickerson H, Harbaugh B, Zhang L. Prevalence of obesity and overweight among children and youth in Mississippi: Current trends in weight status. JMSMA. 2008;49(8):231-237. 5. Molaison EF, Kolbo JR, Speed N, Dickerson E, Zhang, L. Prevalence of overweight among children and youth in Mississippi: A comparison between 2003 and 2005. 2008 Available at http://www.mshealthpolicy. com. Accessed April 4, 2008 6. Arens R, Muzumdar H. Childhood obesity and obstructive sleep apnea syndrome. J Appl Physiol. 2009. Web site. doi: 10.1152/japplphysiol. 00689.2009. Accessed January 5, 2010. 7. Daniels SR, The consequences of childhood overweight and obesity. The Future of Children. 2006;16(1):47-67. 8. Rowland K, Coffey J. Are overweight children more likely to be overweight adults? J Fam Practice. 2009;58(8):431-432. 9. Sjoberg RL, Nilsson KW , Leppert J. Obesity, shame and depression in school aged children: A population-based study. Pediatrics, 2005,116, 389-392. 10. Thompson DR, Obarzanek E, Franko D, Barton B, Morrison J, Biro F, et al. Childhood overweight and cardiovascular disease risk factors: The

JOURNAL MSMA

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2010

24.

25.

26. 27.

28. 29. 30.

31.

National Heart Lung & Blood Institute Growth and Health Study. Pediatrics. 2007;150:18-25. Weiss R, Dziura J, Burgert TS, Tamborlane WV, Taksali SE, Yeckel CW, Allen K, Lopes M, Savoye M, Morrison J, Sherwin RS, Caprio S. Obesity and the metabolic syndrome in children and adolescents. N Engl J Med, 2004;350:2362-2374. Wang Y, Beydoun MA, Liang L, Caballero B, Kumanyika SK. Will all Americans become overweight or obese? Estimating the progression and cost of the US obesity epidemic. Obesity. 2008;16:2323-2330. Boehmer TK, Luke DA, Haire-Joshu DL, Bates HS, Brownson RC. Preventing childhood obesity through state policy: Predictors of bill enactment. AM J Prev Med. 2008;34(4):333-340. Boehmer TK, Brownson RC, Haire-Joshu D, Dreising ML. Patterns of childhood obesity prevention legislation in the United States. Preventing Chronic Disease. 2007;4:(3)1-11. Dodson EA, Fleming C, Boehmer TK, Haire-Joshu D, Luke DA, Brownson RC. Preventing childhood obesity through state policy: Qualitative assessment of enablers and barriers. Journal of Public Health Policy. 2009;30:S161-176. Foster GD, Sherman S, Borradaile KE. A policy-based school intervention to prevent overweight and obesity. Pediatrics. 2008;121(4): 794-802. Nihiser A, Lee SM, Wechsler H, et al. Body mass index measurement in schools. Journal of School Health. 2007;77(10):651-672. Story M, Nanney MS, Schwartz MB. Schools and obesity prevention: Creating school environments and policies to promote healthy eating and physical activity. The Milbank Quarterly. 2009;87(1):71-100. SB 2369, amending Mississippi Code of 1972 Annotated Section 37-13134. Web site. http://billstatus.ls.state.ms.us/documents/2007/html/SB/ 2300-2399/SB2369SG.htm. Accessed December 15, 2009. United States Department of Agriculture, Food and Nutrition Services. Section 204 of Public Law 108-265-Child Nutrition and WIC Reauthorization Act of 2004. 2004. Web site. http://www.fns.usda.gov/ TN/Healthy/108-265.pdf. Accessed September 23, 2008. Mississippi Department of Education, Mississippi Office of Healthy Schools. Beverage Regulations for Mississippi Schools. 2006. Website. http://www.cn.mde.k12.ms.us/documents/VendingRegForMSSchools06. pdf. Accessed September 20, 2008. Mississippi Legislature, Senate. The Mississippi Students Act. 2007. Web site. http://billstatus.ls.state.ms.us/documents/2007/pdf/ham/ Amendment_Report_for_SB2369.pdf. Accessed September 16, 2008 Mississippi Department of Education, Office of Innovation and School Improvement Office of Accreditation Mississippi Public School Accountability Standards 2007. 2007. Web site. http://www.mde.k12. ms.us/accred/2007_Edition.MS%20Public%20School%20Acct.%20Std s.pdf. Accessed September 17, 2008. Mississippi Department of Education. Mississippi Healthy Students Act Senate Bill 2369 Nutrition Standards. 2007. Web site. http://www. healthyschoolsms.org/documents/MississippiHealthyStudentsActSenate Bill2369NutritionStandards_000.pdf. Accessed September 17, 2008. Mississippi Secretary of State, Administrative Procedures. Physical Education/Comprehensive Health Education Rules and Regulations. 2007. Web site. http://www.sos.state.ms.us/busserv/AdminProcs//PDF/ 00014817b.pdf. Accessed September 17, 2008. Qualtrics [Online Survey Software]. Provo, UT; 2009. Centers for Disease Control. A SAS Program for the CDC Growth Charts. Web site. http://www.cdc.gov/nccd/php/dnpa/growthcharts/ sas.htm. Accessed June 1, 2009. SUDAAN [computer program]. Version 10.0. Research Triangle Park, NC; 2009 American Academy of Pediatrics 2003. Prevention of pediatric overweight and obesity. Pediatrics. 2003;112:424-430. American Academy of Pediatrics, 2010. Screening for Obesity in Children and Adolescents: US Preventive Services Task Force Recommendation Statement: US Preventive Services Task Force Pediatrics 2010;125:361â&#x20AC;&#x201C;367. Web site. www.pediatrics.org/cgi/doi/ 10.1542/peds.2009-2037. Accessed January 20, 2010). American Medical Association, 2007. Expert committee recommendations on the assessment, prevention, and treatment of child and adolescent overweight and obesity. Website. http://www.amaassn.org/ama1/pub/upload/mm/433/ped_obesity_recs.pdf. Accessed January 20, 2010.

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JOURNAL MSMA

MARCH

2010

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â&#x20AC;˘ SCIENTIFIC ARTICLES â&#x20AC;˘

Cardiovascular Disease in Rheumatoid Arthritis: Disease and Treatment Interactions and their Implications on Treatment Decisions Suzanne Sanders, MD and Stephen A. Geraci, MD

INTRODUCTION

BSTRACT

Cardiovascular disease is highly prevalent in rheumatoid arthritis patients, contributing to significant morbidity and mortality. Few randomized trials are available to guide risk assessment and intervention in these complex patients. This paper discusses traditional atherosclerotic and rheumatoid-related risk factors for cardiovascular disease in these patients, reviews the effect of treatment of cardiovascular risk factors on rheumatoid arthritis activity, and describes the effect of rheumatoid arthritis treatment on risk factors for cardiovascular disease. The authors reviewed the existing literature by cross-referencing topics such as cardiovascular disease, rheumatoid arthritis, various risk factors for cardiovascular disease and their treatments, and treatments for rheumatoid arthritis, using Medline and PubMed, reviewing references from 1983-2009. Traditional and rheumatoid-related risk factors (including active inflammation/disease activity and some medications) contribute to this high prevalence of cardiovascular disease in rheumatoid arthritis. Evidence supports aggressive therapy for traditional cardiovascular risk factors, reducing rheumatoid activity, and limiting pro-atherosclerotic medications.

Patients with rheumatoid arthritis (RA) have a reduced life expectancy with 40-50% of deaths attributed to cardiovascular disease (CVD).2,3 Their CVD incidence is greater than that of non-RA patients4 with a standardized incidence ratio of 2.9 for acute myocardial infarction (AMI) compared to the general population.5 Women who have RA for at least 10 years suffer a 3.10 relative risk of AMI,6 while overall patients with RA have a 63% greater 30-day cardiovascular (CV) mortality following first acute cardiovascular events than non-RA patients.7 Twice as likely to experience unrecognized AMI and sudden death, RA patients are also less likely to undergo coronary bypass grafting than non-RA subjects.8 Traditional atherosclerotic risk factors (hypertension, dyslipidemia, glucose intolerance/diabetes, smoking, dietary indiscretion, and physical inactivity) contribute to CVD in RA patients but do not fully explain these observations.8,9 After adjustment for these traditional factors, RA still affords a 3.17 relative risk for major CV events,9 clearly identifying an independent, additive risk afforded by RA itself. Prevention of CVD in RA patients is therefore an important challenge for primary care providers, cardiologists and rheumatologists alike.

METHODS KEY WORDS:

CARDIOVASCULAR DISEASE, RHEUMATOID ARTHRITIS, RISK FACTORS, TREATMENT, PREVENTION

AUTHOR INFORMATION: Dr. Suzanne Sanders is a staff rheumatologist and Assistant Chief of Medical Services at the G.V. (Sonny) Montgomery Veterans Affairs Medical Center and Assistant Professor of Medicine at the University of Mississippi School of Medicine, Jackson, MS. Dr. Stephen Geraci is Professor of Medicine in the Division of Pulmonary and Critical Care Medicine at the University of Mississippi School of Medicine, Jackson, MS. CORRESPONDING AUTHOR: Suzanne Sanders, MD, Medical Service (111), 1500 E. Woodrow Wilson Drive, Jackson, MS 39216. Email: Suzanne.Sanders@va.gov

This article reviews traditional and RA-associated risk factors for cardiovascular disease, interactions between the two diseases, and how treatments for either might benefit or adversely effect either condition. To that end, the authors searched the published literature by cross-referencing topics of cardiovascular disease, rheumatoid arthritis, cardiovascular disease risk factors (including hypertension, dyslipidemia, diabetes/glucose intolerance, smoking, diet, and physical inactivity), treatments for these risk factors, and treatments for rheumatoid arthritis with special attention to those clinical trials that are available. Papers published between 1983-2009 identified using PubMed and Medline search engines were reviewed. MARCH

