January 2010 JMSMA

January

VOL. LI

2010

No. 1

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Lucius M. Lampton, MD Editor D. Stanley Hartness, MD Michael O’Dell, MD AssociAtE Editors Karen A. Evers MAnAging Editor PublicAtions coMMittEE Dwalia S. South, MD Chair Philip T. Merideth, MD, JD Martin M. Pomphrey, MD Leslie E. England, MD, Ex-Officio Myron W. Lockey, MD, Ex-Officio and the Editors thE AssociAtion Randy Easterling, MD President Tim J. Alford, MD President-Elect J. Clay Hays, Jr., MD Secretary-Treasurer Lee Giffin, MD Speaker Geri Lee Weiland, MD Vice Speaker Charmain Kanosky Executive Director JOURNAL OF THE MISSISSIPPI STATE MEDICAL ASSOCIATION (ISSN 0026-6396) is owned and published monthly by the Mississippi State Medical Association, founded 1856, located at 408 West Parkway Place, Ridgeland, Mississippi 39158-2548. (ISSN# 0026-6396 as mandated by section E211.10, Domestic Mail Manual).

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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.

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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.

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JAnUArY 2010

VOlUme 51

nUmBer 1

Scientific ArticleS

Abnormal 1 Hour Glucose challenge test followed by a normal 3 Hour Glucose tolerance test: Does it identify Adverse Pregnancy Outcome?

3

Screening for Vitamin D Deficiency in the elderly

7

Suzanne K. Pugh, LT, MC, USNR; Aaron T. Poole, LT, MC, USNR; James B. Hill, COL, MC, USN; Everett F. Magann, CAPT, MC, USN; Suneet P Chauhan, MD and John C. Morrison, MD

Jatupol Kositsawat, MD, DMSc, MPH and Stephen A. Geraci, MD

clinical Problem-Solving: Uncommon but not rare

11

Lynne A. Orozco, MD

SPeciAl Article

2010 Public Health report card

15

PreSiDent’S PAGe

Have a Good night

19

Randy Easterling, MD; MSMA President

eDitOriAl

Start to finish

22

Stanley Hartness, MD; Associate Editor

relAteD OrGAnizAtiOnS Mississippi State Department of Health

27

DePArtmentS

Physicians’ Bookshelf Una Voce Placement/classified

25 31 32

ABOUt tHe cOVer:

“leAf On tHe trAce” - Martin M. Pomphrey, Jr., MD, a semi-retired orthopaedic surgeon sub-

specializing in sports medicine who practiced with Oktibbeha County Hospital (OCH) Bone and Joint Clinic, took this photograph while enjoying a walk at French Camp located on the Natchez Trace. Come winter, the nearby forest depends on the abundance of pines to remain green as the vibrant autumn colors go out in glory as shown by this red leaf of a Sweetgum tree. American Sweetgum (Liquidambar Styraciflua) leaves turn in most cases brilliant orange, red, and purple colors in the fall, and stay on the tree quite late. They have five sharply pointed lobes, but are easily distinguished from maples in being glossy and leathery in appearance, and arranged alternately, not in opposite pairs. The first historical reference to the tree comes from the author and soldier, Don Bernal Diaz del Castillo, who accompanied Cortez in 1519 and was a witness to ceremonies between Cortez and Montezuma, who both partook of a liquid amber extracted from a Sweetgum tree. Once commercially popular for soaps, adhesives and pharmaceuticals, today its wood is valuable for fine furniture and interior finishing. ❒ VOL. LI

January

No. 1

2010

January

VOL. LI

Official Publication of the MSMA Since 1959

january

2010

No. 1

2010 jOurnaL MSMa

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• SCiEnTiFiC arTiCLES •

Abnormal 1 Hour Glucose Challenge Test Followed by a Normal 3 Hour Glucose Tolerance Test: Does it Identify Adverse Pregnancy Outcome?

Suzanne K. Pugh, LT, MC, USNR; Aaron T. Poole, LT, MC, USNR ; James B. Hill, COL, MC, USN; Everett F. Magann, CAPT, MC, USN; Suneet P Chauhan, MD; John C. Morrison, MD

A

intrODUctiOn

BStrAct

Objective: To determine if pregnancies with an abnormal glucose challenge test (GCT) but a normal (GTT) are at increased risk for fetal macrosomia or an adverse pregnancy outcome. Study Design: This prospective observational study matched women with an abnormal glucose challenge test and a normal GTT with the next patient with a normal GCT. Results: Over 12 months, 107 women with abnormal GCT were matched with 107 women with normal GCT. Women with an abnormal GCT were older (27.3 vs 24.7, p = 0.001) and less likely to be African-American (OR = 2.2, 95% CI 1.06-4.49) but no more likely to have an adverse pregnancy outcome. ROC curves could not differentiate between macrosomic vs non-macrosomic newborns using GCT values. Conclusion: Women with an abnormal GCT but a normal GTT are more likely to be older, less likely to be African-American, but no more likely to have an adverse pregnancy outcome or a macrosomic fetus.

