march 2010 jmsma

VOL. LI No. 3

March 2010

In Appreciation of42 Years of Dedicated Service

1967 through 2009

Mississippi State Medical Association

I In 4 2 Y

n A p p re c i ia reciation of reciation of f D di i

a t i io n of f t d S i4 2 Year Year

1 9 s s of f D e d di ic rrs of Dedicated Servicers of Dedicated Service

9 6 7 t h ro u g r rough 2 rough 2 c a t e d S Se r v i

h 2009 i ic e

M i s s i s s ip p p p i S t a t e M e di i c c al al Associattiionn

MARCH 2010 VOLUME 51 NUMBER 3

SCIENTIFIC ARTICLESPrevalence and Trends in Obesity among Mississippi PublicSchool Students, 2005-2009 67Elaine 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 TreatmentInteractions and their Implications on Treatment Decisions 75Suzanne Sanders, MD and Stephen A. Geraci, MD

Clinical Problem-Solving: Pseudo Seizures Vs Pseudo Zebra 83D. Mark Pogue, MD; Judith G. Gearhart, MD and George Moll, Jr., MD, PhD

PRESIDENT’S PAGEPigs Have Already Flown 89Randy Easterling, MD; MSMA President

EDITORIALSThere is a Tide in the Affairs of Men 91W. Lamar Weems, MD; MSMA Past President

The Great Myth 92Dwalia S. South, MD; MSMA Past President,Chair, MSMA Committee on Publications

RELATED ORGANIZATIONSInformation and Quality Healthcare 94University of Mississippi Medical Center 95

DEPARTMENTSPlacement/Classified 95Una Voce 96

ABOUT THE COVER: “TRICYRTIS HIRTA (TOAD LILY)” - From the botanical family Liliaceae, this Toad lily flower headwas photographed by Brett Tisdale, MD, a board certified emergency physicianpracticing in McComb. Toad lilies add summer and autumn bloom to shadegardens. Unique, its anthers look like the eyes on a slug, its stamens arch likeshowerheads, and its six differently shaded petals (actually tepals) alternate likemen and women at a dinner table. Unless massed and displayed prominently upfront 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 clustersor cymes, purple-spotted with yellow throats, they appear a cross between an orchidand 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 thisselection, if not the entire genus, is an instant attention-getter.❒

2010March

VOL. LI No. 3

Official Publication

of the MSMA Since 1959

JOURNAL OF THE MISSISSIPPI STATEMEDICAL 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, Mississippi38655, Ph: (662) 236-1700, Fax: (662) 236-7011,email: [email protected]

POSTMASTER: send address changes

to Journal of the Mississippi State Medical

Association, P.O. Box 2548, Ridgeland, MS 39158-

2548.

The views expressed in this publication reflect

the opinions of the authors and do not necessarily

state the opinions or policies of the Mississippi State

Medical Association.

Copyright© 2010,

Mississippi State Medical Association.

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

ChairPhilip T. Merideth, MD, JD

Martin M. Pomphrey, MD

Leslie E. England, MD, Ex-OfficioMyron W. Lockey, MD, Ex-Officio

and the Editors

THE ASSOCIATION

Randy Easterling, MD

PresidentTim J. Alford, MD

President-ElectJ. Clay Hays, Jr., MD

Secretary-TreasurerLee Giffin, MD

SpeakerGeri Lee Weiland, MD

Vice SpeakerCharmain Kanosky

Executive Director

MARCH 2010 JOURNAL MSMA 65

©

When it comes to your good name.

Everything matters

nceriexpeer Ouns. tiolusoand erstnduand analyzethef ot uostay nts, patie

web-based of rs uho150 ver ocialty-spesped omizestcu

CruOevreSeW

with rks woaff stnt memanagerisk d ncegnizecorelly fuOnce. cticeprar youin risk

malprar youl ntrocoand sehourtucource resoa courses, CMEaccredited web-based

assessmentsrisk practice n-site ocific, cialty-spelEllAevobAsremotsuC

and ms esysts, echniquteapply touyowith d liminateer od cedurearerisks d, gnizerastactiveproa with ms miuprecticemalpra

emails.management risk and library urce management risk d nalizersoper ffeoWe. assessments

ocusts videproMD , cateAdvo!esl

that ns lutiosoand priateapprowith ntify, eidtogy tera

r uyoct teProemails., gramspromanagement , efrewith rs meo

MD.coetcaov.Adwww2686-800)(

n, visit www.ambestting informatio rast later theFor Mississippi physicians. Ples foelicif pos omany type offer We

r patients. You and yotect youpro

ou DYYoection troP

mMD.co4372

cate2010 Advo©d. rvese.com. All rights ren, visit www.ambestfits. Socy benelis for po contact uaser Mississippi physicians. Ple

ur patie yorvect and sete prour patients. Yo

!woll Ne. Cavrou Dese

st Inc. uthwe Sof the oncera, MD Insucate undect tobje suunts arens may apply. Discostrictio remefits. So

.ur yo fo same thet us donts, leur patie

val. rwriting appro unde

66 JOURNAL MSMA MARCH 2010

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 drop-

ping 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 re-

cently, however, the National Health and Nutrition Examination Survey

(NHANES) showed no significant changes in the percentage of obesity

among US children aged 2 to 19 years between 2003-2004 and 2005-

2006.2 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 Missis-

sippi’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 encourag-

ing 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 ob-

tain weighted YRBS data on high and middle school students. Conse-

quently, 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 over-

weight. 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 preva-

lence of obesity was reported. Between 2005 and 2007, the prevalence

of obese children and youth declined from 25.5% to 23.5%. The preva-

lence 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 sug-

• SCIENTIFIC ARTICLES •

Prevalence and Trends in Obesityamong 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

ABSTRACT

AUTHOR INFORMATION: Dr. Molaison is an Associate Professor in the Department ofNutrition & Food Systems at The University of Southern Mississippi. Dr. Kolbo is aProfessor 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 StateDepartment of Health and an Associate Professor in the School of Nursing at theUniversity of Mississippi Medical Center. Dr. Harbaugh is an Associate Professor in theSchool of Nursing at The University of Southern Mississippi. Dr. Armstrong is theMedical Director for Public Health District V, for the Mississippi State Department ofHealth. Dr. Rushing is an Assistant Professor in the Department of Nutrition & FoodSystems at The University of Southern Mississippi. Dr. Blom is an Assistant Professorof Physical Education at Ball State University. Ms. Green is currently a graduatestudent in the Master of Public Health Program at The University of SouthernMississippi.

CORRESPONDING AUTHOR: Elaine Fontenot Molaison, PhD, The University of SouthernMississippi, Department of Nutrition & Food Systems, 118 College Drive #5172,Hattiesburg, MS 39406, Phone: 601-266-6548, Fax: 601-266-6343, [email protected]



gested that like data from the National YRBS and other national stud-

ies, the prevalence may be leveling off or beginning to drop in Missis-

sippi.4

Whether or not the obesity rates are continuing to increase, lev-

eling off, or declining may have a significant impact on the health and

well-being among children, youth and adults. Evidence has been pro-

gressively 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 es-

timates 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 obe-

sity are expected to reach one trillion dollars annually by 2030.12

Educational InitiativesWith 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 initia-

tives is currently available.13-18

Through a mix of state and federal legislation, Mississippi re-

cently began implementing several state-wide school-based initiatives

to address the problem of childhood obesity. In 2004, Congress en-

acted the Child Nutrition and WIC Reauthorization Act (Section 204 of

Public Law 108-265) mandating any local education agency partici-

pating 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 estab-

lished phased implementation of strict guidelines for the types of bev-

erages 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 stu-

dents at Mississippi schools during the school day. In phase two, bev-

erage vending was further restricted to include only bottled water,

low-fat and non-fat milk, and 100% fruit juice in age-appropriate serv-

ings for elementary and middle schools. High schools are allowed bot-

tled 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

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) Nu-

trition 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 pre-

pared at schools, marketing of healthy foods to students and staff, min-

imum 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/ Com-

prehensive Health Education Rules and Regulations provided time re-

quirements, 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 stu-

dents in grades 9-12.25 By the fall of 2008, all standards and require-

ments 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 pub-

lic 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 en-

rollment in grades K - 12 of each school. In the second stage of sam-

pling, 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 in-

tended to develop sample weights so that the weighted sample esti-

mates 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 Missis-

sippi, as the study protocol matched the 2003, 2005, and 2007 CAY-

POS.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 respon-

sible 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 measure-

ments required that the weight scale be placed on a hard, smooth sur-

face; 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 gath-

ered 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 main-

tained 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 ANALYSISBody 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-calculate-

BIV.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 per-

centile); and (4) obese (BMI is greater than or equal to the 95th per-

centile).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 pre-

vious 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 Non-

white 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.

Results of 2009 CAYPOS Based on Subgroups of ParticipantsAs 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 clas-

sified 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.

GenderIn 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).

RaceIn terms of race, 19.5% of the White students were classified as

obese with another 17.9% as overweight. Among the Non-white stu-

dents, 27.4% were obese and 19% were overweight. There is a statis-

TABLE 1: CHARACTERISTIC OF PARTICIPANTS, CAYPOS, GRADES K-12,MISSISSIPPI, 2009

Characteristic Unweighted count Weighted percent

Gender

Male 1,839 49.8Female 1,864 50.2

Race

White 1,648 43.7Nonwhite

a

2,053 56.3

Missing 2 0.0Grade

Elementary

K 163 4.21st 274 7.92nd 338 8.53rd 271 7.34th 447 11.7

5th 163 4.5Middle school

6th 143 3.77th 344 8.98th 501 13.6

High school

9th 435 12.310th 263 7.6

11th 153 4.112th 208 5.7

Total 3,703 100

aNinety-three percent of Nonwhite Students were African American.


tically significant difference between the prevalence of obesity among

the White and Nonwhite students (Table 2).

Gender and RaceAs 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).