2010 JOURNAL MSMA

TRADITIONAL RISK FACTORS AND TREATMENT Hypertension Up to 70% of RA patients have hypertension; of these, only 61% receive anti-hypertensive therapy (with fewer than 22% of these optimally controlled), while 39% remain undiagnosed.10 Under-diagnosis appears common in young RA patients, while the elderly are more likely to be under-treated.10 Singh and colleagues modeled the potential effect on cardiovascular event occurrence associated with increases in systolic blood pressure among osteoarthritis (OA) and RA patients using risk prediction models from the Framingham Heart Study and data from National Health and Nutrition Examination Survey (NHANES) III. Of the estimated 30 million adults in the U.S. aged ≥ 35 years with OA and RA, roughly 39% receive pharmacologic treatment for hypertension. The authors estimate that increases in systolic blood pressure of 1-5 mm Hg are associated with 7100 -35,700 additional ischemic heart and cerebrovascular events per year, while greater increases in systolic blood pressure (of 20 mm Hg, experienced by 15% of the study population) would result in 21,700 additional events annually.11 The mechanism of hypertension in RA may be multifactorial, but some anti-rheumatoid drugs likely contribute. Glucocorticoids have well-known mineralocorticoid actions including reduced sodium excretion which may elevate blood pressure.12 Prednisolone use appears independently associated with hypertension in RA patients, particularly with long-term exposure to medium-dose (≥ 7.5 mg) daily glucocorticoid therapy.10,13 Non-steroidal anti-inflammatory drugs (NSAIDs) may also have significant effects on blood pressure, most notably in established hypertensives already receiving treatment.14 They can also contribute to nephrotoxicity, particularly when given concurrently with angiotensin-converting enzyme inhibitors (ACEi) or angiotensin II receptor blockers (ARB).15,16 Other medications used to treat RA, such as leflunomide, may also contribute to hypertension.17 It is important to recognize hypertension in RA patients and treat it aggressively with dietary and lifestyle changes, avoidance/limitation of contributory medications, and early initiation of antihypertensive pharmacotherapy with active titration to goal. No good data suggest that deviation from Joint National Commission (JNC-7) guidelines is generally indicated.18 However, ACEi and ARBs reduce the concentrations of pro-inflammatory mediators and oxidative stress products in several inflammatory models19 and may have a theoretical advantage over other agents (although one human study showed no significant effects of quinapril on inflammatory markers in RA patients).20 In one small study, two-thirds of captopril-treated patients reported improved arthritis symptoms, while significant changes were noted in clinical and biochemical measurements (Ritchie articular index; C-Reactive Protein [CRP]).21 The data are conflicting regarding whether ACEi have a significant effect on endothelial function in RA patients.20,22 Whether ACEi or ARB are more effective in reducing hypertensive cardiovascular complications in RA patients has not yet been determined. Dyslipidemia Several studies suggest lipid abnormalities are prevalent in RA patients and correlate with disease activity,23,24,25 with up to 70% of inflammatory arthritis patients demonstrating clinical dyslipidemia.26 The

JOURNAL MSMA

MARCH

2010

most prevalent dyslipidemias in RA are low high-density lipoprotein (HDL) levels and elevated atherogenic index (total cholesterol/HDLcholesterol ratio).23,24,25 In selecting treatment strategies, some providers avoid reductase inhibitors (statins) in RA patients, believing drug-induced myopathy to be more frequent in, or that drug-induced muscle symptoms may confuse the clinical picture of, RA. However, a double-blind, randomized placebo-controlled trial in RA patients showed that a high potency statin (atorvastatin) was well tolerated with similar adverse event frequencies to those in placebo-treated controls.27 Statins improve lipid profiles27,28 and inflammation (including reduced disease activity and inflammatory markers such as CRP and erythrocyte sedimentation rate [ESR]) in RA.27,28 Effective drug treatment of RA itself can lead to improved lipid profiles.25,29 Despite the fact that glucocorticoids can worsen dyslipidemia,30,31 treatment of RA with methotrexate and prednisone (7.5 mg/day with tapering as tolerated) resulted in increased HDL concentrations and significant reductions in atherogenic indices.25 Other studies suggest hydroxychloroquine treatment of RA decreases serum triglycerides, total cholesterol and low density lipoprotein (LDL) concentrations,32 while increasing HDL levels.33 However, while antitumor necrosis factor (TNF) therapy may increase HDL levels in the short term,34,35 available data suggests it may lead to a more atherogenic lipid pattern over time.36 Diabetes/Glucose Intolerance Although no evidence of a strong relationship between RA and diabetes was noted in the NHANES III data of participants ≥ 60 years old,37 a recent study showed an association between type 1 diabetes and anti-cyclic citrullinated peptide-positive RA.38 Rheumatoid arthritis patients also have insulin resistance39 proportionate to the grade of inflammation40 and worsened by glucocorticoid treatment.41 The association between insulin resistance and atherosclerosis is well established and described elsewhere.42 Some medications used to treat RA can improve insulin sensitivity. Disease-modifying anti-rheumatic drug (DMARD) therapy, when combined with dietary modification, decreases insulin resistance by 36% within three months.43 Several studies of anti-TNF-α therapy have demonstrated reduced insulin resistance,44,45,46 though at least one paper failed to confirm this finding.47 The hazard ratio for incident diabetes among RA patients treated with hydroxychloroquine is 0.62 compared to those not treated with this drug, while the risk of diabetes abated with longer duration hydroxychloroquine use in one important study.48 Therefore, it is important to address not only frank diabetes but also those factors that contribute to decreased insulin sensitivity in RA patients. This should include limiting glucocorticoid exposure and treating inflammation. Smoking Smoking increases the risk of developing RA, particularly seropositive RA,49,50 and may also decrease the response of RA to certain medications.51 However, the degree to which smoking contributes to CVD risk in RA is controversial. While Chung and colleagues found

that smoking was associated with more severe coronary artery calcification in RA patients,52 another study concluded that smoking had a weaker relationship with cardiovascular events among RA subjects than among non-RA subjects.53 Smoking does appear to increase rheumatoid factor positivity, disease severity, and extra-articular RA manifestations (rheumatoid nodules, lung disease, and vasculitis).54,55,56 This is important because cardiovascular mortality appears higher in seropositive patients, and severe extra-articular manifestations are associated with an increased risk of CVD events.57,58 At this time, the data support an important, though complex, contribution of smoking to CVD and provides more than reasonable justification for aggressive smoking cessation intervention in RA patients.

be comparable to those in non-RA patients, and appropriate exercise should be regularly recommended.

RA-SPECIFIC RISK FACTORS AND THEIR MODULATION

Diet is linked directly to several cardiovascular risk factors including obesity, hypertension, and dyslipidemia. However, the data supporting any particular dietary treatment of RA are limited. While a few small studies have reported potential benefits from vegan or Mediterranean diets, most had too few (24-130) patients to support broad dietary recommendations.59,60,61 Fish oils (omega-3 fatty acids) have a beneficial anti-inflammatory effect in clinical trials in RA62 and may reduce the incidence of CVD63 and post-AMI mortality.64 Therefore, the best present evidence suggests that preventive cardiovascular diets consistent with American Heart Association guidelines, rich in omega-3 fatty acids, should be recommended to RA patients with or without CVD.

Glucocorticoids The cardiovascular impact of glucocorticoids in RA patients is somewhat controversial. As noted above, glucocorticoids reduce insulin sensitivity,41 may contribute to hypertension,10 and can promote unfavorable lipid profiles.30,31 Conversely, RA activity can worsen insulin resistance and contribute to dyslipidemia, suggesting anti-inflammatory glucocorticoids could have a net beneficial effect. In fact, one recent study suggested that prednisolone at 7.5mg daily did not influence endothelial function or atherosclerosis in patients with early RA.70 Another study, using a large linkage database and adjusting for covariates, defined the relative risk for cardiovascular events in patients receiving >7.5 mg prednisone daily as 2.56, while the relative risk (exclusive of congestive heart failure events) in patients receiving low dose prednisone was similar to that of steroid-naive patients.71 A population-based cohort study showed that rheumatoid factor (RF)-positive patients carry a greater risk of cardiovascular events with glucocorticoid exposure (particularly with higher cumulative dose, higher average daily dose, and recent use of glucocorticoids), but RF-negative patients suffered no such increase regardless of glucocorticoid dosage or timing of use.72 Therefore, limiting the dose and duration of steroid therapy, particularly in RF-positive patients, is the best, though incompletely, supported strategy.

Physical Inactivity Physical inactivity, in part due to its contribution to obesity, glucose intolerance, dyslipidemia, and hypertension, is another risk factor for CVD and particularly frequent in RA patients. Though providers and patients often believe these patients cannot exercise, recent studies suggest they can do so safely, with some rheumatoid symptoms improving as a result.65,66,67,68 A 21-week concurrent strength/endurance training protocol in women with early or long-standing RA resulted in significantly improved maximal strength, walking speed, vertical squat jump distance, and maximal aerobic capacity.66 Participation in a low-impact aerobic exercise program may also reduce fatigue, pain, and depression in RA patients.67 In a larger randomized, controlled, multicenter trial, investigators compared effectiveness and safety between a 2-year intensive exercise program and routine physical therapy. The intensive group showed greater improvement in functional ability and emotional status, while demonstrating no detrimental effects on disease activity or median radiographic damage of the large joints.68 However, subgroup analysis suggested that patients with extensive large joint damage may have accelerated joint destruction with high-intensity weight-bearing exercises and should avoid excessive loading of already damaged joints.69 Therefore, patients with mild to moderate RA can safely pursue moderate exercise programs, adjusting their regimen to avoid excessive loading of damaged large joints or aggressive physical activity during disease flairs. Although yet to be studied prospectively in RA patients, the cardiovascular benefits of exercise would be expected to

Non-steroidal Anti-inflammatory Drugs The contribution of NSAIDs to cardiovascular risk is also controversial. Rofecoxib, a cyclooxygenase (Cox) -2 inhibitor, was withdrawn from the market because of increased incidence of cardiovascular events during chronic administration.73 Presently, celecoxib is the only drug class member remaining on the U.S. market. The safety of Cox-1 inhibitors has similarly been questioned with Federal Drug Administration (FDA) warnings of increased CV risk added to all NSAID package inserts. Several studies have failed to clarify this issue. A meta-analysis of 18 randomized controlled trials showed a relative risk of AMI with rofecoxib use of 2.30 at the end of 2000 (2.24 one year later); there was little evidence that the relative risk differed with control group (placebo, non-naproxen NSAID, or naproxen) or trial duration.74 Another meta-analysis of 39 clinical trials including over 41,000 patients found the incident rates of combined cardiovascular events were not significantly different between patients treated with celecoxib and placebo, or between celecoxib and non-selective NSAIDs.75 A population-based case-control study concluded that current and new users of all available classes of non-aspirin NSAIDs were at higher risk for AMI.76 Conversely, a meta-analysis of case-control and cohort design observational studies showed a dose-related risk with rofecoxib and an elevated summary relative risk with diclofenac (a Cox-1 inhibitor) but no risk increase with celocoxib or the nonselective inhibitors, naproxen, piroxicam, or ibuprofen.77 Additionally, ex vivo platelet studies demonstrate inhibition of aspirinâ&#x20AC;&#x2122;s antiplatelet effect with ibuprofen (but not with rofecoxib, di-