KeY WOrDS:

GluCOse ChAllenGe TesT, GluCOse TOleRAnCe TesT, feTAl mACROsOmIA, AdveRse pReGnAnCy OuTCOme

AUtHOr infOrmAtiOn: Dr. Pugh is a 4th year resident and Dr. Poole is a 3rd year resident in Obstetrics and Gynecology at the naval Medical Center, Portsmouth, Virginia. Dr. Hill is a Maternal Fetal Medicine specialist who is also based at the naval Medical Center – Portsmouth and is a collaborator with the university of Mississippi Medical Center on a number of OB-Gyn projects between the uS navy and uMC. Dr. magann is a Clinical Professor of OB-Gyn at the university of Mississippi Medical Center and a former Maternal Fetal Medicine Fellow here at uMC who is currently serving with the uS navy in Portsmouth and is the navy coordinator of all OB-Gyn research between the uS navy and uMC. Dr. chauhan is currently director of Maternal Fetal Medicine at aurora Heath Care in West allis, Wisconsin and is a former MFM fellow at uMC. Dr. morrison is Professor of Obstetrics and Gynecology at the university of Mississippi Medical Center and is the former Chairman of the Department of OB-Gyn. cOrreSPOnDinG AUtHOr: Everett F. Magann, CaPT, MC, uSn, Department of Obstetrics and Gynecology, naval Medical Center - 620 john Paul jones Circle, Portsmouth, Va; Telephone: (757) 953-4293; Facsimile: (757) 953-7350; E-Mail: Everett.magann@med.navy.mil

An association between gestational diabetes, fetal macrosomia and adverse pregnancy outcomes has been observed in cohort studies.1,2 large population based studies have shown an increased risk of adverse neonatal and maternal pregnancy outcomes with pre-gestational and gestational diabetes compared with pregnancies without diabetes.3 The association between diabetes and pregnancy outcomes is strongest with women who have pre-pregnancy diabetes.3 The question arises about the relationship between women with an abnormal 1 hour glucose challenge test (GCT) but a normal 3 hour glucose tolerance test (GTT) and pregnancy outcomes.

A literature search was undertaken in puBmed from 1966 to July 2008 using the search terms “diabetes – gestational, pregnancy outcome, glucose tolerance tests, false positive reactions, prenatal diagnosis, and predictive value of tests.” Three investigations were found which compared pregnancy outcomes in women with a positive GCT and a negative GTT to women with a negative GCT.3,4,5 One study observed that the risk of fetal macrosomia, antenatal death, shoulder dystocia, endometritis, and cesarean delivery was seen more frequently in the group with the positive GCT but negative GTT compared with the women with a negative GCT.3 The other two investigations4,5 found no difference in intrapartum and perinatal outcomes between women with a positive GCT but negative GTT and women with a negative GCT. All 3 of these studies were retrospective in design, and each of the studies used a different threshold for the screening GCT, ≥130,5 ≥135,3 and ≥1404 mg/dl. Two of the studies4,5 used the criteria for the elevated values for the GTT of the Carpenter/Coustan criteria (≥95, ≥180, ≥155, or ≥ 140 mg/dl for fasting, 1 hour, 2 hour, 3 hour tests after the 100g glucose load respectively using plasma glucose). The other study3 used the national diabetes data Group Conversion (nddG) criteria for the elevated values for the GTT (≥100, ≥190, ≥165, or ≥145 mg/dl for fasting, 1 hour, 2 hour, 3 hour tests after the 100g glucose load) respectively, but authors do not state if this was whole blood or plasma january

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glucose. Although two of these studies used the lower cut offs of the Carpenter/Coustan criteria, many clinicians (including those at university of mississippi medical Center) continue to use the national diabetes data Group (nddG) values and the higher cut off of ≥ 140 mg/dl for the diagnosis of a positive GCT. The purpose of this study was to determine in a prospective cohort study if women having an abnormal 1 hour glucose challenge test (≥140 mg/dl as a cutoff) but a normal GTT using the cutoffs of the nddG group were more likely to have a macrosomic fetus and/or an adverse pregnancy outcome than women having a normal 1 hour GCT.

mAteriAlS AnD metHODS This is a prospective observational study performed at the naval medical Center – portsmouth, virginia between January and december of 2006. This military population was chosen for analysis as this population is more consistent with the general mississippi obstetric population outside of the high risk clinics at the university of mississippi in Jackson and more consistent with the military populations in meridian and Biloxi. Women without pre-gestational diabetes (type 1 or type 2) or risk factors such as a history of an abnormal GTT in the past or a history of an adverse pregnancy outcome usually linked with gestational diabetes mellitus and who were undergoing a GCT at 2428 weeks of gestation were eligible for this study. The study was undertaken using a 50g pure glucose load in 150 ml of fluid. The blood glucose was obtained using venous plasma. All women with a 1 hour GCT that was ≥140 mg/dl underwent a 3 hour oral GTT. Gestational diabetes was diagnosed in women with ≥2 abnormal values for the 3 hour oral GTT using the following values: fasting ≥105 mg/dl; 1 hour ≥190 mg/dl; 2 hours ≥165 mg/dl; and 3 hours ≥145 mg/dl (nddG criteria). Women with one abnormal value on the GTT were then matched to the next low-risk patient undergoing a GCT and with a 1 hour of <140 mg/dl. each patient was assigned a study number, and no patient identifiers were on the data collection sheet. This study was approved by our independent ethics committee which in the us navy is the Chief, navy Bureau of medicine and surgery, Washington, d.C., through the local Clinical Investigation program (p05-051).

A sample size was determined based on the risk of not delivering a macrosomia infant in the women with the abnormal GCT. Assuming the likelihood of macrosomia of 10% among patients with one-hour glucola <140, a sample size of 100 in each group has a 80% power to detect an increase of 0.15 with a significance level (alpha) of 0.05 (two-tailed). statistical analysis was done with Instat (san diego, California). for continuous data, the Kolmogorov-smirnov test was used to determine if the data followed Gaussian distribution, and student t-test or mann-Whitney tests were used where applicable. Categorical data were analyzed by chi-square and fisher exact test, as appropriate. Odds ratio (OR) with 95% confidence intervals (CI) were calculated. Receiver – operating characteristic (ROC) curves were constructed for one-hour post glucola and BmI to differentiate between the abnormal (at least 4000g) and normal (less than 4000g) birth weights. Two-by-two contingency tables were created to calculate true and false positive rates for diagnostic tests to differentiate between macrosomic and non-macrosomic newborns. The true positive rate was plotted against the false

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positive rate for an estimate to predict the adverse outcome to develop the ROC curves. The areas under the curves and the standard error (se) were estimated by a point-to-point trapezoidal method of integration.