Grade LevelAmong elementary level students (grades K – 5), 24.1% were

classified as obese with 17.7% classified as overweight. Among the

middle school students (grades 6 – 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)

Gender and Grade LevelAmong females, the highest rates were at the elementary level

followed by the middle school and high school. For males, the high-

est rates were at the middle school followed by the elementary school

and high school. Specifically, at the elementary level, 24.0% of fe-

males 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

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 LevelAmong 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 stu-

dents 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).

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 preva-

lence of obesity between white and nonwhite students was not statisti-

cally significant (p = 0.069; Figure 2). At the high school level, 19.6%

of White students were obese with 18.4% overweight. For Nonwhite

All (K-12) Elementary (K-5) Middle school (6-8) High school (9-12)

(%, 95% CIc) (%, 95% CI) (%, 95% CI) (%, 95% CI)

All

Overweighta

2005 18.4 (17.0-19.8) 18.0 (16.2-19.8) 19.4 (16.5-22.3) 18.1(15.9-20.3)

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)

Obesityb

2005 25.5 (23.3-27.7) 25.0 (22.3-27.7) 28.9 (24.8-33.0) 23.5 (20.6-26.4)

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)

White

Overweight

2005 17.7 (15.5-19.9) 17.9 (14.4-22.0) 18.2 (13.8-23.7) 16.9 (14.6-19.6)

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)

Nonwhited

Overweight

2005 18.8 (17.2 20.4) 18.2 (16.2-20.5) 20.1 (16.9-23.7) 18.9 (15.8-22.6)

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

2005 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)

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

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

c95% confidence interval.

dIn 2009, 2007, and 2005,

about

93%,

94%, and 95%

of Nonwhite students were African American,

respectively.

TABLE 3: PREVALENCE OF OVERWEIGHT AND OBESITY BY GRADE LEVEL

AND RACE, CAYPOS, MISSISSIPPI 2005, 2007, AND 2009 All (K-12) Elementary (K-5) Middle school (6-8) High school (9-12)

(%, 95% CI) (%, 95% CI) (%, 95% CI) (%, 95% CI)

Male

Overweight

2005 18.6 (16.8-20.4) 18.7 (16.3-21.2) 19.3 (15.3-24.0) 18.1 (15.0-21.7)

2007 17.5 (15.5-19.7) 16.3 (13.9-19.0) 18.5 (13.1-25.5) 19.3 (15.6-23.6)

2009 18.2 (16.5-20.0) 18.0 (15.5-20.8) 17.1 (14.0-20.6) 19.5 (16.3-23.3)

Obesity

2005 25.2 (23.0-27.4) 24.2 (21.6-27.0) 28.4 (23.9-33.3) 24.4 (19.3-30.3)

2007 24.2 (22.0-26.6) 25.7 (22.3-29.4) 20.1 (16.3-24.5) 24.4 (20.0-29.4)

2009 24.8 (22.5-27.4) 24.2 (20.9-27.7) 27.1 (22.9-31.8) 23.7 (19.0-29.1)

Female

Overweight

2005 18.1(15.7-20.5) 17.5 (14.5-20.9) 19.6 (15.6-24.2) 18.2 (14.4-22.9)

2007 19.7 (17.3-22.3) 20.5 (18.1-23.2) 19.7 (15.5-24.6) 18.1 (12.4-25.5)

2009 18.8 (17.2-20.5) 17.4 (14.8-20.3) 18.9 (15.3-23.1) 20.5 (18.4-22.9)

Obesity

2005 25.9 (22.6-29.2) 25.9 (21.8-30.6) 29.4 (23.9-35.6) 22.8 (18.7-27.5)

2007 22.9 (20.4-25.5) 24.8 (20.9-29.2) 24.9 (20.9-29.4) 17.1 (13.4-21.6)

2009 23.0 (20.8-25.3) 24.0 (20.2-28.2) 23.7 (20.0-27.8) 21.1 (17.6-25.2)

White male

Overweight

2005 17.9 (15.3-20.9) 17.7 (14.1-22.0) 18.3 (13.4-24.5)* 18.2 (16.4-20.2)*

2007 17.5 (14.7-20.6) 17.3 (14.2-20.8) 17.4 (9.9-28.7)* 17.8 (12.0-25.5)*

2009 17.8 (15.4-20.6) 18.1 (13.7-23.6) 15.8 (10.8-22.6)* 19.4 (13.9-26.5)*

Obesity

2005 23.6 (21.1-26.4) 21.3 (19.0-23.7) 31.5 (29.5-33.5) 22.3 (18.2-26.9)*

2007 23.6 (20.3-27.2) 23.0 (18.7-27.9) 18.9 (12.1-28.3)* 28.8 (21.8-37.0)

2009 22.5 (19.1-26.4) 18.7 (13.3-25.6) 25.4 (18.4-34.0) 25.2 (18.3-33.5)

Nonwhite male

Overweight

2005 19.2 (16.8-21.9) 19.6 (17.8-21.6) 19.8 (14.8-25.9)* 18.0 (13.2-24.2)*

2007 17.7 (14.8-20.9) 15.3 (11.1-20.7) 19.8 (15.2-25.5)* 20.5 (15.0-27.3)

2009 18.4 (16.0-21.1) 17.9 (14.1-22.5) 18.2 (13.1-24.7)* 19.7 (15.5-24.6)

Obesity

2005 26.4 (22.8-30.4) 26.7 (23.3-30.4) 25.8 (18.5-34.9)* 25.8 (11.4-48.5)*

2007 25.0 (21.9-28.5) 28.3 (23.2-34.0) 20.9 (16.2-26.6)* 22.3 (16.1-30.0)

2009 26.6 (23.8-29.6) 27.9 (23.6-32.7) 28.5 (22.7-35.1) 22.4 (17.2-28.5)

White female

Overweight

2005 17.6 (14.3-21.6) 18.1 (14.9-21.9) 18.1 (12.4-25.7)* 16.0 (14.7-17.5)*

2007 19.1 (15.7-22.9) 18.3 (15.1-22.1) 22.0 (13.9-33.2)* 17.2 (9.8-28.3)*

2009 17.9 (15.7-20.3) 18.4 (14.5-23.1) 17.6 (12.1-24.7) 17.6 (14.1-21.6)*

Obesity

2005 22.3 (18.5-26.7) 22.8 (20.1-25.8) 25.5 (20.9-30.8)* 18.0 (13.0-24.4)*

2007 18.4 (14.9-22.6) 20.7 (15.5-27.2) 20.0 (13.2-29.2)* 10.9 (7.7-15.3)*

2009 16.4 (13.8-19.5) 16.8 (12.3-22.4) 17.9 (12.9-24.4)* 14.8 (10.0-21.3)*

Nonwhite female

Overweight

2005 18.4 (15.8-21.4) 17.0 (14.8-19.4) 20.4 (18.3-22.6)* 19.7 (17.0-22.7)*

2007 20.1 (17.2-23.4) 22.6 (18.9-26.8) 17.1 (14.4-20.2)* 18.7 (12.4-27.2)*

2009 19.6 (17.6-21.8) 16.8 (13.9-20.2) 20.3 (13.5-29.4)* 23.1 (19.2-27.6)

Obesity

2005 28.4 (24.1-33.1) 28.0 (22.6-34.2) 32.0 (23.5-41.9) 26.0 (18.7-34.9)

2007 26.4 (23.2-29.8) 28.5 (23.8-33.8) 29.0 (23.4-35.3) 20.5 (14.8-27.7)

2009 28.1 (25.2-31.2) 28.4 (23.2-34.2) 29.5 (22.9-37.1) 26.6 (22.2-31.5)

* Sample size is less than 50. The estimates may not be reliable.

TABLE 2: PREVALENCE OF OVERWEIGHT AND OBESITY BY GRADE LEVEL,GENDER, AND RACE, CAYPOS, , 2005, 2007, AND 2009

FIGURE 1: OBESITY PREVALENCE BY RACE AMONG MISSISSIPPI

ELEMENTARY SCHOOL STUDENTS

22.9 21.9

17.8

27.4 28.4 28.1

0

5

10

15

20

25

30

35

40

2005 2007 2009

Percent

Year

White

Nonwhite

p = 0.077 p = 0.020 p = 0.006


students, 24.7% were obese and 21.6% were overweight. The differ-

ence in the prevalence of obesity between white and nonwhite students

was not statistically significant (p = 0.071; Figure 3).

Gender, Race, and Grade LevelWhen 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 over-

weight. At the elementary level, these differences between rates of

obesity between White and Nonwhite females were statistically sig-

nificant. 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 CAYPOSWhile no statistically significant differences were found over

the three time periods (2005, 2007, 2009) for overall rates or by gen-

der, 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%

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, com-

pared to 21.0% in 2007 and 22.9% in 2005. Among Nonwhite stu-

dents, 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).

DISCUSSION

Like prevalence rates reported nationally, the prevalence of obe-

sity 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 Non-

white 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 stu-

dents 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 dif-

ferences were found between Nonwhite and White students as well as

among Nonwhite females and White females. Also, although the dif-

ferences 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

FIGURE 2: OBESITY PREVALENCE BY RACE AMONG MISSISSIPPI MIDDLE

SCHOOL STUDENTS

28.4

19.521.6

29.325.4

29.0

0

5

10

15

20

25

30

35

40

2005 2007 2009

Percent

Year

White

Nonwhite

p = 0.825 p = 0.469 p = 0.069

FIGURE 3: OBESITY PREVALENCE BY RACE AMONG MISSISSIPPI HIGH

SCHOOL STUDENTS

19.9 20.1 19.6

25.9

21.424.7

0

5

10

15

20

25

30

35

40

2005 2007 2009

Percent

Year

White

Nonwhite

p = 0.178 p = 0.755 p = 0.071


seeing similar signs of changes among males and Nonwhite students?

What do these findings suggest in light of recent educational initia-

tives? 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 preva-

lence rates to the recent policies, programs, and activities being imple-

mented across the state. It is clear that continued monitoring of the

prevalence rates is critical, especially as educational initiatives con-

tinue to be implemented.