Diet

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clofenac or acetaminophen), a finding of unproven clinical importance.78 Hence, the cardiovascular safety of any chronically administered NSAID is at best questionable. Providers should use caution in prescribing these medications to RA patients, particularly to those with other CV risk factors or those who require prophylactic aspirin. Aggressive RA, Extra-articular Disease, and Inflammation Studies strongly suggest that uncontrolled inflammation and aggressive RA with extra-articular manifestations are associated with an increased risk of CV events. Population-based data from the Rochester Epidemiology Project revealed that cardiovascular deaths were significantly more frequent among RA patients with ≥ 3 ESR values ≥ 60 mm/hour, RA vasculitis, or RA lung disease – suggesting that systemic inflammation confers additional risk for cardiovascular death despite controlling for traditional risk factors and co-morbidities.79 While smoking and ESR elevation are associated with more severe coronaryartery calcification in established RA patients,52 a larger number of swollen joints was a predictor of CV death in Pima Indians with RA.80 A prospective cohort study of male veterans age > 50 showed the RA Disease Activity Score (DAS) to be a significant predictor of major adverse cardiac events independent of traditional cardiovascular risk factors,81 while another study showed C-reactive protein (CRP) to be independently associated with microvascular dysfunction in RA patients.82 In addition, anti-cyclic citrullinated peptide antibodies, which predict poor clinical outcome and radiologic severity, are independently associated with the development of ischemic heart disease in RA patients.83 As noted previously, severe extra-articular disease manifestations also appear to be associated with an increased risk of first-ever cardiovascular events.58 Reducing inflammation with methotrexate or anti-TNF treatment may decrease cardiovascular risk, further supporting the role of systemic inflammation84,85 with methotrexate reducing cardiovascular deaths by 70% in one cohort study.86 In addition to decreasing CRP, TNF inhibitors may improve insulin sensitivity, HDL levels, and endothelial function in RA patients, explaining in part their potential benefits on cardiovascular risk.35,44,45,46,87,88 Although, at least one study suggests that azathioprine, cyclosporine, and leflunomide may be associated with increased CV risk,89 results from a multi-national crosssectional cohort study showed that prolonged use of treatments such as methotrexate, sulfasalazine, leflunomide, glucocorticoids, and TNF inhibitors appears to be associated with a reduced risk of CVD.90 Sum-

mary evidence suggests that patients with continued inflammation and progressive RA should be treated aggressively to help prevent CVD.

CONCLUSION Cardiovascular disease is excessive in RA patients, related to traditional and disease-specific risk factors. Aggressive treatment of traditional risk factors is indicated and may improve the RA itself. Glucocorticoids and NSAIDs should be used with caution, particularly as long-term therapy. Inflammation and progressive RA should also be treated aggressively to decrease CV risk with the current data most strongly supporting methotrexate therapy. Prospective, outcome-based studies are needed to define optimal treatment strategies to reduce cardiovascular morbidity and mortality in rheumatoid arthritis patients.

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Myllykangas-Luosujärvi RA, Aho K, Isomäki HA. Mortality in rheumatoid arthritis. Semin Arthritis Rheum. 1995;25:193-202. Wolfe F, Mitchell DM, Sibley JT, et al. The mortality of rheumatoid arthritis. Arthritis Rheum.1994;37:481-494. Wållberg-Jonsson S, Öhman M, Dahlqvist SR. Cardiovascular morbidity and mortality in patients with seropositive rheumatoid arthritis in northern Sweden. J Rheumatol. 1997;24:445-451. Turesson C, Jarenros A, Jacobsson L. Increased incidence of cardiovascular disease in patients with rheumatoid arthritis: results from a community based study. Ann Rheum Dis. 2004;63:952-955. Södergren A, Stegmayr B, Lundberg V, et al. Increased incidence of and impaired prognosis after acute myocardial infarction among patients with seropositive rheumatoid arthritis. Ann Rheum Dis. 2007;66:263266. Solomon DH, Karlson EW, Rimm EB, et al. Cardiovascular morbidity and mortality in women diagnosed with rheumatoid arthritis. Circulation. 2003;107:1303-1307. Van Doornum S, Brand C, King B, et al. Increased case fatality rates following a first acute cardiovascular event in patients with rheumatoid arthritis. Arthritis Rheum. 2006;54:2061-2068. Maradit-Kremers H, Crowson CS, Nicola PJ, et al. Increased unrecognized coronary heart disease and sudden deaths in rheumatoid arthritis. Arthritis Rheum. 2005;52:402-411. Del Rincón I, Williams K, Stern MP, et al. High incidence of cardiovascular events in a rheumatoid arthritis cohort not explained by traditional cardiac risk factors. Arthritis Rheum. 2001;44:2737-2745. Panoulas VF, Douglas KMJ, Milionis HJ, et al. Prevalence and associations of hypertension and its control in patients with rheumatoid arthritis. Rheumatology (Oxford). 2007;46:1477-1482. Singh G, Miller JD, Huse DM, et al. Consequences of increased systolic blood pressure in patients with osteoarthritis and rheumatoid arthritis. J Rheumatol. 2003;30:714-719. Jacobs JWG, Bijlsma JWJ. Kelley’s Textbook of Rheumatology, ed 7, Harris ED Jr, Budd RC, Firestein GS, et al (ed). Philadelphia, PA: Elsevier Saunders; 2005:859-876. Panoulas VF, Douglas KM, Stavropoulos-Kalinoglou A, et al. Longterm exposure to medium-dose glucocorticoid therapy associates with JACKSON OFFICE 401 East Capitol St., Suite 600, Jackson, MS 39201 Post Office Box 651, Jackson, MS 39205-0651 PH. 601.968.5500 FAX 601.968.5593

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arthritis correlate with a reduction in antibodies to food antigens. Rheumatology (Oxford). 2001;40:1175-1179. McKellar G, Morrison E, McEntegart A, et al. A pilot study of a Mediterranean-type diet intervention in female patients with rheumatoid arthritis living in areas of social deprivation in Glasgow. Ann Rheum Dis. 2007;66:1239-1243. Cleland LG, James MJ, Proudman SM. The role of fish oils in the treatment of rheumatoid arthritis. Drugs. 2003;63:845-853. Kris-Etherton PM, Harris WS, Appel LJ. Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation. 2002;106:2747-2757. Marchioli R, Barzi F, Bomba E, et al. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction. Circulation. 2002;105:1897-1903. Van den Ende CHM, Breedveld FC, le Cessie S, et al. Effect of intensive exercise on patients with active rheumatoid arthritis: a randomised clinical trial. Ann Rheum Dis. 2000;59:615-621. HĂ¤kkinen A, Hannonen P, Nyman K, et al. Effects of concurrent strength and endurance training in women with early or longstanding rheumatoid arthritis: comparison with healthy subjects. Arthritis Rheum. 2003;49:789-797. Neuberger GB, Aaronson LS, Gajewski B, et al. Predictors of exercise and effects of exercise on symptoms, function, aerobic fitness, and disease outcomes of rheumatoid arthritis. Arthritis Rheum. 2007;57:943-952. de Jong Z, Munneke M, Zwinderman AH, et al. Is a long-term highintensity exercise program effective and safe in patients with rheumatoid arthritis? Arthritis Rheum. 2003;48:2415-2424. Munneke M, de Jong Z, Zwinderman AK, et al. Effect of a highintensity weight-bearing exercise program on radiologic damage progression of the large joints in subgroups of patients with rheumatoid arthritis. Arthritis Rheum. 2005;53:410-417. HafstrĂśm I, Rohani M, Deneberg S, et al. Effects of low-dose prednisolone on endothelial function, atherosclerosis, and traditional risk factors for atherosclerosis in patients with rheumatoid arthritis â&#x20AC;&#x201C; a randomized study. J Rheumatol. 2007;34:1810-1816. Wei L, MacDonald TM, Walker BR. Taking glucocorticoid by prescription Is associated with subsequent cardiovascular disease. Ann Intern Med. 2004;141:764-770. Davis JM, Maradit Kremers H, Crowson CS, et al. Glucocorticoids and cardiovascular events in rheumatoid arthritis. Arthritis Rheum. 2007;56:820-830. U.S. Food and Drug Administration [homepage on the internet]. FDA News: FDA issues public health advisory on vioxx as its manufacturer voluntarily withdraws the product; 2004. http://www.fda.gov/bbs/topics/ news/ 2004/NEW01122.html accessed May 27, 2008. Juni P, Nartey L, Reichenbach S, et al. Risk of cardiovascular events and rofecoxib: cumulative meta-analysis. Lancet. 2004;364:2021-2029. White WB, West CR, Borer JS, et al. Risk of cardiovascular events in patients receiving celecoxib: a meta-analysis of randomized clinical trials. Am J Cardiol. 2007;99:91-98. Johnsen SP, Larsson H, Tarone RE, et al. Risk of hospitalization for myocardial infarction among users of rofecoxib, celecoxib, and other NSAIDs. Arch Intern Med. 2005;165:978-984. McGettigan P, Henry D. Cardiovascular risk and inhibition of cyclooxygenase. JAMA. 2006;296:1633-1644. Catella-Lawson F, Reilly MP, Kapoor SC, et al. Cyclooxygenase inhibitors and the antiplatelet effects of aspirin. N Engl J Med. 2001;345:1809-1817. Maradit-Kremers H, Nicola PJ, Crowson CS, et al. Cardiovascular death in rheumatoid arthritis. Arthritis Rheum. 2005;52:722-732. Jacobsson LTH, Turesson C, Hanson RL, et al. Joint swelling as a predictor of death from cardiovascular disease in a population study of Pima Indians. Arthritis Rheum. 2001;44:1170-1176. Banerjee S, Compton AP, Hooker RS, et al. Cardiovascular outcomes in male veterans with rheumatoid arthritis. Am. J. Cardiol. 2008;101:1201-1205. Galarraga B, Khan F, Kumar P, et al. C-reactive protein: the underlying cause of microvascular dysfunction in rheumatoid arthritis. Rheumatology (Oxford). 2008;47:1780-1784. LĂłpez-Longo FJ, Oliver-MiĂąarro D, de la Torre I, et al. Association between anti-cyclic citrullinated peptide antibodies and ischemic heart

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disease in patients with rheumatoid arthritis. Arthritis Rheum. 2009;61:419-424. Van Halm VP, Nurmohamed MT, Twisk JWR, et al. Disease-modifying antirheumatic drugs are associated with a reduced risk for cardiovascular disease in patients with rheumatoid arthritis: a case control study. Arthritis Res Ther [serial on the internet]. 2006 Sep [cited 2008 May 28];8(5):R151 [about 8 p.]. Web site: http://arthritisresearch.com/content/8/5/R151. Jacobsson LT, Turesson C, Gulfe A, et al. Treatment with tumor necrosis factor blockers is associated with a lower incidence of first cardiovascular events in patients with rheumatoid arthritis. J Rheumatol. 2005;32:1213-1218. Choi HK, HernĂĄn MA, Seeger JD, et al. Methotrexate and mortality in patients with rheumatoid arthritis: a prospective study. Lancet. 2002;359:1173-1177. Cardillo C, Schinzari F, Mores N, et al. Intravascular tumor necrosis factor alpha blockade reverses endothelial dysfunction in rheumatoid arthritis. Clin Pharmacol Ther. 2006;80:275-281. Bilsborough W, Keen H, Taylor A, et al. Anti-tumour necrosis factoralpha therapy over conventional therapy improves endothelial function in adults with rheumatoid arthritis. Rheumatol Int. 2006;26:1125-1131. Solomon DH, Avorn J, Katz JN, et al. Immunosuppressive medications and hospitalization for cardiovascular events in patients with rheumatoid arthritis. Arthritis Rheum. 2006;54:3790-3798. Naranjo A, Sokka T, Descalzo MA, et al. Cardiovascular disease in patients with rheumatoid arthritis: results from the QUEST-RA study. Arthritis Res Ther. 2008;10(2):R30. Epub 2008 March 6.