The critical ratio z test for a paired statistical design was used to determine the statistical significance of the curves.6 If the area under the ROC curve was not significantly different from the area under the nondiagnostic line (y = x or when the false positive and true positive rates were identical), then the diagnostic test was considered to be poor. p <0.05 or 95% CI not crossing integer 1 was considered significant. multiple linear regression was used with macrosomia as the dependent variable and the following 6 independent variables: maternal age (<19, 20-34, 35 years or more), ethnicity (Caucasians, AfricanAmerican, hispanic, and others), nulliparous (yes or no), BmI (normal [<25], overweight [25-29.9] and obese [30 or more]), gestational age (preterm [GA <37 weeks], term [37 to 40.6 weeks] and postterm [41 or more weeks]), intrauterine growth restriction (< vs >10% for GA, using nomograms published by Alexander et al).7 In addition to macrosomia (yes or no), the same independent variables were used, and a second multiple linear regression with admission to nICu as the dependent variable was established. multicollinearity was used to determine if the y-variables were independent. To determine which variables made a significant contribution to the correct macrosomia or to nICu admission, the full model was compared with a simpler model omitting the least significant variable one at a time.

reSUltS Two hundred and fourteen women were recruited for this study (107 women with an abnormal GCT but a normal 3 hour oral GTT and 107 with a normal GCT) between January of 2006 and december of 2006. Compared to women with a normal GCT, women with an abnormal GCT were older (27.3 vs. 24.7, p = 0.001), and there were less likely to be African-American women (OR = 2.2, 95% CI 1.06-4.49).

The number of nulliparous women in each group, body mass index at the first prenatal visit, antepartum complication of hypertension (gestational hypertension or preeclampsia) and the number of antepartum hospitalizations were similar between groups. (Table 1) tABle 1: MaTErnaL DEMOGraPHiCS anD anTEParTuM COMPLiCaTiOnS

Age (years) < 19 20-34 > 35 Ethnicity African-American Caucasians Hispanics Others Nulliparous Body mass index < 24 25-29 > 30 Hypertensive disease Antepartum hospitalization

< 140 N = 107 24.7 +5.0 11% (12) 85% (91) 4% (4)

> 140 N = 107 27.3 +5.2 2% (2) 86% (92) 12% (13)

23% 68% 7% 2% 48% 26.0 52% 26% 21% 7% 3%

12% 72% 9% 7% 64% 27.5 45% 23% 32% 6% 4%

(25) (73) (7) (2) (56) +5.3 (56) (28) (23) (7) (3)

(13) (77) (10) (7) (69) +6.8 (48) (25) (34) (6) (4)

P / OR (95% CI) 0.0001 6.63 (1.45, 30.41) 0.93 (0.43, 1.99) 0.28 (0.09, 0.89) 2.20 0.84 0.68 0.27 0.60 1.35 1.16 0.59 1.18 0.85

(1.06, (0.46, (0.25, (0.35, (0.35, 0.158 (0.79, (0.62, (0.32, (0.38, (0.36,

4.49) 1.50) 1.86) 1.05) 1.05) 2.31) 2.16) 1.09) 3.63) 2.03)

The number of women undergoing cervical ripening prior to labor induction, without cervical ripening, and gestational age at the time of delivery were also similar between the two groups. (Table 2) The neonatal birth weight, number of neonates that were small for gestational age, large for gestational age, had Apgar scores <7 at 5 minutes, an umbilical artery ph <7.0 or the number of neonatal deaths were not different between groups. (Table 2) There were 2 cases of shoulder dystocia, one in the group with an abnormal GCT and the other in the group with a negative GCT. There were no transient or permanent injuries in either neonate. The overall number of newborn intensive care unit admissions was greater in the group with a normal 1 hour GCT (7/107, 7%) compared to the group with the abnormal GCT (2/107, 2%, OR 1.59 95% CI 11.09-2.32). (Table 2)

fiGUre 1: rOC CurVES FOr OnE HOur POST GLuCOLa anD BMi TO iDEnTiFy a MaCrOSOMiC

(≥4000 GraM) FETuS

tABle 2: inTraParTuM anD PErinaTaL COMPLiCaTiOnS

Gestational age (weeks) < 37 37-40.6 > 41 Cervical ripening Labor induction Apgar score < 7 at 5 min Birthweight (g) SGA Birthweight >4,000 g NICU admission RDS Others UApH < 7.00 Neonatal death

< 140 N = 107 39.1 +1.3 5% (5) 86% (92) 9% (10)

> 140 N = 107 38.9 +1.3 7% (7) 88% (94) 6% (6)

P / OR (95% CI) 0.480 0.70 (0.21, 2.28) 0.85 (0.38, 1.88) 1.73 (0.61, 4.96)

12% (13) 25% (27) 3% (3)

7% (8) 16% (17) 2% (2)

1.30 (0.98, 1.73) 1.21 (0.58, 2.49)

3428 + 467 8% (9) 11% (12) 7% (7) 4% (4) 3% (3)

3554 + 540 4% (4) 20% (21) 2% (2) 2% (2) 0

0 1

0 0

0.069 2.36 (0.70, 7.93) 0.52 (0.24, 1.11) 1.59 (1.09,2.32) 0.26 (0.00, 7.28) ----

The 1 hour post glucola and the BmI at first visit were assessed to determine if either could be used as a diagnostic test to identify a macrosomic fetus. A ROC was constructed; it revealed that the area under the ROC curve for one-hour post-glucola (0.42 + 0.05) was not significantly different than for BmI (0.43 + 0.05; p >0.05) and both of them were similar to the area under the non-diagnostic line (p >0.05).