While there have been recent pediatric obesity-focused initia-

tives from the American Academy of Pediatrics along with the Amer-

ican Medical Association related to childhood obesity, there have not

been any formal statewide medical initiatives instituted in Missis-

sippi.29-31 However, a recent development provides a new opportunity

for the Mississippi State Medical Association to lead a statewide ini-

tiative to screen school-aged children for obesity. Recent recommen-

dations 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 in-

terventions to promote improvements in weight status.30 These rec-

ommendations differ from 2005 Task Force recommendations, as there

is now stronger evidence that obese and overweight school aged chil-

dren, once identified, can improve weight status with moderate to high

intensity interventions.

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

REFERENCES1. Morbidity and Mortality Weekly Report. Youth Risk Behavior

Surveillance—United States, 2007. Centers for Disease Control Website. www.cdc.gov/mmwr. Accessed December 1, 2009.

2. Ogden CL, Carroll MD, Flegal KM. High body mass index for ageamong 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 studentsin Mississippi compared with prevalence data from the Youth RiskBehavior Surveillance System. Prev Chronic Dis. 2006;3:A84.

4. Kolbo JR, Armstrong MG, Blom L, Bounds W, Molaison E, DickersonH, Harbaugh B, Zhang L. Prevalence of obesity and overweight amongchildren 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. Prevalenceof overweight among children and youth in Mississippi: A comparisonbetween 2003 and 2005. 2008 Available at http://www.mshealthpolicy.com. Accessed April 4, 2008

6. Arens R, Muzumdar H. Childhood obesity and obstructive sleep apneasyndrome. 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 beoverweight adults? J Fam Practice. 2009;58(8):431-432.

9. Sjoberg RL, Nilsson KW , Leppert J. Obesity, shame and depression inschool 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

National Heart Lung & Blood Institute Growth and Health Study.Pediatrics. 2007;150:18-25.

11. 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 EnglJ Med, 2004;350:2362-2374.

12. Wang Y, Beydoun MA, Liang L, Caballero B, Kumanyika SK. Will allAmericans become overweight or obese? Estimating the progressionand cost of the US obesity epidemic. Obesity. 2008;16:2323-2330.

13. Boehmer TK, Luke DA, Haire-Joshu DL, Bates HS, Brownson RC.Preventing childhood obesity through state policy: Predictors of billenactment. AM J Prev Med. 2008;34(4):333-340.

14. Boehmer TK, Brownson RC, Haire-Joshu D, Dreising ML. Patterns ofchildhood obesity prevention legislation in the United States. PreventingChronic Disease. 2007;4:(3)1-11.

15. 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 PublicHealth Policy. 2009;30:S161-176.

16. Foster GD, Sherman S, Borradaile KE. A policy-based schoolintervention to prevent overweight and obesity. Pediatrics. 2008;121(4):794-802.

17. Nihiser A, Lee SM, Wechsler H, et al. Body mass index measurement inschools. Journal of School Health. 2007;77(10):651-672.

18. Story M, Nanney MS, Schwartz MB. Schools and obesity prevention:Creating school environments and policies to promote healthy eatingand physical activity. The Milbank Quarterly. 2009;87(1):71-100.

19. SB 2369, amending Mississippi Code of 1972 Annotated Section 37-13-134. Web site. http://billstatus.ls.state.ms.us/documents/2007/html/SB/2300-2399/SB2369SG.htm. Accessed December 15, 2009.

20. United States Department of Agriculture, Food and Nutrition Services.Section 204 of Public Law 108-265-Child Nutrition and WICReauthorization Act of 2004. 2004. Web site. http://www.fns.usda.gov/TN/Healthy/108-265.pdf. Accessed September 23, 2008.

21. Mississippi Department of Education, Mississippi Office of HealthySchools. Beverage Regulations for Mississippi Schools. 2006. Website.http://www.cn.mde.k12.ms.us/documents/VendingRegForMSSchools06.pdf. Accessed September 20, 2008.

22. 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

23. Mississippi Department of Education, Office of Innovation and SchoolImprovement Office of Accreditation Mississippi Public SchoolAccountability Standards 2007. 2007. Web site. http://www.mde.k12.ms.us/accred/2007_Edition.MS%20Public%20School%20Acct.%20Stds.pdf. Accessed September 17, 2008.

24. Mississippi Department of Education. Mississippi Healthy Students ActSenate Bill 2369 Nutrition Standards. 2007. Web site. http://www.healthyschoolsms.org/documents/MississippiHealthyStudentsActSenateBill2369NutritionStandards_000.pdf. Accessed September 17, 2008.

25. Mississippi Secretary of State, Administrative Procedures. PhysicalEducation/Comprehensive Health Education Rules and Regulations.2007. Web site. http://www.sos.state.ms.us/busserv/AdminProcs//PDF/00014817b.pdf. Accessed September 17, 2008.

26. Qualtrics [Online Survey Software]. Provo, UT; 2009.27. 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.

28. SUDAAN [computer program]. Version 10.0. Research Triangle Park,NC; 2009

29. American Academy of Pediatrics 2003. Prevention of pediatricoverweight and obesity. Pediatrics. 2003;112:424-430.

30. American Academy of Pediatrics, 2010. Screening for Obesity inChildren and Adolescents: US Preventive Services Task ForceRecommendation Statement: US Preventive Services Task ForcePediatrics 2010;125:361–367. Web site. www.pediatrics.org/cgi/doi/10.1542/peds.2009-2037. Accessed January 20, 2010).

31. American Medical Association, 2007. Expert committeerecommendations on the assessment, prevention, and treatment of childand adolescent overweight and obesity. Website. http://www.ama-assn.org/ama1/pub/upload/mm/433/ped_obesity_recs.pdf. AccessedJanuary 20, 2010.

Medical Assurance Company of Mississippi

“ “

Defense of Claims

AlacideM

CecnarraussA

foynapmoC

AM

ippiipssissiMf

fihhfMCAfedsihnI

hfi, esneffe

“fo“was“Since

myandMACM

, suppoyy,stand bunderstandIdidlawsuit

notBut,sippi.insurancemalpractice

onfocused“wasinception,ts

“it

AM

foughtCounselDefensemy

, support, and fight for their insureds. muchhowjustunderstand

threatenedwasIuntilinphysiciansforinsurance

medical ofbusinesscoreitsonMACM thatunderstoodIinception,

fiehtthguoffoMCA

a fought

, support, and fight for their insureds. they much

a with-Missis

medical MACM

. thgfifig

choose it over any other carrieMississippito

sounds’MACM

and they were honest with me. wasIit.forget

battlemulti-yearmyandMACM

“carrie

“rea

“the

“s

“r

““. any other c

“r.

IreasontheisdoctorsMississippicommitment andfootingsound

and they were honest with me. withhonestbetoablewaswillIwon.andmeforbattlefoughtCounselDefensemy

Cardiologist David Irwin, MD

would Icommitment

them withnever will

a fought

Cardiologist David Irwin, MD

ddd

hs mialcr oirepushtfotraplargetnilanoisseforprieht

ussAlacideMot,sraey03revoroF

upelo, MTTuCardiologist

lhd

usnir uoo ts ecivresg nildnapytinummocerachtlaehehCAM,yy,adoTTo.sdeenytilibaillssissiMfoynnyapmoCecnaru

vahsnaicisyhhypippississiM,

upelo, Mississippi Cardiologist

. sderug nidivorn asiMCr ofippisd ekoolev

motehtniamersre

seetnaraugelvelatsdetacidedA

.sdeenssaotsuonllaC

. ippissuswollatahwsiyolf os raeyynnya

denibmoc,sihT.ytiroirppolopruofostseretniehttaht

tnemevlovninaicisyhhypdna

27145230081

lanoisseforpruoyhtiwtsis

nieciohcforeirracehtebotir uom orft roppusd nay tlay

e hthtiw-dlohycily reveta

y tilibail

-sissiMn, sderusn

w

eD

ten.mcam.www2714.523.008.1

allaCfoesneffee

smia


MRI’s in flexion and extensionpositions offer the most accurate diagnosis of

herniated disc .

call 504.934.40004 3 4 9 L o v e l a n d S t . • M e t a i r i e , L A 7 0 0 0 6 Watch TV during procedure.

Patients are usually scanned in a comfortable seated position watchinga 42” plasma screen television throughout the procedure.Conventional lie down MRIs can miss information that is onlyvisible when patients are scanned in an upright position. Our ACRaccredited facility offers physicians the choice to scan the patient intheir position of pain. Both our technologist and radiologist have over50 combined years of MRI expertise. We offer same day scheduling, 24hour reports and transportation in the metro area. Appointmentsstarting at 7 a.m.

Subscribe to MSMA e-mail news...

MSMAonline.com

@• Give your fax machine a break

• Save trees and “go green”

• Share news by clicking Forward

• Receive legislative alerts

• Learn news you can use as soon as it’s available

If you want to be “in the know” send an emailmessage to [email protected]. Ifyour email has changed make sure you send

your new address to the MSMA. You may updateyour profile information online anytime.


Cardiovascular disease is highly prevalent in rheumatoid arthri-

tis patients, contributing to significant morbidity and mortality. Few

randomized trials are available to guide risk assessment and interven-

tion in these complex patients. This paper discusses traditional athero-

sclerotic 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 dis-

ease.

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 refer-

ences 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. Ev-

idence supports aggressive therapy for traditional cardiovascular risk

factors, reducing rheumatoid activity, and limiting pro-atherosclerotic

medications.

KEY WORDS: CARDIOVASCULAR DISEASE, RHEUMATOID

ARTHRITIS, RISK FACTORS, TREATMENT,PREVENTION

INTRODUCTION

Patients with rheumatoid arthritis (RA) have a reduced life ex-

pectancy 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 infarc-

tion (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 over-

all patients with RA have a 63% greater 30-day cardiovascular (CV)

mortality following first acute cardiovascular events than non-RA pa-

tients.7 Twice as likely to experience unrecognized AMI and sudden

death, RA patients are also less likely to undergo coronary bypass graft-

ing than non-RA subjects.8

Traditional atherosclerotic risk factors (hypertension, dyslipi-

demia, 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 fac-

tors, RA still affords a 3.17 relative risk for major CV events,9 clearly

identifying an independent, additive risk afforded by RA itself. Pre-

vention of CVD in RA patients is therefore an important challenge for

primary care providers, cardiologists and rheumatologists alike.