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2010

• CLINICAL PROBLEM-SOLVING • Presented and edited by the Department of Family Medicine, University of Mississippi Medical Center, Diane K. Beebe, MD, Chair

Pseudo Seizures Vs Pseudo Zebra D. Mark Pogue, MD; Judith G. Gearhart, MD and George Moll, Jr., MD, PhD

n 11-year-old African American male presented to Emergency Department (ED) via ambulance with complaint of seizure. He reported being unaccompanied during the seizure described as loss of consciousness for about a minute. History of present illness revealed this was his “second seizure at school.” Review of systems was negative. The ED physician noted vital signs and physical examination normal for age with the exception of slurred speech. The patient’s Glasgow Coma Scale was normal at 15, and he was able to follow 3-step commands. A basic metabolic panel was collected on presentation. His cardiac rhythm strip and bedside glucose were normal. The basic metabolic panel was normal with the exception of a low serum calcium of 6.0 mg/dL (reference range 8.4-10.2). The ED physician’s impression was possible seizure disorder and hypocalcemia. The patient was stable, and family medicine was consulted for admission. Causes of hypocalcemia are numerous (Figure 1) in an 11-yearold male with possible seizures.1 I worry about tetany and risk of laryngospasm secondary to hypocalcemia as the likely cause of the patient’s “seizure” episodes. Serum prolactin (PRL) concentrations can be informative, as elevated PRL can reflect mid-brain lesions and be elevated for up to 6 hours after a seizure.2 Family medicine’s initial patient interview was performed 5 hours after his ED presentation. The patient was a poor historian and was noted to have a flat affect. The patient reported he was alone in the restroom at school, became dizzy and awoke on the floor. He admitted to loss of consciousness but was unsure how long it lasted. The patient remembered “seeing” objects and friends from his old school just before “passing out.” He had no bowel or bladder incontinence, muscle jerking, weakness or numbness. He denied confusion following the event. The patient’s mother revealed he had experienced a similar episode requiring pediatric ED treatment near their home several weeks ago. She stated, “A scan was negative for seizures.” When asked about her son’s flat affect and slurred speech, his mother was adamant he was at his baseline. The family history was negative for seizures. Remainder of medical his-

AUTHOR INFORMATION: D. Mark Pogue, MD†, Family Medicine Resident and George Moll, Jr., MD, PhD, Professor Pediatrics and Chief Pediatric Endocrinology, University of Mississippi Medical Center. CORRESPONDING AUTHOR: Judith G. Gearhart, MD, Professor of Family Medicine, University of Mississippi Medical Center, 2500 North State St., Jackson, MS 39216

FIGURE 1: HYPOCALCEMIA – DIAGNOSTIC PATHWAYS Low Serum Calcium – Confirmed with ionized Calcium and/or serum protein concentrations High Creatinine/BUN Renal Failure

High Serum Phosphorous

Low/Normal Serum Phosphorous

Low Urine

High Urine

Phosphorous

Calcium

Low Urine Calcium Functional PTH Deficiency deficiency Normal Alkaline Phosphatase Phosphatase (normal for bone/age) No Clinical Rickets Low PTH or High PTH Inappropriate “Normal” PTH Severe HypoMagnesemia Calcium (<1.0 mg/dL) Sequestration

Functional Vit D Elevated Alkaline (normal for bone/age) Clinical Rickets

High PTH

Activating Calcium Receptor Mutations (High urine

High PTH

Excessive Phosphorous Load -

RTA Vit. D deficiency

Tumor Lysis,

Calcium)

Excessive

High PTH

Vit. D resistance VDDR types 1,2

“Hungry Phosphorous Bone Intake Syndrome” Hypo-PTH Transient, Familial, Autoimmune, 2nd to metabolic disease

PTH Resistance PHP

Malabsorption Liver Disease Drugs

PHP – Diagnostic Pathways PTH TEST: determine PTH stimulated plasma or urinary cAMP, TmP/GFR PHP type 2 – cAMP equivocal or normal, TmP/GFR decreased PHP type 1 – cAMP decreased, then erythrocyte Gs decreased (PHP 1A) or normal (PHP 1B) Abbreviations: BUN=blood urea nitrogen, PTH=Intact Parathyroid Hormone, Vit. D=Vitamin D analogues as primarily 25OH-VitaminD (calcifediol), RTA=renal tubular acidosis, VDDR=Vit. D dependent rickets, PHP=pseudohypoparathyroidism, cAMP=cyclic Adenosine MonoPhosphate, TmP/GFR=quotient maximum rate of tubular phaophate reabsorption and glomerular filtration, Gs =guanine nucleotide stimulating regulatory intra-membrane multi-subunit protein

tory was noncontributory. The social history was negative for abuse. He was in 6th grade with declining grades. The history is the most important tool for diagnosing syncope; however, our patient is a poor historian. For loss of consciousness in this age group, I would be concerned with neurocardiogenic syncope.3 This is the most common type of syncope with typical age of onset 12 years in boys and often confused with epilepsy.4 Thirty to fifty percent of children are estimated to have at least one episode of syncope by MARCH

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†Dr. Pogue died February 11, 2009.

Mark Pogue, MD Sketch by Judith G. Gearhart, MD

Dr. Mark Pogue attended elementary school in Columbus, MS. He was an Eagle Scout at age 15. After graduation from Neshoba Central High School in Philadelphia in 1990, Mark had several occupations. He was a mechanic, factory worker and in construction before he decided to pursue the medical field. Dr. Pogue started as a phlebotomist, as he worked his way through lab school. Dr. Pogue graduated from Meridian Community College with a degree in Laboratory Medicine in 1995. He worked in the lab until he decided to venture into physician practice management and recruitment. He worked at Neshoba County General Hospital as Director of Physician Services until he enrolled in medical school in 2002. Dr. Pogue’s dream of becoming a doctor took him to the Caribbean, then England where he graduated from St. Christopher’s College of Medicine in 2005. Dr. Pogue served his fourth year medical school training at Emory University, and Johns Hopkins and Habor Hospital in Baltimore, MD. Dr. Pogue entered residency training in the Department of Family Medicine at the University of Mississippi Medical Center in 2006. At UMMC, Dr. Pogue was awarded the “Gary W. Jefcoats” teaching award for residents who exemplify outstanding teaching characteristics in the areas of medical student, resident, and patient education. Upon completion of his residency in 2009, Dr. Pogue planned to practice family medicine in rural Dewitt, Arkansas. Dr. Pogue was an extraordinary person who touched the lives of everyone he met; he is deeply missed.

adolescence, accounting for only about 1% of pediatric ED visits. Though most are benign, neurologic imaging in the ED should be considered.5 On physical examination the patient had temperature, pulse and blood pressure normal for age. His tongue protruded in midline without lesions. He had normal cardiac, pulmonary, abdomen and musculoskeletal examinations. His neurologic examination revealed intact cranial nerves and reflexes. Chvostek and Trousseau’s signs were negative. Slurred speech and flat affect were noted. Test results from his ED visit 6 weeks ago revealed normal blood glucose, negative urine drug screen and normal computed tomography (CT) of the head. An electroencephalogram (EEG) was scheduled in 2 weeks. The normal CT from 6 weeks earlier is reassuring and not indicative of acute hemorrhage or stroke though a head magnetic resonance imaging (MRI) + contrast would better assess brain development concerns and neither modality rules out seizures. EEG might reveal a seizure disorder. The patient may have experienced pseudoseizures, conversion disorder symptoms;6 however, he has documented hypocalcemia. A repeat serum calcium concentration was 5.8 mg/dL. His serum albumin and magnesium concentrations were within normal limits. An electrocardiogram (EKG) indicated borderline prolonged QT interval. The patient’s prolonged QT interval is typical of hypocalcemia.8 Major symptoms noted at his two ED visits are fatigue, slurred speech and flat affect. Absence of Chvostek and Trousseau’s signs suggest a chronic condition; however, acute versus chronic hypocalcemia cannot be determined as he has no prior serum calcium determinations for comparison.7 Calcium replacement should immediately be instituted. A 12 lead EKG is most important for recurrent syncope assessment and for monitoring management of severe hypocalcemia.3,8 The patient was administered oral calcium carbonate 1000