Thus, neither maternal BmI at first visit nor the results of 1 hour GCT can be used as diagnostic tests to identify macrosomic (≥4000g) fetus. (figure 1) Analysis using multiple regression analysis reveals that the only factor that made a significant independent contribution to macrosomia was gestational age at delivery (R2 = 8%; p <0.010). In the analysis of factors that might influence nICu admission, none of the other assessed independent variables made a significant contribution to prediction of nICu admission (p = 0.238).

DiScUSSiOn Gestational diabetes is correlated with an increased risk of fetal macrosomia and adverse pregnancy outcomes when compared to women without gestational diabetes.1,2 studies that compared pregnancy outcomes and the risk of fetal macrosomia in women with a pos-

itive GCT but a negative GTT and the risk of fetal macrosomia and adverse pregnancy outcomes have found conflicting results. Other investigators have compared pregnancy outcomes in women with a positive GCT and one abnormal value of a GTT (2 out of the 4 values must be abnormal for a positive test) to women with a negative GCT. The study by mclaughlin8 found that the risks of cesarean delivery, preeclampsia, chorioamnionitis, birth weight >4000g and admission to a neonatal intensive care unit (nICu) were greater in the group with one abnormal value on the GTT. The study by lindsey9 found that both preeclampsia/eclampsia and macrosomia were more frequently seen in the group with one abnormal value on the GTT compared to women with a negative GCT. Our investigation prospectively compared a cohort of women with a positive GCT but a negative GTT with women with a negative GCT. We found no increased risk of either an abnormal adverse pregnancy outcome or greater risk for macrosomia in women with an abnormal GCT but a normal GTT. like our study, the retrospective cohort study by dudhbhai4 found no difference in rates of macrosomia (7 vs 8 %), shoulder dystocia (0%), or cesarean delivery (20 vs 17%) for those with abnormal 1 hr GCT compared to normal GTT. These findings were also similar to Gumus5 who observed no difference in maternal/fetal outcomes but did observe patient characteristics that put the population with abnormal GCT at risk for the subsequent development of diabetes later in life (family history of diabetes, gestational weight gain). In contrast, stamilio3 found a significant increase in adverse perinatal outcomes including macrosomia (4500g, OR 3.66), antenatal death (OR 4.61), shoulder dystocia (OR 2.85), and cesarean delivery (OR 1.76). however, in the assessment of this data it appears to be unadjusted for maternal complications including higher rates of obesity (OR 1.8), chronic hypertension (OR 2.7), and older age (28.5 vs 25.5) which influence the risk of an adverse perinatal outcome and the risk of macrosomia. By not adjusting for maternal complications, his conclusions become somewhat suspect.3 Additionally stamilio used the lower threshold of ≥130mg/dl (Carpenter/Coustan criteria) rather than the cutoff of 140mg/dl (nddG criteria) for the diagnosis of gestational diabetes. should patients like those in our study be treated even though january

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they do not meet the diagnostic criteria for gestational diabetes by GTT? Treatment of patients with an abnormal GCT but a normal GTT is controversial. Bevier10 randomized patients to an experimental group with diet and intensive glucose monitoring compared to a control group. A reduction in macrosomia from 25% in the treatment group compared with 3% in the control group and a mean reduction in fetal weight of 289 grams were found. however, this study excluded patients from an experimental group who were noncompliant (14 of 49, 29%), thus avoiding those patients with likely the worst control and perhaps influencing the results. We feel that treatment should not be begun unless there is a positive GTT (2 abnormal values).

Our study showed that African American women were less likely than “other women” (white, hispanic and Asian women) to have an abnormal GCT, the opposite of what one usually notes in pregnancy.

The inclusion of Asian and hispanic women along with white women may have lead to this increased risk among the other women as hispanic, Asian, and African American women are all at increased risk for gestational diabetes.11 secondly, the number of active-duty African American women in this study, while increased over numbers found in the general population, are all screened for diabetes prior to entering military service and yearly thereafter and must maintain certain fitness standards. This subset of the African American population then would be less likely to have glucose intolerance than those in the general population, perhaps explaining the paradox.

One of the limitations of this investigation is the number of women recruited, observed, and matched with the next patient with a normal GCT. There was a trend in this study toward increased macrosomia in those patients with abnormal 1 hour GCT (20 vs 11%), (OR 0.52, 95% CI 0.24, 1.11). It is possible that with more patients, a statistically significant difference might have been identified. Also, the difference in rates of obesity (23 vs 34%) might have proved statistically significant with more recruits. This limitation is balanced by the study design being prospective with the recruited women matched to the next patient with a normal 1 hour GCT. Additionally, the management of both groups of women was similar and pre-study power calculation was met. finally, none of the women had their management altered because of a concern for an adverse outcome, and n ROC curves were utilized to detect any links between a GCT, maternal BmI and fetal weight in excess of 4000g. Therefore, it is unlikely that bias played a role in our results.