METHODS

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 con-

dition. To that end, the authors searched the published literature by

cross-referencing topics of cardiovascular disease, rheumatoid arthri-

tis, cardiovascular disease risk factors (including hypertension, dys-

lipidemia, diabetes/glucose intolerance, smoking, diet, and physical

inactivity), treatments for these risk factors, and treatments for rheuma-

toid arthritis with special attention to those clinical trials that are avail-

able. Papers published between 1983-2009 identified using PubMed

and Medline search engines were reviewed.

Cardiovascular Disease in RheumatoidArthritis: Disease and Treatment

Interactions and their Implications onTreatment Decisions

Suzanne Sanders, MD and Stephen A. Geraci, MD

ABSTRACT

AUTHOR INFORMATION: Dr. Suzanne Sanders is a staff rheumatologist and Assistant Chiefof Medical Services at the G.V. (Sonny) Montgomery Veterans Affairs Medical Centerand 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 Pulmonaryand Critical Care Medicine at the University of Mississippi School of Medicine, Jackson,MS.

CORRESPONDING AUTHOR: Suzanne Sanders, MD, Medical Service (111), 1500 E. WoodrowWilson Drive, Jackson, MS 39216. Email: [email protected]

• SCIENTIFIC ARTICLES •


TRADITIONAL RISK FACTORS AND TREATMENT

HypertensionUp to 70% of RA patients have hypertension; of these, only 61%

receive anti-hypertensive therapy (with fewer than 22% of these opti-

mally 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 poten-

tial 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 treat-

ment for hypertension. The authors estimate that increases in systolic

blood pressure of 1-5 mm Hg are associated with 7100 -35,700 addi-

tional 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 an-

nually.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 ap-

pears independently associated with hypertension in RA patients, par-

ticularly 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 concen-

trations 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 ef-

fects 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 car-

diovascular complications in RA patients has not yet been determined.

DyslipidemiaSeveral studies suggest lipid abnormalities are prevalent in RA

patients and correlate with disease activity,23,24,25 with up to 70% of in-

flammatory arthritis patients demonstrating clinical dyslipidemia.26 The

most prevalent dyslipidemias in RA are low high-density lipoprotein

(HDL) levels and elevated atherogenic index (total cholesterol/HDL-

cholesterol ratio).23,24,25

In selecting treatment strategies, some providers avoid reduc-

tase inhibitors (statins) in RA patients, believing drug-induced myopa-

thy to be more frequent in, or that drug-induced muscle symptoms may

confuse the clinical picture of, RA. However, a double-blind, ran-

domized placebo-controlled trial in RA patients showed that a high po-

tency 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 dyslipi-

demia,30,31 treatment of RA with methotrexate and prednisone (7.5

mg/day with tapering as tolerated) resulted in increased HDL concen-

trations and significant reductions in atherogenic indices.25 Other stud-

ies suggest hydroxychloroquine treatment of RA decreases serum

triglycerides, total cholesterol and low density lipoprotein (LDL) con-

centrations,32 while increasing HDL levels.33 However, while anti-

tumor 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 IntoleranceAlthough 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 in-

flammation40 and worsened by glucocorticoid treatment.41 The associ-

ation between insulin resistance and atherosclerosis is well established

and described elsewhere.42

Some medications used to treat RA can improve insulin sensi-

tivity. 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 di-

abetes 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.

SmokingSmoking increases the risk of developing RA, particularly

seropositive RA,49,50 and may also decrease the response of RA to cer-

tain 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 calcifi-

cation 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 rheuma-

toid factor positivity, disease severity, and extra-articular RA manifes-

tations (rheumatoid nodules, lung disease, and vasculitis).54,55,56 This is

important because cardiovascular mortality appears higher in seropos-

itive 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 ces-

sation intervention in RA patients.

DietDiet is linked directly to several cardiovascular risk factors in-

cluding 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 There-

fore, 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.

Physical InactivityPhysical inactivity, in part due to its contribution to obesity, glu-

cose 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 im-

proving as a result.65,66,67,68 A 21-week concurrent strength/en-

durance 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 Partici-

pation in a low-impact aerobic exercise program may also reduce fa-

tigue, pain, and depression in RA patients.67

In a larger randomized, controlled, multicenter trial, investiga-

tors compared effectiveness and safety between a 2-year intensive ex-

ercise 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 me-

dian 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 exces-

sive 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

be comparable to those in non-RA patients, and appropriate exercise

should be regularly recommended.

RA-SPECIFIC RISK FACTORS AND THEIR MODULATION

GlucocorticoidsThe cardiovascular impact of glucocorticoids in RA patients is

somewhat controversial. As noted above, glucocorticoids reduce in-

sulin sensitivity,41 may contribute to hypertension,10 and can promote

unfavorable lipid profiles.30,31 Conversely, RA activity can worsen in-

sulin resistance and contribute to dyslipidemia, suggesting anti-in-

flammatory glucocorticoids could have a net beneficial effect. In fact,

one recent study suggested that prednisolone at 7.5mg daily did not in-

fluence 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 (ex-

clusive of congestive heart failure events) in patients receiving low

dose prednisone was similar to that of steroid-naive patients.71 A pop-

ulation-based cohort study showed that rheumatoid factor (RF)-positive

patients carry a greater risk of cardiovascular events with glucocorti-

coid exposure (particularly with higher cumulative dose, higher aver-

age 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 in-

completely, supported strategy.

Non-steroidal Anti-inflammatory DrugsThe contribution of NSAIDs to cardiovascular risk is also con-

troversial. Rofecoxib, a cyclooxygenase (Cox) -2 inhibitor, was with-

drawn from the market because of increased incidence of

cardiovascular events during chronic administration.73 Presently, cele-

coxib 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-analy-

sis 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 An-

other 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 popu-

lation-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

aspirin’s antiplatelet effect with ibuprofen (but not with rofecoxib, di-


clofenac or acetaminophen), a finding of unproven clinical impor-

tance.78

Hence, the cardiovascular safety of any chronically administered

NSAID is at best questionable. Providers should use caution in pre-

scribing 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 InflammationStudies strongly suggest that uncontrolled inflammation and ag-

gressive 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 signif-

icantly 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 coronary-

artery 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 ad-

verse cardiac events independent of traditional cardiovascular risk fac-

tors,81 while another study showed C-reactive protein (CRP) to be

independently associated with microvascular dysfunction in RA pa-

tients.82 In addition, anti-cyclic citrullinated peptide antibodies, which

predict poor clinical outcome and radiologic severity, are independ-

ently associated with the development of ischemic heart disease in RA

patients.83 As noted previously, severe extra-articular disease manifes-

tations also appear to be associated with an increased risk of first-ever

cardiovascular events.58

Reducing inflammation with methotrexate or anti-TNF treat-

ment 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 en-

dothelial function in RA patients, explaining in part their potential ben-

efits on cardiovascular risk.35,44,45,46,87,88 Although, at least one study

suggests that azathioprine, cyclosporine, and leflunomide may be as-

sociated with increased CV risk,89 results from a multi-national cross-

sectional 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. Glu-

cocorticoids 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 car-

diovascular morbidity and mortality in rheumatoid arthritis patients.

REFERENCES1. Myllykangas-Luosujärvi RA, Aho K, Isomäki HA. Mortality in

rheumatoid arthritis. Semin Arthritis Rheum. 1995;25:193-202. 2. Wolfe F, Mitchell DM, Sibley JT, et al. The mortality of rheumatoid

arthritis. Arthritis Rheum.1994;37:481-494. 3. Wållberg-Jonsson S, Öhman M, Dahlqvist SR. Cardiovascular

morbidity and mortality in patients with seropositive rheumatoidarthritis in northern Sweden. J Rheumatol. 1997;24:445-451.

4. Turesson C, Jarenros A, Jacobsson L. Increased incidence ofcardiovascular disease in patients with rheumatoid arthritis: results froma community based study. Ann Rheum Dis. 2004;63:952-955.

5. Södergren A, Stegmayr B, Lundberg V, et al. Increased incidence of andimpaired prognosis after acute myocardial infarction among patientswith seropositive rheumatoid arthritis. Ann Rheum Dis. 2007;66:263-266.

6. Solomon DH, Karlson EW, Rimm EB, et al. Cardiovascular morbidityand mortality in women diagnosed with rheumatoid arthritis.Circulation. 2003;107:1303-1307.

7. Van Doornum S, Brand C, King B, et al. Increased case fatality ratesfollowing a first acute cardiovascular event in patients with rheumatoidarthritis. Arthritis Rheum. 2006;54:2061-2068.

8. Maradit-Kremers H, Crowson CS, Nicola PJ, et al. Increasedunrecognized coronary heart disease and sudden deaths in rheumatoidarthritis. Arthritis Rheum. 2005;52:402-411.

9. Del Rincón I, Williams K, Stern MP, et al. High incidence ofcardiovascular events in a rheumatoid arthritis cohort not explained bytraditional cardiac risk factors. Arthritis Rheum. 2001;44:2737-2745.

10. Panoulas VF, Douglas KMJ, Milionis HJ, et al. Prevalence andassociations of hypertension and its control in patients with rheumatoidarthritis. Rheumatology (Oxford). 2007;46:1477-1482.

11. Singh G, Miller JD, Huse DM, et al. Consequences of increasedsystolic blood pressure in patients with osteoarthritis and rheumatoidarthritis. J Rheumatol. 2003;30:714-719.

12. 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.