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mg (400 mg elemental calcium) about 8 hours apart by mouth and slow infusion of 10 mL 10% calcium gluconate (100 mg elemental calcium) in 500 mL 0.45% sodium chloride (1/2 normal saline) as recommended by endocrine consult to achieve 50 to 75 mg elemental calcium per kilogram body weight per day. I am concerned about risk for tetany and laryngospasm. Patient serum from his ED presentation is unavailable for additional tests such as PRL. The patient’s normal serum magnesium and albumin exclude hypomagnesemia or hypoalbuminemia as contributors to his hypocalcemia. His normal blood urea nitrogen, creatinine, potassium and electrolyte balance do not support renal failure or hypokalemia to promote decreased serum calcium. Simultaneously obtained serum intact parathyroid hormone (PTH), vitamin D, calcium and phosphorous would help narrow the broad differential for hypocalcemia by delineating PTH related disorders. A thyroid stimulating hormone (TSH) can also help delineate specific PTH response deficiency such as pseudohypoparathyroidism (PHP) type 1b or 2 from general peptide hormone receptor response deficiencies such as PHP type 1a and type 1c.1 More laboratory values became available. The patient’s intact PTH was 297 pg/mL (reference 15-65 for normal range serum calcium). The post infusion serum ionized calcium was still critically low at 3.50 mg/dL (reference 4.8-5.3). The patient’s serum PRL 31.1 ng/mL (reference 2.7-17.7) was elevated. His serum phosphorous was 5.2 mg/dL (reference 3.0-6.8 with normal serum calcium). His TSH was normal for age. Intravenous and oral infusions of calcium to achieve daily maintenance (50 mg elemental calcium per kilogram body weight per day) should raise serum calcium for up to 3 hours.7 Our patient’s serum calcium declines rapidly 1 hour after his initial calcium gluconate infusion that may reflect relative hyperphosphatemia with chronic calcium and vitamin D deficiencies. Our patient’s lack of anticipated response to his elevated intact PTH also supports target organ resistance as seen in

patients with PHP who would have at least relative hyperphosphatemia. Deficiencies in vitamin D active metabolites (e.g., decreased intake or production) can contribute to hypocalcemia and elevated PTH. Such secondary hyperparathyroidism is characteristically associated with low serum phosphate unless countered by PTH resistance as in PHP patients. Vitamin D (25-Hydroxy- and 1,25-diHydroxy-) would help to identify vitamin D deficiency and distinguish it from rare forms of vitamin D dependent rickets (VDDR type 1 or 2) that can be expressed from infancy to adolescence and typically support normal serum phosphate. Head MRI + contrast and EEG should assist exclusion of central nervous system (CNS) anomalies contributing to seizures. My impression is secondary hyperparathyroidism due to hypocalcemia likely encouraged by preexisting vitamin D deficiency and poor calcium intake resulting in neuromuscular irritability in a patient with the rare occurrence of PHP. These diagnoses can be clarified by focused medical history, record review and physical examination. Although the patient reported he was alone, the ambulance report listed a teacher as a witness. According to the teacher, “he stiffened and then started shaking for less than a minute” as she helped patient to floor to prevent injury. No further seizure activity was reported. The patient again related he did not like his new school. The patient admitted to disliking milk that, according to his mother, started at age 4 when sour milk made him sick. Despite an average size mother, our 11 year-old patient was as tall as an average 14 year-old male. The patient admitted to tiring faster than other kids his age and denied diarrhea or change in bowel habits with fatty foods. Poor dentition was noted along the lower mandible. The musculoskeletal examination did not demonstrate limb weakness, varus or valgus deformity, but his Achilles reflexes were noted delayed bilaterally. His milk aversion and poor dentition suggest vitamin D deficiency. Hypocalcemia due to dietary vitamin D deficiency is more common in African Americans as their increased skin melanin can decrease vitamin D production from ultraviolet light exposure. Although there are exceptions to short stature with PHP, our patient’s tall stature is inconsistent with the majority of PHP. The absence of diarrhea, erratic bowel patterns or hypoproteinemia makes malabsorption an unlikely contributor to our patient’s hypocalcemia. I will obtain fasting metabolic panel with blood counts to assess general medical status, consider anemia and sepsis and follow his serum calcium response to therapy. The results of his EEG and head MRI should assist consideration of seizures.9 On hospitalization day 2, the serum calcium concentration increased to 6.2 mg/dL following additional infusions of calcium gluconate with 3000 mg oral calcium carbonate (about 30-50 mg/kilogram body weight per 24 h). The oral regimen was changed to a combination of calcium citrate and vitamin D to supply 1200 mg elemental calcium and 800 units vitamin D per day. Two additional infusions of 20 mL calcium gluconate were ordered to be given 6 hours apart. The serum alkaline phosphatase was elevated 608 U/L (reference 9-15 year-old 60-285 U/L). His uric acid, albumin and liver function results were within normal limits for age. His physical examination was unchanged with no further seizure

activity. The patient and his mother denied recent medication or drug ingestion, use of fluoride supplements or fungal treatments. The history and laboratory test results eliminate many causes of hypocalcemia. His elevated serum alkaline phosphatase is seen with any metabolically active bone condition including secondary hyperparathyroid, PHP in the presence of vitamin D deficiency or the rare VDDR subtypes as well as normal childhood and adolescent bone growth. An MRI of the brain was read as within normal limits. The EEG showed slowing activity with small burst spikes in the right central region. The neurologist’s interpretation was pending. The EEG pattern typical of hypocalcemia may demonstrate generalized slowing with bursts of spiking activity.9 Pseudoseizures are psychogenically stimulated epileptic attacks without central nervous system dysfunction noted in EEG. Our patient’s signs and symptoms are inconsistent with pseudoseizures.6 His hypocalcemia is real yet his serum calcium is not rapidly responsive to appropriate therapy. Acute hypocalcemia should show a rapid response; chronic hypocalcemia is more resistant to replacement therapy. I believe his dietary deficiency in both calcium and vitamin D contributes to his sluggish response to therapy. Vitamin D metabolites would be helpful to his diagnosis. On hospitalization day 3, the patient’s calcium increased only 0.6 mg/dL to 6.8 mg/dL despite multiple additional infusions and oral supplementation. His nurse noted he had difficulty taking oral medications, and his mother reported he nearly always found it difficult to swallow pills even when crushed in applesauce. The patient is not consuming enough oral vitamin D and calcium due to his difficulty swallowing pills. I will prescribe calcitriol (Rocaltrol) as the preferred preparation for relatively rapid vitamin D activity within 36 hours of ingestion.10 I will consult speech pathology for swallowing study. Speech therapists noted normal swallow but also a flat affect with their impression of “almost Asperger’s like behavior” and recommended additional developmental testing. His mother again considered his behavior baseline. The patient was scheduled for follow-up with pediatric neurology and endocrinology and Child Development Center assessment. The neurologist read his EEG to be abnormal, showing few episodes of spike discharges from the right central region, possibly associated with benign rolandic epilepsy but correlation with medical history was recommended. Requested medical records documented new onset seizures 6 weeks prior to presentation with clonic activity for about 1 minute, dull affect, dilated pupils and small contusion on left lateral aspect of tongue. The patient and caretakers were given seizure precaution literature and instructions to schedule repeat EEG. The patient’s serum calcium was improving with his acceptance of therapy assisted by liquid calcitriol 0.25 mcg TID, calcium carbonate suspension 1875 mg divided TID and a chewable multi-vitamin added to a regimen of oxcarbazepine (Trileptial) at 10 mg/kg BID. A pediatric general clinic report from 7 years prior to this ED presentation indicated normal serum calcium concentration 9.8 mg/dL. Our patient’s history with lack of familial seizure disorder is consistent with tetany induced seizures rather than rolandic epilepsy. NorMARCH

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mal serum calcium 7 years prior to this hospitalization is also consistent with an acquired rather than a congenital cause. The inherited defect of PHP type 2 is not known and some cases are considered acquired with severe vitamin D deficiency. Our patient’s pending vitamin D analogues should help to distinguish among vitamin D related disorders with or without PHP.11 On day 4 the calcium concentration was stable near 7 mg/dL. The nurse noted hemiballismus when he awoke but he denied seizures over night. He admitted to cramps in his proximal lower extremities when exposed to cold environments. His mother now reported a decline in her son’s mental status and poor grades for approximately 6 months. Changes in dentition had occurred over the past year. A focused neurologic examination revealed horizontal nystagmus and chorea symptoms. A funduscopic examination revealed bilateral papilledema. Our patient’s profound hypocalcemia is responding slowly to supplementation with calcitriol and high dose calcium carbonate. Despite weight-based oxcarbazepine, neuromuscular excitability persists. Cognitive deficits, neuropsychiatric abnormalities and extra-pyramidal symptoms resembling chorea are associated with calcification of basal ganglia, which occurs in all forms of hypoparathyroidism with chronic hypocalcemia. Although our patient’s brain CT from 6 weeks ago does not show such calcifications, his history with decline in mentation and development of dental abnormalities over the past 6 months supports the development of his hypocalcemia over at least this 6month interval. A rare target organ (kidney) resistance to vitamin D can cause hypercalcuria despite hypocalcemia.12,13 This may contribute to our patient’s slow recovery from hypocalcemia. VDDR type 1 is characterized by target organ resistance due to vitamin D receptor defect. VDDR usually presents in children under age 3 years but some present in adolescents. VDDR is associated with elevated alkaline phosphatase but should cause hypophosphatemia. Spot urinary calcium and assessment of patient’s calcium and phosphate reabsorption capability should assist consideration of VDDR.14 I will again consult pediatric endocrinology to review therapy. On day 5 of hospitalization, his serum calcium declined to 6.1 mg/dL and phosphorous increased to 6.7 mg/dL. The patient had received a total of 15,125 mg calcium orally and 60 cc of calcium gluconate infusion since admission. His spot urinary calcium post infusion was minimal at 2 mg/dL, and his post infusion serum calcium concentration increased to 7.1 mg/dL. The parents were anxious for the patient to be discharged, but the pediatric endocrinologist agreed with therapy and recommended not discharging the patient until stable serum calcium concentration greater than 7.0 mg/dL. The parents want to take their child home as they think he can continue oral therapy at home. However, their son must be monitored in hospital for his anticipated response to long-term oral therapy. Serum phosphate concentration may also increase with calcitriol supplementation as it acts upon the kidney to reabsorb phosphate in the renal tubule. Serum phosphorus would not increase after supplementation in a patient with calcitriol receptor defect such as with VDDR. Because