There is likely a spectrum of glucose intolerance in pregnancy, but the management of patients without a clear diagnosis of gestational

diabetes is unclear. from our study, there appears to be no adverse perinatal complications with an abnormal GCT but normal OGTT. like other studies have shown, these patients may be at higher risk for diabetes later in life. We speculate that pregnancies outside of the indigent population in the university setting would have similar findings as those patients more closely resemble our military population which is a cross section of the us population. future research is required to determine if treating patients with abnormal 1 hour GCT with oral agents and/or insulin can improve perinatal outcomes and prevent macrosomia.

referenceS 1.

langer O, levy J, Brustman l, Anyaegbunam A, merkatz R, divon m.

Glycemic control in gestational diabetes mellitus – how tight is tight enough: small for gestational age versus large for gestational age? Am J Obstet Gynecol. 1989;161:646-53.

Casey Bm, lucas mJ, mcIntire dd, leveno KJ. pregnancy outcomes in 2. women with gestational diabetes compared with the general obstetric population. Obstet Gynecol. 1997;90:869-73.

3. stamilio dm, Olsen T, Ratcliffe s, sehdev hm, macones GA. false positive 1-houir glucose challenge test and adverse perinatal outcomes.

Obstet Gynecol. 2004;103:148-156.

4. dudhbhai m, lim l, Bombard A, Julliard K, meenakshi B, Trachelenberg y, Weiner Z. Characteristics of patients with abnormal glucose challenge test and normal oral glucose tolerance test results: Comparison with normal and gestational diabetic patients. Am J Obstet Gynecol. 2006;194:e42-e45.

5.

Gumus II, Turhan nO. Are patients with positive screening but negative diagnostic test for gestational diabetes under risk for adverse pregnancy outcomes? J Obstet Gynaecol Res. 2008;34:359-63.

6.

Beck JR, schultz eK. The use of relative operating characteristic (ROC) curves in test performance evaluation. Arch Pathol Lab Med. 1986;110:13-20.

7.

Alexander GR, himes Jh, Kaufman RB, mor Joanne, Kogan m. A united states national reference for fetal growth. Obstet Gynecol.

1996;87:163-8.

8. mclaughlin GB, Cheng yW, Caughey AB. Women with one elevated 3hour glucose tolerance test value: Are they at risk for adverse outcomes?

Am J Obstet Gynecol. 2006;194:e16-e19.

9. lindsay mK, Graves W, Klein l. The relationship of one abnormal glucose tolerance test value and pregnancy complications. Obstet Gynecol. 1989;73:103-6.

10. Bevier WC, fischer R, Jovanovic l. Treatment of women with an abnormal glucose challenge test (But a normal oral glucose tolerance test) decreases the prevalence of macrosomia. Am J Perinatol.

1999;16:269-75.

11. American diabetes Association. Gestational diabetes mellitus. Diabetes Cared. 2001;24:s77-79.

Disclaimer: The views expressed in this article are the view of the authors and do not necessarily reflect the official policy or position of the Department of the Navy, Department of Defense, or the US Government.

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• SCiEnTiFiC arTiCLES •

Screening for Vitamin D Deficiency in the Elderly Jatupol Kositsawat, MD, DMSc, MPH; Stephen A. Geraci, MD

A

VitAmin D AVAilABilitY AnD metABOliSm

BStrAct

The importance of vitamin d to normal physiologic function is well established. With deficiency becoming increasingly frequent, the potential for preventing and treating diseases through vitamin d supplementation is gaining in appreciation. deficiency is particularly common in the geriatric population based on both behavioral and biologic factors, and has been associated with increased risk of musculoskeletal, neuropsychiatric, cardiovascular, endocrine and oncologic disease.

Although some experts recommend empiric supplementation for all elderly persons, a strategy of routine screening and documented adequacy of replacement in deficient patients appears superior.

KeY WOrDS:

vITAmIn d defICIenCy, levels, sCReenInG, eldeRly

intrODUctiOn vitamin d deficiency in patients aged ≥65 years has become increasingly common. The national health and nutritional examination survey (nhAnes) 2000-2004 estimated the prevalence at 30-35% for females, and 25-30% for males, over age 70,1 while the longitudinal Aging study Amsterdam (lAsA) found these figures to be 56% and 38% respectively.2 vitamin d serum concentrations depend upon several factors including race/ethnicity, age, gender, sun exposure, obesity, and dietary intake.3 non-hispanic whites have higher average concentrations than non-hispanic blacks, with levels in mexican Americans intermediate between these. The elderly are at higher risk of deficiency, due to a combination of reduced sun exposure, impaired cutaneous ability to synthesize vitamin d, lower dietary intake, reduced hepatic metabolism, and lower tissue responsiveness. females and obese individuals typically demonstrate lower levels and may be at higher risk of deficiency-related disease.4 AUtHOr infOrmAtiOn: Jatupol Kositsawat, mD, DmSc, mPH, Medical Service, G.V. (Sonny) Montgomery Va Medical Center, Division of Geriatric Medicine, university of Mississippi School of Medicine and Stephen A. Geraci, mD, Division of Pulmonary and Critical Care Medicine, university of Mississippi School of Medicine, jackson. cOrreSPOnDinG AUtHOr: jatupol Kositsawat, Medical Service (111), 1500 E. Woodrow Wilson Dr., jackson, MS 39216; Telephone: 601-364-1251, Facsimile: 601-364-1278 Email: jatupol.Kositsawat@va.gov.