13. Panoulas VF, Douglas KM, Stavropoulos-Kalinoglou A, et al. Long-term exposure to medium-dose glucocorticoid therapy associates with

Benefit PlansCompliance ProgramsFraud & Abuse/StarkLabor & EmploymentMalpractice DefenseMedicare Law & RegulationCONSTARK

HIPAAMedical StaffTaxationWorkers’ CompensationGovernment RelationsMergers, Acquisitions

& Joint Ventures

JACKSON OFFICE401 East Capitol St., Suite 600, Jackson, MS 39201

Post Office Box 651, Jackson, MS 39205-0651PH. 601.968.5500 FAX 601.968.5593

GULF COAST OFFICE 2781 C.T. Switzer, Sr. Drive, Suite 307

Biloxi, MS 39531 PH. 228.385.9390 FAX 228.385.9394

HATTIESBURG OFFICE 601 Adeline St., Hattiesburg, MS 39401

P.O. Box 990, Hattiesburg, MS 39403-0990 PH. 601.582.5551 FAX 601.582.5556

www.wisecarter.com


hypertension in patients with rheumatoid arthritis. Rheumatology(Oxford). 2008;47:72-75.

14. Frishman WH. Effects of nonsteroidal anti-inflammatory drug therapyon blood pressure and peripheral edema. Am J Cardiol.2002;89(6A):18D-25D.

15. Adhiyaman V, Asghar M, Oke A, et al. Nephrotoxicity in the elderlydue to co-prescription of angiotensin converting enzyme inhibitors andnonsteroidal anti-inflammatory drugs. J R Soc Med. 2001;94:512-514.

16. Juhlin T, Erhardt LR, Ottosson H, et al. Treatments with losartan orenalapril are equally sensitive to deterioration in renal function fromcyclooxygenase inhibition. Eur J Heart Fail. 2007;9:191-196.

17. Rozman B, Praprotnik D, Logar D, et al. Leflunomide andhypertension. Ann Rheum Dis. 2002;61:567-569.

18. Chobanian AV, Bakris GL, Black HR, et al. Seventh report of the jointnational committee on prevention, detection, evaluation, and treatmentof high blood pressure. Hypertension. 2003;42:1206-1252.

19. Dagenais NJ, Fakhreddin J. Protective effects of angiotensin IIinterruption: evidence for antiinflammatory actions. Pharmacotherapy.2005;25:1213-1229.

20. Takiz C, Utuk O, Pirildar T, et al. Effects of angiotensin-convertingenzyme inhibition and statin treatment on inflammatory markers andendothelial functions in patients with longterm rheumatoid arthritis. JRheumatol. 2005;32:2095-2101.

21. Martin MF, Surrall KE, McKenna F, et al. Captopril: a new treatmentfor rheumatoid arthritis?. Lancet. 1984;1:1325-1328.

22. Flammer AJ, Sudano I, Hermann F, et al. Angiotensin-convertingenzyme inhibition improves vascular function in rheumatoid arthritis.Circulation. 2008;117:2262-2269.

23. Boers M, Nurmohamed MT, Doelman CJA, et al. Influence ofglucocorticoids and disease activity on total and high density lipoproteincholesterol in patients with rheumatoid arthritis. Ann Rheum Dis.2003;62:842-845.

24. Yoo W. Dyslipoproteinemia in patients with active rheumatoid arthritis:effects of disease activity, sex, and menopausal status on lipid profiles.J Rheumatol. 2004;31:1746-1753.

25. Georgiadis AN, Papavasiliou EC, Lourida ES, et al. Atherogenic lipidprofile is a feature characteristic of patients with early rheumatoidarthritis: effect of early treatment – a prospective, controlled study.Arthritis Res Ther [serial on the internet]. 2006 Apr [cited 2008 May28];8(3):R82 [about 9 p.]. Web site: http://arthritis-research.com/content/8/3/R82.

26. Dessein PH, Joffe BI, Stanwix A, et al. The acute phase response doesnot fully predict the presence of insulin resistance and dyslipidemia ininflammatory arthritis. J Rheumatol. 2002;29:462-466.

27. McCarey DW, McInnes IB, Madhok R, et al. Trial of atorvastatin inrheumatoid arthritis (TARA): double-blind, randomized placebo-controlled trial. Lancet. 2004;363:2015-2021.

28. Maki-Petaja KM, Booth AD, Hall FC, et al. Ezetimibe and simvastatinreduce inflammation, disease activity, and aortic stiffness and improveendothelial function in rheumatoid arthritis. J Am Coll Cardiol.2007;50:852-858.

29. Park Y, Choi HK, Kim M, et al. Effects of antirheumatic therapy onserum lipid levels in patients with rheumatoid arthritis: a prospectivestudy. Am J Med. 2002;113:188-193.

30. Becker DM, Chamberlain B, Swank R, et al. Relationship betweencorticosteroid exposure and plasma lipid levels in heart transplantrecipients. Am J Med. 1988;85:632-638.

31. Fernandez-Miranda C, Guijarro C, De La Calle A, et al. Lipidabnormalities in stable liver transplant recipients: effects ofcyclosporine, tacrolimus, and steroids. Transpl Int. 1998;11:137-142.

32. Wallace DJ, Metzger AL, Stecher VJ, et al. Cholesterol lowering effectof hydroxychloroquine in patients with rheumatic disease: reversal ofdeleterious effects of steroids. Am J Med. 1990;89:322-326.

33. Munro R, Morrison E, McDonald AG, et al. Effect of diseasemodifying agents on the lipid profiles of patients with rheumatoidarthritis. Ann Rheum Dis. 1997;56:374-377.

34. Vis M, Nurmohamed MT, Wolbink G, et al. Short term effects ofinfliximab on the lipid profile in patients with rheumatoid arthritis. JRheumatol. 2005;32:252-255.

35. Popa C, Netea MG, Radstake T, et al. Influence of anti-tumour necrosisfactor therapy on cardiovascular risk factors in patients with activerheumatoid arthritis. Ann Rheum Dis. 2005;64:303-305.

36. Popa C, van den Hoogen FHJ, Radstake TRDJ, et al. Modulation of

lipoprotein plasma concentrations during long-term anti-TNF therapy inpatients with active rheumatoid arthritis. Ann Rheum Dis.2007;66:1503-1507.

37. Simard JF, Mittleman MA. Prevalent rheumatoid arthritis and diabetesamong NHANES III participants aged 60 and older. J Rheumatol.2007;34:469-473.

38. Liao KP, Gunnarsson M, Källberg H. Specific association of type 1diabetes mellitus with anti-cyclic citrullinated peptide-positiverheumatoid arthritis. Arthritis Rheum. 2009;60:653-660.

39. Svenson KL, Pollare T, Lithell H, et al. Impaired glucose handling inactive rheumatoid arthritis: relationship to peripheral insulin resistance.Metabolism. 1988;37:125-130.

40. Dessein PH, Joffe BI. Insulin resistance and impaired beta cell functionin rheumatoid arthritis. Arthritis Rheum. 2006;54:2765-2775.

41. Dessein PH, Joffe BI, Stanwix AE, et al. Glucocorticoids and insulinsensitivity in rheumatoid arthritis. J Rheumatol. 2004;31:867-874.

42. La Montagna G, Cacciapuoti F, Buono R, et al. Insulin resistance is inindependent risk factor for atherosclerosis in rheumatoid arthritis. DiabVasc Dis Res. 2007;4:130-135.

43. Dessein PH, Joffe BI, Stanwix AE. Effects of disease modifying agentsand dietary intervention on insulin resistance and dyslipidemia ininflammatory arthritis: a pilot study. Arthritis Res. 2002;4(6):R12.Epub 2002 Sep 16.

44. Gonzalez-Gay MA, De Matias JM, Gonzalez-Juanatey C, et al. Anti-tumor necrosis factor-alpha blockade improves insulin resistance inpatients with rheumatoid arthritis. Clin Exp Rheumatol. 2006;24:83-86.

45. Tam LS, Tomlinson B, Chu TT, et al. Impact of TNF inhibition oninsulin resistance and lipid levels in patients with rheumatoid arthritis.Clin Rheumatol. 2007;26:1495-1498.

46. Oguz FM, Oguz A, Uzunlulu M. The effect of infliximab treatment oninsulin resistance inpatients with rheumatoid arthritis. Acta Clin Belg.2007;62:218-222.

47. Rosenvinge A, Krogh-Madsen R, Baslund B, et al. Insulin resistanceinpatients with rheumatoid arthritis: effect of anti-TNF alpha therapy.Scand J Rheumatol. 2007;36:91-96.

48. Wasko MCM, Hubert HB, Lingala VB, et al. Hydroxychloroquine andrisk of diabetes in patients with rheumatoid arthritis. JAMA.2007;298:187-193.

49. Costenbader KH, Feskanich D, Mandl LA, et al. Smoking intensity,duration, and cessation, and the risk of rheumatoid arthritis in women.Am J Med. 2006;119:503-511.

50. Stolt P, Bengtsson C, Nordmark B, et al. Quantification of the influenceof cigarette smoking on rheumatoid arthritis: results from a populationbased case-control study, using incident cases. Ann Rheum Dis.2003;62:835-841.

51. Mattey DL, Brownfield A, Dawes PT. Relationship between pack-yearhistory of smoking and response to tumor necrosis factor antagonists inpatients with rheumatoid arthritis. J Rheumatol. 2009;36:1180-1187.

52. Chung CP, Oeser A, Raggi P, et al. Increased coronary-arteryatherosclerosis in rheumatoid arthritis. Arthritis Rheum. 2005;52:3045-3053.

53. Gonzalez A, Maradit Kremers H, Crowson CS, et al. Do cardiovascularrisk factors confer the same risk for cardiovascular outcomes inrheumatoid arthritis patients as in non-rheumatoid arthritis patients?Ann Rheum Dis. 2008;67:64-69.

54. Wolfe F. The effect of smoking on clinical, laboratory, and radiographicstatus in rheumatoid arthritis. J Rheumatol. 2000;27:630-637.

55. Albano SA, Santana-Sahagun E, Weisman MH. Cigarette smoking andrheumatoid arthritis. Semin Arthritis Rheum. 2001;31:146-159.