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this patient’s phosphorous is increasing, vitamin D deficiency with secondary hyperparathyroidism in the presence of PHP is more likely than VDDR. Hyperparathyroidism has an inhibitory effect on phosphate reabsorption in the renal tubule; therefore, the patient’s elevated phosphorus concentration reflects a resistance to PTH within his kidneys as expected with PHP. In PHP, serum phosphate concentrations may rise as high as 8 mg/dL owing to loss of aforementioned inhibitory effect of PTH.14 Our patient’s response is consistent with PHP type 2 at this point. In PHP type 2, PTH infusions usually increase urinary and serum cyclic adenosine monophosphate; however, PTH does not elicit a phosphaturic response. I will discuss the option of infusing exogenous PTH to diagnose PHP. These test results have long turnaround times and should await serum calcium normalization. On day 6, the patient’s calcium dropped to 6.1 mg/dL. The parents declined PTH infusion testing as they desired discharge and were leery of exogenous hormone. The patient’s vitamin D analogues returned very low total 25OH-vitamin D (calcifediol) <4 (20100ng/mL), 25OH-vitamin D2 <4 (20-100 ng/mL), 25OH-vitamin D3 <4 (11-71 ng/mL) and 1,25diOH-vitamin D (calcitriol) 83 pg/mL (27-71 pg/mL). Reference laboratory results are consistent with severe vitamin D deficiency. The patient’s undetectable calcifediol likely represents the lack of sunlight-produced and dietary vitamin D that is converted to calcifediol as the 25OH-vitamin D storage pool from which the body produces active 1,25diOH-vitamin D or calcitriol. The results are consistent with our patient’s dietary history and decreased sun exposure. Undetectable calcifediol is uncommon; secondary hyperparathyroidism and hypophosphatemia occur with calcifediol below 15 ng/dL. The low serum calcifediol excludes VDDR type 1 which typically is associated with normal to high calcifediol. In VDDR type 2, one typically would expect extremely high concentrations of calcitriol with a normal concentration of calcifediol and loss of urinary calcium. The high serum calcitriol concentration is expected as PTH stimulates production of calcitriol in the kidneys. The normal and rising serum phosphate concentrations may be due to a renal resistance to PTH as seen in PHP type 2. Some authors suggest PHP type 2 is a manifestation of vitamin D deficiency rather than a distinct entity, implying prolonged vitamin D deficiency can induce the acquired defect responsible for PHP type 2.14 Repeat intact PTH and serum phosphate, elevated despite correction of vitamin D and calcium, are consistent with PHP. On day 7 the parents wanted to leave regardless of serum calcium concentration. A compromise was reached with his parents to complete one more calcium infusion and a 24-hour urine calcium assessment prior to his discharge with attention to his appointment with endocrinologist in only 2 days. An additional 30 cc’s of calcium gluconate was infused. The serum calcium concentration rose to 7.0 mg/dL, and our patient was discharged home in guarded condition. He was instructed to continue calcium carbonate suspension, calcitriol and oxcarbazepine with once daily adult or teen vitamin. The discharge diagnoses were profound vitamin D deficiency with PHP type 2 variant and seizure disorder. His 24hour urine calcium was low at 17 mg/24 hours (100-300 mg).

I am extremely uncomfortable with the patient leaving the hospital. If I allow the parents to sign him out against medical advice, the patient will not receive the additional infusion needed because his calcium is much lower than the recommended 7.0 mg/dL or greater. Pediatric endocrinology confirms his follow-up appointment. The decreased 24-hour urine calcium excretion reaffirms the patient is retaining urinary calcium and does not support VDDR type 2. The pediatric endocrinologistâ&#x20AC;&#x2122;s clinic note 3 days later indicated therapeutic improvements with serum calcium, phosphorus and intact PTH concentrations of 7.4 mg/dL, 7.2 mg/dL and 393.0 pg/mL, respectively. Serum thyroid stimulating hormone, magnesium and glucose concentrations were all normal. The parents were counseled on lifelong compliance to reduce his risks for life threatening hypocalcemia. The patient was continued on current liquid medicines at adjusted doses to achieve therapeutic goals. The patient was to follow up in 1 month with the endocrinologist. Subsequent laboratory analysis revealed improving 25OH-vitamin D and normal calcium, 17 ng/mL and 9.7 mg/dL, respectively. Oxcarbazepine was discontinued, and seizure activity ceased with normalization of serum calcium. The patientâ&#x20AC;&#x2122;s affect, mentation and grades have improved substantially. Both PHP and vitamin D deficiency are to be considered less likely due to the misleading normal serum phosphate concentration that subsequently increased in our patient. His normal phosphorus can be explained by the concomitant profound vitamin D deficiency and presence of PHP that is proposed to develop with prolonged vitamin D deficiency. The resistance to PTH found in PHP type 2 results in hyperphosphatemia. However, our patientâ&#x20AC;&#x2122;s elevated calcitriol prior to exogenous treatment indicates a normal renal 1alpha-hydroxylase reaction response to elevated PTH. Once replacement occurred via calcitriol and calcium supplementation, the patientâ&#x20AC;&#x2122;s phosphorus transiently increased in a pattern consistent with PHP. PHP type1B is unlikely without the classic phenotype characteristics and youthful age of onset with an inherited pattern. PTH regulation of growth factor production by bone cells can promote our patients tall stature, but PHP type 2 effects reduce bone mineralization.14,15

KEY WORDS:

DIAGNOSIS, SYNCOPE, HYPOCALCEMIA, VITAMIN D DEFICIENCY, PSEUDOHYPOPARATHYROIDISM

6. 7. 8.

9. 10. 11. 12. 13.

14.

15.

Gordon TA, Moodie DS, Passalacqua M, et al. A retrospective analysis of the cost-effective workup of syncope in children. Cleve Clin J Med. 1987;54:391â&#x20AC;&#x201C;394. Harden CL. Pseudoseizures and dissociative disorders: a common mechanism involving traumatic experiences. Seizure. 1997;6:151â&#x20AC;&#x201C;155. Tohme JF, Bilezikian JP. Hypocalcemic emergencies. Endocrinol Metab Clin North Am. 1993;22:363-375. Desai TK, Carlson RW, Geheb MA. Prevalence and clinical implications of hypocalcemia in acutely ill patients in a medical intensive care setting. Am J Med. 1988;84:209-214. Swash M, Rowan AJ. Electroencephalographic criteria of hypocalcemia and hypercalcemia. Arch Neurol. 1972;26:218-228. Gupta MM. Medical emergencies associated with disorders of calcium homeostasis. J Assoc Physicians India. 1989;37:629-631. Becker KL. Calcium and Bone Metabolism Principles and Practice of Endocrinology and Metabolism, 2nd ed. JB Lippincott, 1995.pp.452 Kumar R. Vitamin D and calcium transport. Kidney Int. 1991;40:11771189. Slatopolsky, E; Robson, AM; Elkan, I; Bricker, NS. Control of phosphate excretion in uremic man. J Clin Invest. 1968 Aug;47(8): 1865â&#x20AC;&#x201C;1874. Murer H, Lotscher M, Kaissling B, Levi M, Kempson SA, Biber J. Renal brush border membrane Na/Pi-cotransport: molecular aspects in PTH-dependent and dietary regulation. Kidney Int. 1996 Jun;49(6): 1769-1773. Abugassa S, Nordenstrom J, Eriksson S, Sjoden G. Bone mineral density in patients with chronic hypoparathyroidism. J Clin Endocrinol Metab. 1993;76:1617-1621.

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Acknowledgment: We are grateful to William Nicholas, MD, for review of this manuscript.

REFERENCES 1.

3. 4.

Diaz R. Calcium Disorders in Children and Adolescents. In: Pediatric Endocrinology, 5th edition, Section IV: Disorders of Calcium and Mineral Metabolism. Lifshitz F (Ed), Informa Healthcare, New York 2009; pp.475-495 Chen DK, So YT, Fisher RS. Use of serum prolactin in diagnosing epileptic seizures: Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology, Sep 2005;65:668-675. McLeod KA. Syncope in children. Arch Dis Child. 2003;88:350-353. Boehm KE, Morris EJ, Kip KT, Karas B, Grubb BP. Diagnosis and management of neurally mediated syncope and related conditions in adolescents. J Adolesc Health. 2001;28:2-9.

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MARCH

2010 JOURNAL MSMA

Wishing You A

Happy Doctorsâ&#x20AC;&#x2122; Day March 30, 2010

For all you do and all the ways you care, for your endless hours of concern and compassion, for your perseverance to do what is best, you are making a difference in the lives of others. From your Mississippi State Medical Association Alliance Board Rachel Aultman Gelinda Barrett Rachel Becker Kathy Carmichael Peggy Crawford

JOURNAL MSMA

Connie Derhgawen Kathy Fletcher Amy Gammel Shoba Gaymes Cathy Gersh

MARCH

2010

Jean Hill Danita Horne Angela Ladner Louise Lampton Nancy Leader

Nancy Lindstrom Brinda ManiSundaram Eileene McRae Melanie Moore Karen Morris

Jeanne Morrison Sondra Pinson Mollie Pontius Brenda Sumrall Smith Donna Witty

• PRESIDENT’S PAGE •

Pigs Have Already Flown he old saying applies, “I never thought I would live long enough to see it.” As I pen this President’s Page, I am sitting in Bovina, Mississippi surrounded by 6 inches of freshly fallen snow. I am, however, being warmed by the earthshaking events of the past several weeks. Walk backward with me down memory lane as we relive the first 6 weeks of 2010. First, on January 7, 2010, my children's alma mater, the University of Alabama, went from an average team in the S.E.C. to national champions by defeating the University of Texas in the B.C.S. title game in Pasadena, California. My, what a difference three short years and a lot of money in a coach’s banking account can make. Secondly, just as the Democrats were poised to inflict their final blow on health system reform, the increasingly unpopular Obama Care was brought to its knees by a near fatal slap in the face by the election of moderate Republican Scott Brown to the

RANDY EASTERLING, MD 2009-10 MSMA PRESIDENT

sacred “Kennedy Seat” in the United States Senate. And just when you thought it was safe to go back in the water, the earth was shaken on her very axis when the Saints not only made it to the Super Bowl but won! This was a victory of immeasurable proportions to those of us in the “Who Dat” nation who have struggled through 44 seasons hand-in-hand with our beloved “Aints.” The Super Bowl victory was particularly sweet for me as I was one of the 83,000 fans who attended the first Saints game ever in September 1967 in the old Sugar Bowl stadium in New Orleans, Louisiana. I will never forget the first play of the Saints franchise: the old Los Angeles Rams kicked off, and John Gilliam caught the ball on the 1-yard line and ran it back 100-yards for a touchdown. The ensuing 44 years were not nearly as promising. Finally, to top off the first six weeks of 2010, a recent snow storm blanketed almost every corner of Mississippi. Stick a fork in me; I am done! Pigs have flown and hell has frozen over! I repeat, who would have ever thought they would have lived long enough to see the events of the past six weeks? While football games and snow storms in Mississippi are certainly noteworthy and a whole lot of fun, neither has the lasting effect on what you and I do everyday like the special election to the United States Senate seat in Massachusetts. Let’s take a moment to put the election in historical perspective. John F. Kennedy was elected to the United States House of Representatives from Massachusetts in 1946. He held that seat until 1952 when he defeated the Republican U.S. Senator Henry Cabot Lodge, Jr. (Lodge would become Nixon’s vice presidential running mate in 1960). At age 35, John Kennedy became one of the younger individuals to ever be seated as a United States Senator. Staking claim to this previously held Republican seat, Kennedy served in the United States Senate until resigning in December 1960 shortly after defeating Vice President Richard Nixon for the presidency. Kennedy then recommended to the governor of Massachusetts that he appoint a close Kennedy family friend, Benjamin A. Smith, II, as a seat warmer until his younger brother Teddy was old enough to run for the United States Senate (the constitution requires that senators be 30-years-old). After what I am sure was a healthy donation from father Joe Kennedy to his campaign war chest, the Governor of Massachusetts agreed. Benjamin Smith was United States Senator from Massachusetts for less than two years until Ted was elected in a special election in November 1962 and sworn in shortly thereafter. An interesting caveat, Teddy was even younger than his older brother John was when he ascended to the United States Senate, having just reached the ripe old age of 30. However, neither was as young as now Vice President Joe Biden who was elected to the United States Senate from Delaware at age 29. He did, however, turn 30 several weeks after his election, thus fulfilling the constitutional requirement by the time he was sworn in to office. I am sure you have done the math by now. At the time of Ted Kennedy’s passing in 2009, with the exception of the 22-month stint of Kennedy confidant Benjamin Smith, there has been a Kennedy in the United States Congress for 63 years straight. MARCH