There are two forms of vitamin d: d2 (ergocalciferol) and d3 (cholecalciferol).5 The former is synthesized by plants and yeast, the latter in humans by cutaneous synthesis in response to ultraviolet light. dietary sources of d2 include fortified foods and mushrooms, while the best source of d3 is oily fish. exposure of the extremities to direct sunlight for 5-10 minutes produces a mass of vitamin d approximating that from an oral 3000 Iu dose of d3.5 As a dietary supplement, d3 is available over-the-counter (400-10,000 Iu) or in combination with either calcium or alendronate, while d2 is available at the prescription dose of 50,000 Iu. since d2 is only 10-30% as effective as d3 in maintaining serum concentrations of the biologically active form, d3 may be a superior therapeutic formulation.6 Both d2 and d3 are inactive moieties converted through hepatic hydroxylation to calcifediol [25(Oh)d], a storage form of the vitamin, and then to the active calcitriol [1,25 (Oh)2d] via a second hydroxylation primarily in the kidneys. This molecule is then available to bind to vitamin d receptors in most organs and immune cells.

lABOrAtOrY teStinG Blood levels may be measured in either serum or plasma. The 25(Oh)d form is used to assess clinical status and has a serum half-life of ~15 days. Conversely, 1,25(Oh)2d has a ~15 hours half-life; serum concentrations vary with parathyroid hormone (pTh) levels and other variables, leaving its measurement of little use in diagnosing clinical deficiency. Reported levels are most often the sum of 25(Oh)d2 and 25(Oh)d3.7 Although there is no universally accepted serum value which defines vitamin d deficiency, the lower limit of normal is generally considered to be 30 ng/ml8 (optimal range ~36-40 ng/ml). This value was determined from multiple health outcome studies, where lower levels associated with increased disease risk. vitamin d levels are considered marginal (with increased risk of clinical deficiency) at 20-30 ng/ml, frankly deficient between 10-20 ng/ml and severely deficient at <10 ng/ml. This lowest range is most consistently associated with clinical illness. serum pTh should be measured concurrently, since it can be elevated from secondary hyperparathyroidism at vitamin d levels <40 ng/ml and can thus confirm the pathologic nature of reduced vitamin d levels. january

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clinicAl VitAmin D DeficiencY Musculoskeletal System In elderly persons, independent living parallels functional status, determined in part by muscle performance, fall avoidance, bone mass maintenance, and fracture prevention.9 vitamin d deficiency, and the accompanying secondary hyperparathyroidism, causes proximal muscle weakness, increasing the risk of falls.10 Clinical data suggest levels ≥26 ng/ml are needed to maintain muscle performance and limit falls. lAsA determined that elderly persons with levels <20 ng/ml have twice the 3-year incidence of pathologically reduced muscle performance (coordination, proximal muscle strength, and balance).3 A meta-analysis found fall risk was reduced by 22% with 2-36 months of oral vitamin d supplementation, with most dramatic benefits in women receiving active vitamin d analogs.11 vitamin d levels correlate well with Bmd in white patients, but less so in black and hispanic populations.12-13 elderly persons with levels >30 ng/ml are more likely to demonstrate both suppression of pTh release and less frequent nonvertebral factures. data from the Women’s health Initiative suggest that females age 50-79 years with vitamin d levels <19 ng/ml are 71% more likely to suffer hip fractures; pTh and Bmd were not measured in this study however.14 Over an 18 month period, elderly women receiving 800 Iu vitamin d3 plus calcium suffered fewer hip and other non-vertebral fractures; significantly increased serum 25(Oh)d levels, decreased pTh concentrations and increased Bmd were documented.15 This finding was supported by dawson-hughes who showed that daily vitamin d3 (700 Iu) administration for 3 years moderately reduced bone loss and the incidence of non-vertebral fractures.16 Cardiovascular System vitamin d modulates the renin-angiotensin system, vascular smooth muscle and endothelial cells, and when deficient triggers secondary hyperparathyroidism which promotes myocyte hypertrophy and vascular remodeling. deficiency may thus constitute a modifiable risk factor.17 The health professionals follow-up study of men ages 40-75 showed that persons with vitamin d levels <15 ng/ml have twice the 10-year risk of myocardial infarction.18 The framingham Offspring study demonstrated that hypertensive patients with moderate (10-15 ng/ml) or severe (<10 ng/ml) vitamin d deficiency were 53% and 80% (respectively) more likely to develop incident cardiovascular disease.19 systolic blood pressure varies inversely with serum vitamin d levels in non-hypertensive white persons.20 however, the effect of supplementation with vitamin d and calcium on hypertension is unclear.21-23 Conflicting results from several reports may be explained by: the degree, magnitude and frequency of vitamin d deficiency not being reported; supplement doses not having been adequate; outcome benefits being diluted by inclusion of patients without deficiency; and the possibility that vitamin d and blood pressure may not have a cause-effect relationship.

In a study of multi-ethnic u.s. adults (one-third over age 60), the prevalence of cardiovascular risk factors was directly correlated with vitamin d levels.24 The odds ratios for adjusted prevalence of hypertension (1.30), diabetes (1.98), obesity (2.29), and hypertriglyc-

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eridemia (1.47) were significantly higher in patients with the lowest (<21 ng/ml) compared to the highest (>36 ng/ml) quartile of serum levels.