56. Turesson C, Schaid DJ, Weyand CM, et al. Association of HLA-C3 andsmoking with vasculitis in patients with rheumatoid arthritis. ArthritisRheum. 2006;54:2776-2783.

57. Goodson NJ, Wiles NJ, Lunt M, et al. Mortality in early inflammatorypolyarthritis. Arthritis Rheum. 2002;46:2010-2019.

58. Turesson C, McClelland RL, Christianson TJH, et al. Severe extra-articular disease manifestations are associated with an increased risk offirst ever cardiovascular events in patients with rheumatoid arthritis.Ann Rheum Dis. 2007:66:70-75.

59. McDougall J, Bruce B, Spiller G, et al. Effects of a very low-fat, vegandiet in subjects with rheumatoid arthritis. J Altern Complement Med.2002;8:71-75.

60. Hafstrom I, Ringertz B, Spangberg A, et al. A vegan diet free of glutenimproves the sign and symptoms of rheumatoid arthritis: the effects on

arthritis correlate with a reduction in antibodies to food antigens.Rheumatology (Oxford). 2001;40:1175-1179.

61. McKellar G, Morrison E, McEntegart A, et al. A pilot study of aMediterranean-type diet intervention in female patients with rheumatoidarthritis living in areas of social deprivation in Glasgow. Ann RheumDis. 2007;66:1239-1243.

62. Cleland LG, James MJ, Proudman SM. The role of fish oils in thetreatment of rheumatoid arthritis. Drugs. 2003;63:845-853.

63. Kris-Etherton PM, Harris WS, Appel LJ. Fish consumption, fish oil,omega-3 fatty acids, and cardiovascular disease. Circulation.2002;106:2747-2757.

64. Marchioli R, Barzi F, Bomba E, et al. Early protection against suddendeath by n-3 polyunsaturated fatty acids after myocardial infarction.Circulation. 2002;105:1897-1903.

65. Van den Ende CHM, Breedveld FC, le Cessie S, et al. Effect ofintensive exercise on patients with active rheumatoid arthritis: arandomised clinical trial. Ann Rheum Dis. 2000;59:615-621.

66. Häkkinen A, Hannonen P, Nyman K, et al. Effects of concurrentstrength and endurance training in women with early or longstandingrheumatoid arthritis: comparison with healthy subjects. ArthritisRheum. 2003;49:789-797.

67. Neuberger GB, Aaronson LS, Gajewski B, et al. Predictors of exerciseand effects of exercise on symptoms, function, aerobic fitness, anddisease outcomes of rheumatoid arthritis. Arthritis Rheum.2007;57:943-952.

68. de Jong Z, Munneke M, Zwinderman AH, et al. Is a long-term high-intensity exercise program effective and safe in patients with rheumatoidarthritis? Arthritis Rheum. 2003;48:2415-2424.

69. Munneke M, de Jong Z, Zwinderman AK, et al. Effect of a high-intensity weight-bearing exercise program on radiologic damageprogression of the large joints in subgroups of patients with rheumatoidarthritis. Arthritis Rheum. 2005;53:410-417.

70. Hafström I, Rohani M, Deneberg S, et al. Effects of low-doseprednisolone on endothelial function, atherosclerosis, and traditionalrisk factors for atherosclerosis in patients with rheumatoid arthritis – arandomized study. J Rheumatol. 2007;34:1810-1816.

71. Wei L, MacDonald TM, Walker BR. Taking glucocorticoid byprescription Is associated with subsequent cardiovascular disease. AnnIntern Med. 2004;141:764-770.

72. Davis JM, Maradit Kremers H, Crowson CS, et al. Glucocorticoids andcardiovascular events in rheumatoid arthritis. Arthritis Rheum.2007;56:820-830.

73. U.S. Food and Drug Administration [homepage on the internet]. FDANews: FDA issues public health advisory on vioxx as its manufacturervoluntarily withdraws the product; 2004. http://www.fda.gov/bbs/topics/news/ 2004/NEW01122.html accessed May 27, 2008.

74. Juni P, Nartey L, Reichenbach S, et al. Risk of cardiovascular events androfecoxib: cumulative meta-analysis. Lancet. 2004;364:2021-2029.

75. White WB, West CR, Borer JS, et al. Risk of cardiovascular events inpatients receiving celecoxib: a meta-analysis of randomized clinicaltrials. Am J Cardiol. 2007;99:91-98.

76. Johnsen SP, Larsson H, Tarone RE, et al. Risk of hospitalization formyocardial infarction among users of rofecoxib, celecoxib, and otherNSAIDs. Arch Intern Med. 2005;165:978-984.

77. McGettigan P, Henry D. Cardiovascular risk and inhibition ofcyclooxygenase. JAMA. 2006;296:1633-1644.

78. Catella-Lawson F, Reilly MP, Kapoor SC, et al. Cyclooxygenaseinhibitors and the antiplatelet effects of aspirin. N Engl J Med.2001;345:1809-1817.

79. Maradit-Kremers H, Nicola PJ, Crowson CS, et al. Cardiovasculardeath in rheumatoid arthritis. Arthritis Rheum. 2005;52:722-732.

80. Jacobsson LTH, Turesson C, Hanson RL, et al. Joint swelling as apredictor of death from cardiovascular disease in a population study ofPima Indians. Arthritis Rheum. 2001;44:1170-1176.

81. Banerjee S, Compton AP, Hooker RS, et al. Cardiovascular outcomes inmale veterans with rheumatoid arthritis. Am. J. Cardiol.2008;101:1201-1205.

82. Galarraga B, Khan F, Kumar P, et al. C-reactive protein: the underlyingcause of microvascular dysfunction in rheumatoid arthritis.Rheumatology (Oxford). 2008;47:1780-1784.

83. López-Longo FJ, Oliver-Miñarro D, de la Torre I, et al. Associationbetween anti-cyclic citrullinated peptide antibodies and ischemic heart

disease in patients with rheumatoid arthritis. Arthritis Rheum.2009;61:419-424.

84. Van Halm VP, Nurmohamed MT, Twisk JWR, et al. Disease-modifyingantirheumatic drugs are associated with a reduced risk forcardiovascular disease in patients with rheumatoid arthritis: a casecontrol study. Arthritis Res Ther [serial on the internet]. 2006 Sep[cited 2008 May 28];8(5):R151 [about 8 p.]. Web site: http://arthritis-research.com/content/8/5/R151.

85. Jacobsson LT, Turesson C, Gulfe A, et al. Treatment with tumornecrosis factor blockers is associated with a lower incidence of firstcardiovascular events in patients with rheumatoid arthritis. JRheumatol. 2005;32:1213-1218.

86. Choi HK, Hernán MA, Seeger JD, et al. Methotrexate and mortality inpatients with rheumatoid arthritis: a prospective study. Lancet.2002;359:1173-1177.

87. Cardillo C, Schinzari F, Mores N, et al. Intravascular tumor necrosisfactor alpha blockade reverses endothelial dysfunction in rheumatoidarthritis. Clin Pharmacol Ther. 2006;80:275-281.

88. Bilsborough W, Keen H, Taylor A, et al. Anti-tumour necrosis factor-alpha therapy over conventional therapy improves endothelial functionin adults with rheumatoid arthritis. Rheumatol Int. 2006;26:1125-1131.

89. Solomon DH, Avorn J, Katz JN, et al. Immunosuppressive medicationsand hospitalization for cardiovascular events in patients with rheumatoidarthritis. Arthritis Rheum. 2006;54:3790-3798.

90. Naranjo A, Sokka T, Descalzo MA, et al. Cardiovascular disease inpatients with rheumatoid arthritis: results from the QUEST-RA study.Arthritis Res Ther. 2008;10(2):R30. Epub 2008 March 6.


n i PV PMT FV

STO RCL % f g

ENTER CHS x y>< CLx

CustomizedAsset ManagementIf you have $500,000 or more to invest, we invite your inquiry as to our investment record, background, and fee structure. Call us at 601-982-4123 or 1-800-844-4123 or visit our web-site at www.medleybrown.com

Fee Only Financial Advisors

MEDLEY & BROWNF I N A N C I A L A D V I S O R S

P.O. Box 16725Jackson, MS 39236-6725795 Woodlands Parkway, Suite 104Ridgeland, MS 39157601- -800-844-4123Fax 601-366-0013www.medleybrown.com

Contact: Collier SimpsonBedford Realty 601-506-6622

[email protected]

NOW PRELEASING PROFESSIONAL OFFICE SPACEPremier Madison Office Space

Highland Colony Parkway Near Baptist Complex

Expect more financial health for your practice and your portfolio.At Regions, we understand the medical fi eld. We realize that you face daily challenges such as the continual reductions in reimbursement rates. When you turn to Regions as your banking partner, you get easy access to some of the nation’s leading medical-fi nance professionals. In addition, we offer products designed for individuals in the medical industry. Enjoy special pricing on premium personal and business checking accounts, merchant services and special offers on home equity lines of credit,* unsecured lines of credit and access to a specialized mortgage product built just for your needs. Call Regions today, and see why it’s time to expect more.

1.800.regions | regions.com

© 2010 Regions Bank. Opening deposit varies by account type. Credit approval and other restrictions may apply. All accounts subject to the terms and conditions of the Regions Deposit Agreement. Offer subject to approval, including credit approval. *For properties in Texas, Regions must receive a valid real estate lien under Article XVI, Section 50(a)(6) of the Texas Constitution.



An 11-year-old African American male presented to

Emergency Department (ED) via ambulance with

complaint of seizure. He reported being unaccom-

panied during the seizure described as loss of consciousness for

about a minute. History of present illness revealed this was his “sec-

ond 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 hypocal-

cemia. The patient was stable, and family medicine was consulted

for admission.