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While President Kennedy might be considered by most a moderate Democrat, there is no question in anyone’s mind that Ted Kennedy set the bar for left wing liberals in the United States Senate for 47 years. Political pundits will cuss and discuss the United States Senate special election in Massachusetts for years to come. I think we all will agree that the fundamental significance of this election was not that the Democrats no longer have a coveted 60 vote majority in the United States Senate but that the long held “Kennedy seat” (the most liberal seat in congress) is now occupied by a moderate Republican. What does this likely mean for medicine in Mississippi and the United States? 1. The Democratic health system reform that we have all grown to fear will likely not come to fruition. If health care reform comes at all, it will look much different than the present house and senate versions. 2. Total revision of the flawed SGR is unlikely to take place. Fixing the SGR in 2010 will cost an estimated 300 billion dollars. A more moderate senate is not likely to spend that kind of money just to make doctors happy. 3. Midterm elections, which historically have not looked kindly on the party in the White House, will most certainly result in more Republicans elected to both houses of Congress. This will go a long way, in my opinion, to solidify projections one and two. In my opinion, the best we in medicine can expect for our patients in the year 2010 is the beginning of a meaningful health system reform debate: • Reform that will cover most U.S. citizens, while at the same time preserving the imperative doctor/patient relationship. • Reform that will not bankrupt the states by expanding Medicaid rolls. • Reform that will center on private sector market forces while at the same time loosening the grip that insurance companies have on both doctors’ and patients’ throats. • Reform that will result in fair compensation to physicians for taking care of our nation’s elderly. • Reform that will give all health care providers reasonable protection from plaintiff attorneys whose sole interest is that of fattening their purses, even at the expense of our nation’s health. Well, I admit that this is a tall order for 2010. But take heart. Stranger things have happened. After all, remember...pigs have already flown! Your partner in making Mississippi healthier,

Randy Easterling, MD President, Mississippi State Medical Association

Mark Your Calendar! The 142nd Annual Session of the MSMA House of Delegates and Medical Affairs Forum 2010 will be held

June 3-6, 2010 in Natchez.

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• EDITORIALS •

There is a Tide in the Affairs of Men There is a tide in the affairs of men which, taken at the flood, leads on to fortune omitted, all the voyage of their life is bound in shallows and in misery. JULIUS CEASAR — Shakespeare he importance of this moment to the future of the practice of medicine in the United States cannot be overemphasized. The abrupt demise of Obamacare, punctuated by the senatorial election in Massachusetts, was as unexpected as it was fortuitous when viewed from the perspective of the 2008 elections. Physicians generally may revel in this outcome, but, candidly, organized medicine was not instrumental in bringing it about. The waning influence of the profession is no less a legitimate concern now than it was before the deflation of the Reid-Pelosi balloon. Neither should anyone be deluded that the issue of health care reform has been dealt a fatal blow. All major players seem to agree that the current system has deep flaws in terms of access and cost. The receding waters of support for the Democratic plan very likely only portend a tsunami in the making. Physicians need to prepare without delay for the crest of the next wave. The first order of business is to decide who will lead. Like it or not, the AMA is the only player in the field which has the resources to mount an effective campaign on such short notice. The AMA, I believe, is not beyond redemption in spite of its recent obsequious courting of the political power structure when passage of a Democratic crafted plan of some sort seemed inevitable. Now is an unexpected opportunity to start all over because previous leadership has been discredited and all players are momentarily confused about where to go from here. The tide is truly at the flood. We need a game plan, and we need it now. The issue is, of course, complex. Nevertheless, physicians in the main believe, and our ethical principles codify, that all people should have access to health care regardless of ability to pay. To meet this assumed societal obligation, it shouldn’t be necessary to create yet another bureaucracy. The problems of the uninsured, catastrophic illness, etc., can be effectively and efficiently addressed simply by adjusting eligibility requirements and reimbursement rates in the Medicaid program. As a separate issue, the escalating cost of health care must be confronted. The rate of increase in recent years cannot be sustained in the long run. The process of controlling costs is bound to be painful to physicians and all other providers, but who is better qualified to set priorities and oversee the maintenance of quality than medical practitioners? This is a burden that the profession had better assume expeditiously and effectively or else the voyage of the rest of the professional lives of this and future generations of physicians is likely to be bound in the shallows and the misery of a government operated health care system.

—W. Lamar Weems, MD Past President, MSMA

The Pen is Mightier than the Sword! Express your opinion in the JMSMA through a letter to the editor or guest editorial. The Journal MSMA welcomes letters to the editor. Letters for publication should be less than 300 words. Guest editorials or comments may be longer, with an average of 600 words. All letters are subject to editing for length and clarity. If you are writing in response to a particular article, please mention the headline and issue date in your letter. Also include your contact information. While we do not publish street addresses, e-mail addresses or telephone numbers, we do verify authorship, as well as try to clear up ambiguities, to protect our letter-writers.

You can submit your letter via email to KEvers@MSMAonline.com or mail to the Journal office at MSMA headquarters: P.O. Box 2548, Ridgeland, MS 39158-2548. MARCH

2010 JOURNAL MSMA

• EDITORIALS •

The Great Myth he Great Myth is that the Journal of the MSMA is expendable and totally replaceable by something online, something that exists somewhere out there in the ether, in some cyber-never land. The Great Myth is that the production of your monthly Journal MSMA is an expense that this organization can no longer afford. Tonight, I sit staring at two medical journals that arrived in tandem in my home mailbox today. I am looking at the Journal MSMA and the JAMA. Both are works of art and indeed have works of art on the cover. If I were so inclined, I could frame either cover to tastefully and interestingly decorate my wall. I hold them in my hands and feel the sleek coolness of each magazine whisked just this afternoon from my letter box, smell their inviting fresh newsprint. The JAMA slightly outweighs us, but they have no less than 100 names on their masthead: managing editors, sales, marketing folk and the like. The JMSMA has one staff person as managing editor whose attentions are very divided by other pressing tasks of communication at our Headquarters. She does not complain of this. The JMSMA has three hard working, unpaid physician Editors who also do not complain of this. The Journal of the AMA has two features that I always read faithfully…the usually kooky or nebulous poem that may or may not be comprehensible, and the essay section called “A Piece of My Mind.” This isn’t always written by a physician, but it is unfailingly touching and medically thought provoking. The rest of the JAMA can be taken or left depending on one’s interest and available time. But the JAMA is not the voice of the AMA President, Board of Trustees or its Executive Staff. It is a publication by and for its Physician membership. The arrival of the Journal of the Mississippi State Medical Association is quite a different matter. It gives me the same thrill as a long awaited letter from home, an opportunity to reconnect with the people that I have chosen as my extended family, the family of all Mississippi physicians. I feel a connection to every photo and every article it contains. I laugh out loud at some quirk or quip that Scott has penned, learn something new from an article by someone down at the University Hospital, savor Dr. Pomphrey’s photography, ponder Stanley’s wry observations, wonder again why Randy Easterling ever shaved off his beard, appreciate our MSMA history through something Luke has commemorated, and then cry when I read an article on Ed Thompson’s passing. It is no secret that I love the Journal. And I am not alone. I have really never felt the need to look at the Journal MSMA on line. Indeed, I have never looked at any medical periodical/ publication on line on a continuing basis. Except for the requisite exchanging of e-mail with my friends and relatives and the occasional Googling of weird questions that come to mind, the Internet mostly proves basically a nuisance, a major league time-waster and source of daily irritation. I don’t have the membership stats at hand, but I suspect an unbiased poll (i.e. one not done via the Internet) of over age 50 MSMA physicians might yield a similar opinion. I doubt most would ever look at an online Journal MSMA. I am sure that in some future time warp, which thankfully I will not survive to exist in, this will not be the case. My guess is there will be something beyond my current imagination extant for the dissemination of information to members of an organization such as ours, if such an organization continues to exist. These are my limitations, not those of this organization. But I maintain that the time is not now ripe to cease production of a hard copy Journal MSMA. I would vigorously veto this move with all my heart and energies. Today, I also received the gift of a wrinkled and yellowed “back issue” of the Journal MSMA. When I think of it, this unsolicited delivery could not have arrived in a more timely fashion. It was given to me by a long time patient of mine whose mother had died about a week after my own husband’s funeral. This was a ‘purloined’ copy of the Journal MSMA that her Mom had obtained quite accidentally by virtue of a US Postal Service delivery error. The originally intended recipient was a long-retired local physician with advanced dementia who has resided for several years in a personal care home many miles from our town. (Remember we live in a rural hamlet where everyone knows everything about everybody.) Because the magazine cover was attractive, her mother had taken the time to actually open and read it. Because it contained information that she perceived as important and noteworthy to her (and of no use to the doctor to whom it was addressed), she chose to hang on to it. Her reason? It was the August 2007 Journal MSMA containing a lengthy interview article filled with photographs about her own family doctor and long time friend (i.e. yours truly as President of MSMA at the time). This patient’s daughter discovered the issue while cleaning out her Mom’s cedar chest and had decided that I “might not have a copy of this magazine” so she wanted me to have it! Her quote…. “Momma loved you and meant to keep this always, but now that she’s gone, I thought you might need it for your own kids to keep.” She inscribed the front with a purple magic marker, “For Dr. South, I love you, Pam, Feb. 2010.” Such a treasure to be given!