Central Nervous System vitamin d deficiency may be a modifiable risk factor for dementia and depression. In the health survey for england 2000, participants ≥65 years old with the lowest quartile of serum vitamin d levels (3-12 ng/ml) were 2.3 times as likely to demonstrate cognitive impairment than those with levels in the highest quartile (26-68 ng/ml).25 This observation is supported by another cross-sectional longitudinal study of memory and aging in mild Alzheimer’s disease patients and non-demented (control) persons, suggesting vitamin d deficiency associates with active mood disorders and cognitive impairment.26 In another lAsA investigation, patients 65-95 years old demonstrated a strong correlation between depression, reduced vitamin d levels and elevated pTh levels.27 similar associations have been found in a study of norwegians aged 21-70 years: those with serum vitamin d levels <16 ng/ml had more depressive symptoms than those with levels ≥16 ng/ml, and high dose vitamin d supplementation for one year afforded significant improvement.28 Cancer several studies suggest a consistent relationship between vitamin d and risk for colorectal cancer,29-31 with less well defined correlations for prostate, breast and pancreatic malignancies. In a large 4-year trial, healthy white postmenopausal women over age 55 receiving 1100 Iu vitamin d3 and >1400 mg calcium (increasing their mean vitamin d levels from 22.8 to 38.4 ng/ml) enjoyed a 77% reduction in 1-year total cancer risk.32 Baseline and treatment-induced serum vitamin d concentrations in this study were also strong predictors of cancer risk. lower dose (400 Iu) supplementation did not reduce colorectal or breast cancer risk in other trials.33-34 There are also consistent findings of an inverse relationship between colorectal cancer mortality and vitamin d levels in the nurses’ health study, health professionals follow-up study, and nhAnes,35-36 the latter showing levels >32 ng/ml associate with a 72%, race-independent, relative risk reduction in colorectal cancer mortality.36 Type 2 diabetes several reports have shown inverse relationships between vitamin d levels and fasting plasma glucose, insulin resistance, pancreatic beta-cell dysfunction, hemoglobin A1c concentrations, and incidence of metabolic syndrome.37-41 Baseline vitamin d levels also appear to predict future development of type 2 diabetes.40 no randomized controlled trials address whether vitamin d supplementation can prevent diabetes. however, post-hoc analyses suggest that administration of 700 Iu of vitamin d3 combined with 500 mg calcium for ≥3 years may attenuate insulin resistance in healthy older adults with pre-diabetes.42 In the nurses’ health study,43 subjects with a daily intake of >1200 mg calcium and >800 Iu vitamin d3 enjoyed a 33% lower risk of developing type 2 diabetes over 20 years, and data from the Women’s health Initiative support these findings.44 Case re-

ports have suggested that some vitamin d-deficient diabetic patients may show improved glycemic control with replacement.45

APPrOAcHeS tO VitAmin D DeficiencY in tHe GeriAtric POPUlAtiOn

maintaining an optimal vitamin d status could thus afford considerable benefits to elderly patients. Two strategies could potentially meet this need: screening of serum vitamin d concentrations, and empiric supplementation.

Although holick suggested serum monitoring of vitamin d and pTh be a routine part of elder care in 2004,46 screening is not widely performed. Cost-effectiveness of such a strategy is the major consideration; one major nationwide clinical laboratory charges $25.00 for a serum vitamin d measurement and $12.00 for serum pTh level; this compares with $16.00 for a comprehensive lipid panel (spring 2009).

Application of screening concentrations carries several practical caveats. values must be interpreted in light of the latitude (sunlight intensity) where the patient resides and the season during which they are sampled. variation from late winter (lowest) to late summer (highest) can range from 6-20 ng/ml.47-48 With documented deficiency, initial vitamin d3 doses should be 800-2000 Iu or vitamin d2 50000 Iu weekly, with 1000-1500 mg calcium supplementation, daily. On-treatment levels should be repeated after 2-3 months to document adequacy of replacement or direct dose adjustment if needed. Target levels should be >30 ng/ml.

An alternative strategy is to place all elderly persons on empiric supplementation. The cost of 800 Iu vitamin d3 is approximately $72 annually, making this approach more expensive than screening. Additionally, as many as 2/3 to 3/4 of individuals so treated would not expect to enjoy health benefits from supplementation, based on present evidence.1,2,49 since most elderly persons already take medications for one or more chronic illness, introducing another daily medication could contribute to the complications of polypharmacy. finally, empiric dosing could leave moderately-to-severely deficient patients inadequately replaced and not afford the full potential benefit of therapeutic supplementation. hence, this appears to be an inferior approach to annual screening.

cOnclUSiOn elderly patients are at high but variable risk for vitamin d deficiency. many serious and common disorders might be improved if deficiency is identified and treated effectively. empiric supplementation appears to be an inferior strategy to annual measurement of serum concentrations and level-guided replacement when indicated. healthcare providers might consider screening as a part of cost-effective routine health maintenance in the geriatric population, particularly among patients at otherwise increased risk for diabetes or musculoskeletal, cardiovascular, neuropsychiatric, or malignant diseases.

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Armas lA, hollis BW, heaney Rp. vitamin d2 is much less effective than vitamin d3 in humans. J Clin Endocrinol Metab.

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Jones G. pharmacokinetics of vitamin d toxicity. Am J Clin Nutr.

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Bischoff-ferrari hA, Giovannucci e, Willett WC, et al. estimation of optimal serum concentrations of 25-hydroxyvitamin d for multiple health outcomes. Am J Clin Nutr. 2006;84:18-28. dawson-hughes B. serum 25-hydroxyvitamin d and functional outcomes in the elderly. Am J Clin Nutr. 2008:88(suppl):537s-540s.

Janssen hC, samson mm, verhaar hJ. vitamin d deficiency, muscle function, and falls in elderly people. Am J Clin Nutr. 2002;75(4):611615.

Bischoff-ferrari hA, dawson-hughes B, Willett WC, et al. effect of vitamin d on falls: a meta-analysis. JAMA. 2004;291(16):1999-2006.