Causes of hypocalcemia are numerous (Figure 1) in an 11-year-

old male with possible seizures.1 I worry about tetany and risk of laryn-

gospasm secondary to hypocalcemia as the likely cause of the patient’s

“seizure” episodes. Serum prolactin (PRL) concentrations can be in-

formative, as elevated PRL can reflect mid-brain lesions and be ele-

vated 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 treat-

ment 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-

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

• CLINICAL PROBLEM-SOLVING •

Pseudo Seizures Vs Pseudo Zebra

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

AUTHOR INFORMATION: D. Mark Pogue, MD†, Family Medicine Resident and George Moll,Jr., MD, PhD, Professor Pediatrics and Chief Pediatric Endocrinology, University ofMississippi Medical Center.

CORRESPONDING AUTHOR: Judith G. Gearhart, MD, Professor of Family Medicine,University of Mississippi Medical Center, 2500 North State St., Jackson, MS 39216

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

FIGURE 1: HYPOCALCEMIA – DIAGNOSTIC PATHWAYS

Low Serum Calcium – Confirmed with ionized Calcium and/or serum protein

concentrations

High Creatinine/BUN

Renal Failure High Serum Low/Normal Serum

Phosphorous Phosphorous

Low Urine High Urine High Urine

Low Urine

Phosphorous Phosphorous Calcium

Calcium

Functional PTH Deficiency Functional Vit D

deficiency

Normal Alkaline Phosphatase Elevated Alkaline

Phosphatase

(normal for bone/age) (normal for bone/age)

No Clinical Rickets Clinical Rickets

Low PTH or High PTH High PTH High PTH High PTH

High PTH

Inappropriate

“Normal” PTH

Severe Activating Excessive RTA

Hypo- Calcium Receptor Phosphorous

Magnesemia Mutations Load - Vit. D deficiency

Calcium

(<1.0 mg/dL) (High urine Tumor Lysis, Vit. D resistance

Sequestration

Calcium) Excessive VDDR types 1,2

“Hungry

Phosphorous

Bone

Intake

Syndrome”

Hypo-PTH PTH Resistance Malabsorption

Transient, PHP Liver Disease

Familial, Drugs

Autoimmune,

2nd

to metabolic disease

PHP – Diagnostic Pathways

PTH TEST: determine PTH stimulated plasma or urinary cAMP, TmP/GFRPHP type 2 – cAMP equivocal or normal, TmP/GFR decreasedPHP 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


adolescence, accounting for only about 1% of pediatric ED visits.

Though most are benign, neurologic imaging in the ED should be con-

sidered.5

On physical examination the patient had temperature, pulse

and blood pressure normal for age. His tongue protruded in mid-

line without lesions. He had normal cardiac, pulmonary, abdomen

and musculoskeletal examinations. His neurologic examination re-

vealed 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 glu-

cose, negative urine drug screen and normal computed tomogra-

phy (CT) of the head. An electroencephalogram (EEG) was

scheduled in 2 weeks.

The normal CT from 6 weeks earlier is reassuring and not in-

dicative of acute hemorrhage or stroke though a head magnetic reso-

nance 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 hypocal-

cemia.

A repeat serum calcium concentration was 5.8 mg/dL. His

serum albumin and magnesium concentrations were within nor-

mal limits. An electrocardiogram (EKG) indicated borderline pro-

longed 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 can-

not 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

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 ele-

mental 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 hypocal-

cemia. His normal blood urea nitrogen, creatinine, potassium and elec-

trolyte 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 delin-

eating 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 in-

tact PTH was 297 pg/mL (reference 15-65 for normal range serum

calcium). The post infusion serum ionized calcium was still criti-

cally 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 phos-

phorous was 5.2 mg/dL (reference 3.0-6.8 with normal serum cal-

cium). His TSH was normal for age.

Intravenous and oral infusions of calcium to achieve daily main-

tenance (50 mg elemental calcium per kilogram body weight per day)

should raise serum calcium for up to 3 hours.7 Our patient’s serum cal-

cium 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

†Dr. Pogue died February 11, 2009.

Dr. Mark Pogue attended elementary school in Columbus, MS. He was an EagleScout at age 15. After graduation from Neshoba Central High School in Philadelphia in1990, Mark had several occupations. He was a mechanic, factory worker and inconstruction 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 LaboratoryMedicine in 1995. He worked in the lab until he decided to venture into physician practicemanagement and recruitment. He worked at Neshoba County General Hospital asDirector of Physician Services until he enrolled in medical school in 2002. Dr. Pogue’sdream of becoming a doctor took him to the Caribbean, then England where he graduatedfrom St. Christopher’s College of Medicine in 2005. Dr. Pogue served his fourth yearmedical school training at Emory University, and Johns Hopkins and Habor Hospital inBaltimore, MD.

Dr. Pogue entered residency training in the Department of Family Medicine at theUniversity of Mississippi Medical Center in 2006. At UMMC, Dr. Pogue was awardedthe “Gary W. Jefcoats” teaching award for residents who exemplify outstanding teachingcharacteristics in the areas of medical student, resident, and patient education. Uponcompletion of his residency in 2009, Dr. Pogue planned to practice family medicine inrural Dewitt, Arkansas.

Dr. Pogue was an extraordinary person who touched the lives of everyone he met;he is deeply missed.

Mark Pogue, MDSketch by Judith G. Gearhart, MD


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 phos-

phate. Head MRI + contrast and EEG should assist exclusion of cen-

tral nervous system (CNS) anomalies contributing to seizures. My

impression is secondary hyperparathyroidism due to hypocalcemia

likely encouraged by preexisting vitamin D deficiency and poor cal-

cium 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 activ-

ity 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 defi-

ciency. Hypocalcemia due to dietary vitamin D deficiency is more com-

mon 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 in-

consistent 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 meta-

bolic 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 addi-

tional 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, albu-

min 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 hyper-

parathyroid, 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 gen-

eralized 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 cal-

cium 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 af-

fect 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 as-

sisted by liquid calcitriol 0.25 mcg TID, calcium carbonate sus-

pension 1875 mg divided TID and a chewable multi-vitamin added

to a regimen of oxcarbazepine (Trileptial) at 10 mg/kg BID. A pe-

diatric general clinic report from 7 years prior to this ED presen-

tation indicated normal serum calcium concentration 9.8 mg/dL.

Our patient’s history with lack of familial seizure disorder is con-

sistent with tetany induced seizures rather than rolandic epilepsy. Nor-


mal serum calcium 7 years prior to this hospitalization is also consis-

tent with an acquired rather than a congenital cause. The inherited de-

fect of PHP type 2 is not known and some cases are considered acquired

with severe vitamin D deficiency. Our patient’s pending vitamin D ana-

logues 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 horizon-

tal 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. De-

spite weight-based oxcarbazepine, neuromuscular excitability persists.

Cognitive deficits, neuropsychiatric abnormalities and extra-pyrami-

dal 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 men-

tation and development of dental abnormalities over the past 6 months

supports the development of his hypocalcemia over at least this 6-

month interval.

A rare target organ (kidney) resistance to vitamin D can cause

hypercalcuria despite hypocalcemia.12,13 This may contribute to our pa-

tient’s slow recovery from hypocalcemia. VDDR type 1 is character-

ized by target organ resistance due to vitamin D receptor defect. VDDR

usually presents in children under age 3 years but some present in ado-

lescents. 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 as-

sist consideration of VDDR.14 I will again consult pediatric en-

docrinology 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 cal-

cium 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 en-

docrinologist agreed with therapy and recommended not dis-

charging 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 supplemen-

tation 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

this patient’s phosphorous is increasing, vitamin D deficiency with sec-

ondary hyperparathyroidism in the presence of PHP is more likely than

VDDR.

Hyperparathyroidism has an inhibitory effect on phosphate re-

absorption in the renal tubule; therefore, the patient’s elevated phos-

phorus 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 phos-

phaturic 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 ana-

logues returned very low total 25OH-vitamin D (calcifediol) <4 (20-

100ng/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 con-

sistent 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 con-

centration 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 con-

centrations 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 de-

ficiency rather than a distinct entity, implying prolonged vitamin D de-

ficiency 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 par-

ents to complete one more calcium infusion and a 24-hour urine

calcium assessment prior to his discharge with attention to his ap-

pointment with endocrinologist in only 2 days. An additional 30

cc’s of calcium gluconate was infused. The serum calcium concen-

tration rose to 7.0 mg/dL, and our patient was discharged home in

guarded condition. He was instructed to continue calcium carbon-

ate 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 24-

hour urine calcium was low at 17 mg/24 hours (100-300 mg).


I am extremely uncomfortable with the patient leaving the hos-

pital. If I allow the parents to sign him out against medical advice, the

patient will not receive the additional infusion needed because his cal-

cium is much lower than the recommended 7.0 mg/dL or greater. Pe-

diatric endocrinology confirms his follow-up appointment. The

decreased 24-hour urine calcium excretion reaffirms the patient is re-

taining urinary calcium and does not support VDDR type 2.

The pediatric endocrinologist’s clinic note 3 days later indi-

cated 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, magne-

sium and glucose concentrations were all normal. The parents were

counseled on lifelong compliance to reduce his risks for life threat-

ening hypocalcemia. The patient was continued on current liquid

medicines at adjusted doses to achieve therapeutic goals. The pa-

tient was to follow up in 1 month with the endocrinologist. Subse-

quent laboratory analysis revealed improving 25OH-vitamin D and

normal calcium, 17 ng/mL and 9.7 mg/dL, respectively. Oxcar-

bazepine was discontinued, and seizure activity ceased with nor-

malization of serum calcium. The patient’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 pres-

ence of PHP that is proposed to develop with prolonged vitamin D de-

ficiency. The resistance to PTH found in PHP type 2 results in

hyperphosphatemia. However, our patient’s elevated calcitriol prior to

exogenous treatment indicates a normal renal 1alpha-hydroxylase re-

action response to elevated PTH. Once replacement occurred via cal-

citriol and calcium supplementation, the patient’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 pro-

duction 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

Acknowledgment: We are grateful to William Nicholas, MD, for re-view of this manuscript.