JOURNAL MSMA

MARCH

2010

Yes, today I am in receipt of three medical Journals: the latest JAMA, the January JMSMA and that dog-eared August 2007 JMSMA…all of which I opened and perused and two of which I will cherish always. I’m sure I received some on-line Journals that I had neither the time nor the energy to click on and digest. They are floating on the web out there somewhere… unopened, unknelled, uncoffined, and (to at least one reader) unknown. What about the other 3000 or so hard copies of the January 2010 JMSMA that have made their way into member doctor’s home and offices around our state? What are they doing tonight? Some are in the loving hands of a spouse/alliance member. Some have made into the doctor’s waiting room where they are read by hundreds of Mississippi patients. Some are in the hospital doctor’s lounge being read on the sly by non-member physicians. The pull-out Mississippi Public Health Report Card adorns many exam room walls. So you see, the Journal MSMA has a readership that goes beyond the one physician’s address on the back cover…nurses, office managers, drug reps, healthcare vendors and the like. I know this because they tell me so from time to time. Hey, times are hard. A few of them may even end up being recycled at the deer camp ‘out house,’ but you get the picture. The influence of our Journal MSMA is further reaching than many of you have before considered. It is no less than the tangible face and soul of the Mississippi State Medical Association: “The Physicians Who Care for Mississippi.” A bit like the well-preserved 10,000-year-old wall paintings done by cave-dwellers in the Lascaux Caverns of Southwestern France, our old paper Journals of the MSMA still survive and recount to us the interesting stories and pictures of what life was like back in ‘the day.’ The leading characters change from year to year of course; the basic plots don’t. We never fail to be entertained by the bull chasing, rock throwing, and spear-chucking activities of our tribal leaders which have apparently gone on since the beginning of recorded time. Like the group of healers for whom it is written and produced, the Journal MSMA is neither expendable nor replaceable. I predict that the death of the publicly visible and palpable spirit of the Mississippi Physician through the proposed demise of the Journal MSMA could very well signal the beginning of the end of this hallowed organization. This cannot be allowed to happen. — Dwalia S. South, MD Past President, MSMA Chair, MSMA Committee on Publications

BlueCross BlueShield of Mississippi Committed to a Healthier Mississippi.

MARCH

2010 JOURNAL MSMA

• IQH •

1-800-784-8669 = QUITNOW hysicians have often termed tobacco cessation counseling for their patients as a “no brainer.” Many patients very addicted to nicotine often need more than an admonition to stop their use of tobacco. That’s where the Mississippi Tobacco Quitline staff can offer valuable assistance to physicians in taking patients to another level in the process of giving up the use of tobacco. The Tobacco Quitline utilizes a Consent/Referral form which is HIPAA-compliant and allows the counselor to make a proactive contact with the patient instead of waiting for the patient to call. The form also specifies that the patient will allow the Quitline to provide follow-up information to the referring physician on the patient’s cessation treatment. Qualified callers may be eligible for up to eight weeks of the nicotine replacement gum or patch at no cost. When a caller reports any conditions that may inhibit or question the use of nicotine replacement products or medications, a Medical Clearance Form is sent to the physician. In these cases, no products will be distributed without a medical clearance form signed by the physician. Working together, patients can be helped by taking advantage of professional, trained staff who will offer a quit plan, quit date and counseling. Physicians can rely on the Tobacco Quitline staff to engage the patient and provide the behavior change counseling that has been proven to succeed. For more information on the Fax/Referral program or to receive the form for office or clinic use, contact Pamela Luckett, Mississippi Tobacco Quitline manager, at 601-957-1575 ext. 212 or 1-800-784-8669.

Regional Centers for Certified EHRs he Office of the National Coordinator for Health Information Technology (ONC) recently released a funding opportunity titled the American Recovery and Reinvestment Act of 2009, Health Information Technology Extension Program: Regional Centers. To enable priority primary care providers throughout the nation to move rapidly, effectively and efficiently towards the objective of achieving meaningful use of certified EHRs, ONC will identify, through merit-based selection, applicants qualified to serve as Regional Centers. It is expected that each regional center will provide federally supported individualized technical assistance to a minimum of 1,000 priority primary care providers in the first two years of the four-year cooperative agreement project. Over those same two years, the regional centers in the national aggregate will support over 100,000 priority primary care providers to achieve successful adoption and meaningful use of certified EHRs. Regional centers will be selected and awarded in two application cycles completed in FY2010. Successful full applications from each cycle will result in four-year cooperative agreements. Cycle one applicants were to be notified at the end of January 2010 with cycle two applicants notified by March 31, 2010.

—James S. McIlwain, MD IQH President 94

JOURNAL MSMA

MARCH

2010

• UMMC • Dr. James Keeton Becomes New Vice Chancellor ast month the JMSMA reported two candidates were finalists in the national search for vice chancellor for health affairs and dean of the school of medicine at the University of Mississippi Medical Center. In a twist that surprised many, both Dr. Scott Stringer, chairman of the Department of Otolaryngology and Communicative Sciences, and Dr. Robert Robbins, chief of cardiovascular surgery at Stanford University, withdrew from consideration during the final step of the selection process. In collaboration with the search committee in a message to Medical Center employees, University of Mississippi Chancellor Dr. Dan Jones reported the appointment of three experienced faculty to key leadership responsibilities. Pending approval of the Board of Trustees of State Institutions of Higher Learning, Dr. James E. Keeton will assume the role of vice chancellor for health affairs and dean of the school of medicine. Dr. Keeton was interim vice chancellor for seven months after having served as chief-of-staff for Dr. Jones when he was UMMC vice chancellor. The announcement was made February 9th, just one week before Dr. Keeton turns 70. Dr. Jones said in the memo, “Dr. LouAnn Woodward, vice dean of the medical school who has served as interim dean of medicine over the same period, will be named associate vice chancellor for health affairs. Dr. Scott Stringer, chair of the Department of Otolaryngology and Communicative Sciences and associate vice chancellor for clinical affairs, will assume additional administrative oversight of our clinical enterprise, including University Hospitals and Health System and University Physicians.” “I have the utmost confidence in Jimmy Keeton, LouAnn Woodward and Scott Stringer, and am grateful for their willingness to serve in these leadership roles. Over the last seven months, during a time of challenges in the economy, health care and higher education, they have positioned the Medical Center for continued success. I am confident we have a strong leadership group that will serve the Medical Center and the state extremely well,” he added. “I am grateful to Dr. Keeton for making himself available for leadership of the medical center. His wisdom, keen judgment and superlative communication skills have benefited us all over these last seven months. He has gained the confidence of the Medical Center family and important external stakeholders.” Dr. Jones said he is grateful to Drs. Woodward and Stringer, as well, for making themselves available for these key positions. “Dr. Woodward will continue to play a major role in medical school and Medical Center leadership, and Dr. Stringer brings strong skills and experience to leadership of the clinical enterprise. This dual leadership role allows us to continue the important integration of decision making between the physician practice and hospital.”

Dr. James Keeton

•

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PHYSICIANS NEEDED Physicians (specialists such as cardiologists, ophthalmologists, pediatricians, orthopedists, neurologists, etc.) interested in performing consultative evaluations (according to Social Security guidelines) should contact the Medical Relations Office. Toll Free 1-800-962-2230 Jackson 601-853-5487 Leola Meyer (Ext. 5487)

DISABILITY DETERMINATION SERVICES

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2010 JOURNAL MSMA

• UNA VOCE •

A Note of Thanks

In Memoriam Robert “Rob” Walter Bitter 1928 - 2009

[The following note will perhaps explain my lengthy silence and unexplained absence from the pages of the JOURNAL MSMA and particularly the “Una Voce” column. My husband, Robert Bitter, died on October 14, 2009, after an approximate two month struggle with adenocarcinoma of both lungs. Near the end of October, I sent out the following letter to those who had sent flowers or memorials. I continue receiving cards and calls from time to time as friends around the state learn belatedly of his loss. There are probably quite a few folks reading even now who were also unaware of Robert’s death. Try as I might, I could never hope to thank everyone personally and would like to take the liberty of reaching out to our many physician/spouse friends through this month’s column.] —D.S.

hen sending out the thank-you notes graciously provided by the funeral home somehow did not seem sufficient, I decided to write a more personal message to those who shared in my grief. Deciding this was easy, finding the words was not. This fall again proved to be an unwelcomed season of changes for us. Just one year ago, Rob and I celebrated the last day of my two months of cancer treatments. Rob was with me at every moment in that life-altering process of becoming a “cancer victim,” then a “cancer patient,” then finally, hopefully, a “cancer survivor.” Prior to that time, it did not seem possible that anything could have happened to us as a married couple that could make us any closer or more ‘as one’ than we already were. That difficult course of events, however, did just that. Robert was my cheerleader, my chauffeur, my confidante, my constant companion, and my earthly rock. Though throughout the eleven years of our marriage he had always been these things for me, Rob’s deep significance in my life became even more magnified during that physical and spiritual season of change.

This August, the tables were turned on us. Robert had always seemed so timeless and unchanging to me. But when his lung cancer struck, my Rob was toppled like a giant oak by a woodsman’s blade. Once the destructive process was set in motion, no amount of scientific knowledge, force of will, or human strength could we summon to reverse or even slow it. I prayed constantly to God primarily asking for grace and peace for the both of us as we trekked through this forest of raging devastation. Inevitably, the outcome was not what we as a selfish pair of humans would have chosen but rather one consistent with His ultimate plan for our lives. The October sun is finally out this morning and allowing me to contemplate a particularly gorgeous sugar maple tree in our yard. Chard (my first husband who died in 1996) and I transplanted it to this spot from the woods nearby over twenty five years ago. Rob always loved to make pictures of this tree every fall season when she unfailingly provides us with a spectacular golden show. This year, possibly because of all the rain, her color is somehow different and has taken on almost an electric orange glow. In just a few days these bright leaves will be falling, papery brown and scattered by the wind. Her limbs will turn stark and skeletal. But I possess the knowledge that life still abides within, the spirit of this tree will be simply resting… for a season. I don’t suppose that, if left up to me, I would ever choose for this tree or any other to undergo that required transition from supple greenness to that of barren sleeping limbs for even a season. Thankfully, this is God’s call to make. And make it He does, all within His eternal plan… all within His chosen season. I realize that my grief for “the passing” of my husband and earthly best friend is selfish in nature and at times seems almost unbearable to me. Though it brings tears, it helps so much when others also express the weight of their grief at his loss. Robert Bitter’s death has ended his physical life but not our relationship to him. Shakespeare wrote, “They do not truly love, who do not show their love.” Dear friends, this is exactly what you have done for my Rob, shown the lasting deep love and tribute of your friendship with him. Your friendship is the best kinship on earth and I thank you for it. A heart of love goes out to you. —Dwalia South-Bitter, MD

JOURNAL MSMA

MARCH

2010

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