REFERENCES1. Diaz R. Calcium Disorders in Children and Adolescents. In: Pediatric

Endocrinology, 5th edition, Section IV: Disorders of Calcium andMineral Metabolism. Lifshitz F (Ed), Informa Healthcare, New York2009; pp.475-495

2. Chen DK, So YT, Fisher RS. Use of serum prolactin in diagnosingepileptic seizures: Report of the Therapeutics and TechnologyAssessment Subcommittee of the American Academy of Neurology.Neurology, Sep 2005;65:668-675.

3. McLeod KA. Syncope in children. Arch Dis Child. 2003;88:350-353.4. Boehm KE, Morris EJ, Kip KT, Karas B, Grubb BP. Diagnosis and

management of neurally mediated syncope and related conditions inadolescents. J Adolesc Health. 2001;28:2-9.

5. Gordon TA, Moodie DS, Passalacqua M, et al. A retrospective analysisof the cost-effective workup of syncope in children. Cleve Clin J Med.1987;54:391–394.

6. Harden CL. Pseudoseizures and dissociative disorders: a commonmechanism involving traumatic experiences. Seizure. 1997;6:151–155.

7. Tohme JF, Bilezikian JP. Hypocalcemic emergencies. Endocrinol MetabClin North Am. 1993;22:363-375.

8. Desai TK, Carlson RW, Geheb MA. Prevalence and clinical implicationsof hypocalcemia in acutely ill patients in a medical intensive caresetting. Am J Med. 1988;84:209-214.

9. Swash M, Rowan AJ. Electroencephalographic criteria of hypocalcemiaand hypercalcemia. Arch Neurol. 1972;26:218-228.

10. Gupta MM. Medical emergencies associated with disorders of calciumhomeostasis. J Assoc Physicians India. 1989;37:629-631.

11. Becker KL. Calcium and Bone Metabolism Principles and Practice ofEndocrinology and Metabolism, 2nd ed. JB Lippincott, 1995.pp.452

12. Kumar R. Vitamin D and calcium transport. Kidney Int. 1991;40:1177-1189.

13. Slatopolsky, E; Robson, AM; Elkan, I; Bricker, NS. Control ofphosphate excretion in uremic man. J Clin Invest. 1968 Aug;47(8):1865–1874.

14. Murer H, Lotscher M, Kaissling B, Levi M, Kempson SA, Biber J.Renal brush border membrane Na/Pi-cotransport: molecular aspects inPTH-dependent and dietary regulation. Kidney Int. 1996 Jun;49(6):1769-1773.

15. Abugassa S, Nordenstrom J, Eriksson S, Sjoden G. Bone mineraldensity in patients with chronic hypoparathyroidism. J Clin EndocrinolMetab. 1993;76:1617-1621.

We specialize in the business of healthcare

Rachel Aultman Connie Derhgawen Jean Hill Nancy Lindstrom Jeanne Morrison Gelinda Barrett Kathy Fletcher Danita Horne Brinda ManiSundaram Sondra Pinson Rachel Becker Amy Gammel Angela Ladner Eileene McRae Mollie Pontius Kathy Carmichael Shoba Gaymes Louise Lampton Melanie Moore Brenda Sumrall Smith Peggy Crawford Cathy Gersh Nancy Leader Karen Morris Donna Witty

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.

Wishing You A

Happy Doctors’ Day

From your Mississippi State Medical Association Alliance Board

March 30, 2010


• PRESIDENT’S PAGE •

Pigs Have Already Flown


The 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

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.

RANDY EASTERLING, MD2009-10 MSMA PRESIDENT


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, MDPresident, Mississippi State Medical Association

The 142nd Annual Session of

the MSMA House of

Delegates and Medical

Affairs Forum 2010

will be held

June 3-6, 2010in Natchez.

MarkYour

Calendar!

• EDITORIALS •

There is a Tide in the Affairs of Men

The importance of this moment to the future of the practice of medicine in the United States cannot be over-emphasized. The abrupt demise of Obamacare, punctuated by the senatorial election in Massachusetts, was asunexpected 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 theprofession is no less a legitimate concern now than it was before the deflation of the Reid-Pelosi balloon. Neither should anyonebe deluded that the issue of health care reform has been dealt a fatal blow. All major players seem to agree that the current systemhas deep flaws in terms of access and cost. The receding waters of support for the Democratic plan very likely only portend atsunami 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 theresources to mount an effective campaign on such short notice. The AMA, I believe, is not beyond redemption in spite of itsrecent obsequious courting of the political power structure when passage of a Democratic crafted plan of some sort seemedinevitable. Now is an unexpected opportunity to start all over because previous leadership has been discredited and all players aremomentarily 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 allpeople should have access to health care regardless of ability to pay. To meet this assumed societal obligation, it shouldn’t benecessary to create yet another bureaucracy. The problems of the uninsured, catastrophic illness, etc., can be effectively andefficiently addressed simply by adjusting eligibility requirements and reimbursement rates in the Medicaid program. As a separateissue, the escalating cost of health care must be confronted. The rate of increase in recent years cannot be sustained in the longrun. The process of controlling costs is bound to be painful to physicians and all other providers, but who is better qualified to setpriorities and oversee the maintenance of quality than medical practitioners? This is a burden that the profession had betterassume expeditiously and effectively or else the voyage of the rest of the professional lives of this and future generations ofphysicians is likely to be bound in the shallows and the misery of a government operated health care system.

—W. Lamar Weems, MDPast 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 shouldbe 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 arewriting 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 publishstreet 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 [email protected] or mail to the Journal office at MSMA headquarters: P.O. Box 2548,Ridgeland, MS 39158-2548.

There is a tide in the affairs of men which, taken at the flood, leads on to fortuneomitted, all the voyage of their life is bound in shallows and in misery.

JULIUS CEASAR— Shakespeare


The 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 JournalMSMA 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!

The Great Myth


• EDITORIALS •

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, MSMAChair, MSMA Committee on Publications


BlueCross BlueShieldof Mississippi

Committed to a Healthier Mississippi.

• I Q H •

1-800-784-8669 = QUITNOW

Physicians have often termed tobacco cessation counseling for their patients as a “no brainer.” Many patientsvery addicted to nicotine often need more than an admonition to stop their use of tobacco. That’s where theMississippi 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 willallow 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 acaller reports any conditions that may inhibit or question the use of nicotine replacement products or medications, aMedical Clearance Form is sent to the physician. In these cases, no products will be distributed without a medical clearanceform 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 behaviorchange 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 PamelaLuckett, Mississippi Tobacco Quitline manager, at 601-957-1575 ext. 212 or 1-800-784-8669.

Regional Centers for Certified EHRs

The Office of the National Coordinator for Health Information Technology (ONC) recently released a fundingopportunity titled the American Recovery and Reinvestment Act of 2009, Health Information TechnologyExtension Program: Regional Centers.

To enable priority primary care providers throughout the nation to move rapidly, effectively and efficiently towardsthe objective of achieving meaningful use of certified EHRs, ONC will identify, through merit-based selection, applicantsqualified to serve as Regional Centers.

It is expected that each regional center will provide federally supported individualized technical assistance to aminimum 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 careproviders 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 fullapplications from each cycle will result in four-year cooperative agreements. Cycle one applicants were to be notified atthe end of January 2010 with cycle two applicants notified by March 31, 2010.

—James S. McIlwain, MD IQH President


Last 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.”

• PLACEMENT/CLASSIFIED •

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.

DISABILITY DETERMINATION SERVICES

1-800-962-2230

Toll Free 1-800-962-2230

Jackson 601-853-5487

Leola Meyer (Ext. 5487)


• UMMC •

Dr. James Keeton Becomes New Vice Chancellor

Dr. James Keeton

• UNA VOCE •

A Note of Thanks

When 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

In MemoriamRobert “Rob” Walter Bitter

1928 - 2009

[The following note will perhaps explain my lengthy silence andunexplained absence from the pages of the JOURNAL MSMA and particularlythe “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 sentflowers or memorials. I continue receiving cards and calls from time to time asfriends around the state learn belatedly of his loss. There are probably quite afew folks reading even now who were also unaware of Robert’s death. Try as Imight, I could never hope to thank everyone personally and would like to takethe liberty of reaching out to our many physician/spouse friends through thismonth’s column.]

—D.S.


Faster is better. Sometimes you need to get quality life insurance protection for your family - fast.

is the answer.Quick Life offers an excellent selection of personalized life insurance quotes all from highly-rated life insurance companies and offered by MSMA and The Executive Planning Group.Online. Fast. It’s easy to get free life insurance quotes for competitively priced policies. Apply on online. We ask the right questions about your specific objectives and then guide you through the application process. We provide the important information you need to make the right decisions for yourself and your loved ones. If you prefer personal service, Larry Fortenberry and The Executive Planning Group can give you straight answers you need to make informed decisions.Call1-888-285-9477 or visit MSMAquicklife.comShave three to four weeks off the old way of doing business using technology to get you the right protection, right away!

Life Insurance. Quickly.


If you prefer personnaall service, Larry FortenGroup can give you straight answers you needCall1-888-285-9477 or visit MSMAquiLife ILife ILife I

Faster is better. Sometimes you need to get quality life

insurance protection for your family - fast.

is the answer.Quick Life offers an excellent selection of personalized life insurance quotes all from highly-rated life insurance companies and offered by MSMA and The Executive Planning Group.

Online. Fast. It’s easy to get free life insurance quotes for competitively priced policies. Apply on online. We ask the right questions about your specific objectives and then guide you through the application process. We provide the important information you need to make the

right decisions for yourself and your loved ones.

If you prefer personal service, Larry Fortenberry and The Executive Planning Group can give you straight answers you need to make informed decisions.Call1-888-285-9477 or visit MSMAquicklife.com

Shave three to four weeks off the old way of doing business using technology to get you the right protection, right away!



If you prefer personnaall service, Larry FortenGroup can give you straight answers you needCall1-888-285-9477 or visit MSMAqui

Life ILife ILife I

march 2010 jmsma

Documents

s s of f d e d

t i io n of f t d s

t e d s se r

md judith

blossom of t

c i ia reciation of

msma committee

t h ro u g r rough