Bischoff-ferrari hA, dietrich T, Orav eJ, et al. positive association between 25-hydroxyvitamin d levels and bone mineral density: A population-based study of younger and older adults. Am J Med. 2004;116:634-639. hannan mT, litman hJ, Araujo AB, et al. serum 25-hydroxyvitamin d and bone mineral density in a racially and ethnically diverse group of men. J Clin Endocrinol Metab. 2008;93:40-46.

Cauley JA, laCroix AZ, Wu ll, et al. serum 25-hydroxyvitamin d concentrations and risk for hip fractures. Ann Intern Med. 2008;149:242-250.

Chapuy mC, Arlot me, duboeuf f, et al. vitamin d3 and calcium to prevent hip fractures in the elderly women. N Engl J Med. 1992;327(23):1637-1642. dawson-hughes B, harris ss, Krall eA, et al. effect of calcium and vitamin d supplementation on bone density in men and women 65 years of age or older. N Engl J Med. 1997;337(10):670-676. lee Jh, O'Keefe Jh, Bell d, et al. vitamin d deficiency an important, common, and easily treatable cardiovascular risk factor? J Am Coll Cardiol. 2008;52(24):1949-1956.

Giovannucci e, liu y, hollis BW, et al. 25-hydroxyvitamin d and risk of myocardial infarction in men. Arch Intern Med. 2008;168:1174-1180.

Wang TJ, pencina mJ, Booth sl, et al. vitamin d deficiency and risk of cardiovascular disease. Circulation. 2008;117:503-511.

Judd se, nanes ms, Ziegler TR, et al. Optimal vitamin d status attenuates the age-associated increase in systolic blood pressure in white Americans: results from the third national health and nutrition examination survey. Am J Clin Nutr. 2008;87:136-141.

Wang l, manson Je, Buring Je, et al. dietary intake of dairy products, calcium and vitamin d and the risk of hypertension in middle-aged and older women. Hypertension. 2008;51:1073-1079. forman Jp, Bischoff-ferrari hA, Willett WC, et al. vitamin d intake and risk of incident hypertension: results from three large prospective cohort studies. Hypertension. 2005;46(4):676-682. margolis Kl, Ray Rm, van horn l, et al. effect of calcium and vitamin d supplementation on blood pressure: the Women's health Initiative Randomized Trial. Hypertension. 2008;52(5):847-855. martins d, Wolf m, pan d, et al. prevalence of cardiovascular risk factors and the serum levels of 25-hydroxyvitamin d in the united states: data from the Third national health and nutrition examination survey. Arch Intern Med. 2007;167(11):1159-1165. llewellyn dJ, langa K, lang I. serum 25-hydroxyvitamin d Concentration and Cognitive Impairment. J Geriatr Psychiatry Neurol.

2009 feb 4. [epub ahead of print] Wilkins Ch, sheline yI, Roe Cm, et al. vitamin d deficiency is associated with low mood and worse cognitive performance in older adults. Am J Geriatr Psychiatry. 2006;14(12):1032-1040. hoogendijk WJ, lips p, dik mG, et al. depression is associated with decreased 25-hydroxyvitamin d and increased parathyroid hormone levels in older adults. Arch Gen Psychiatry. 2008;65(5):508-512.

Jorde R, sneve m, figenschau y, et al. effects of vitamin d supplementation on symptoms of depression in overweight and obese january

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subjects: randomized double blind trial. J Intern Med. 2008;264(6):599609.

Gorham ed, Garland Cf, Garland fC, et al. Optimal vitamin d status for colorectal cancer prevention: a quantitative meta analysis. Am J Prev Med. 2007;32(3):210-216.

Tangrea J, helzlsouer K, pietinen p, et al. serum levels of vitamin d metabolites and the subsequent risk of colon and rectal cancer in finnish men. Cancer Causes Control. 1997;8(4):615-625.

Garland Cf, Comstock GW, Garland fC, et al. serum 25hydroxyvitamin d and colon cancer: eight-year prospective study.

Lancet. 1989;2(8673):1176-1178. lappe Jm, Travers-Gustafson d, davies Km et al. vitamin d and calcium supplementation reduces cancer risk: results of a randomized trial. Am J Clin Nutr. 2007;85(6):1586-1591.

Wactawski-Wende J, Kotchen Jm, Anderson Gl, et al. Calcium plus vitamin d supplementation and the risk of colorectal cancer. N Engl J Med. 2006;354(7):684-696.

Chlebowski RT, Johnson KC, Kooperberg C, et al. Calcium plus vitamin d supplementation and the risk of breast cancer. J Natl Cancer Inst.

2008;100(22):1581-1591. ng K, meyerhardt JA, Wu K, et al. Circulating 25-hydroxyvitamin d levels and survival in patients with colorectal cancer. J Clin Oncol.

2008;26(18):2984-2991. freedman dm, looker AC, Chang s-C, et al. prospective study of serum vitamin d and cancer mortality in the united states. J Natl Cancer Inst. 2007;99:1594-1602. need AG, Oâ&#x20AC;&#x2122;loughlin pd, horowitz m, et al. Relationship between fasting serum glucose, age, body mass index and serum 25hydroxyvitamin d in postmenopausal women. Clin Endocrinol.

2005;62:738-741.

Chiu KC, Chu A, Go vl, et al. hypovitaminosis d is associated with insulin resistance and beta cell dysfunction. Am J Clin Nutr.

2004;79(5):820-825. scragg R, sowers m, Bell C. serum 25-hydroxyvitamin d, diabetes,

and ethnicity in the Third national health and nutrition examination survey. Diabetes Care. 2004;27(12):2813-2818. forouhi nG, luan J, Cooper A, et al. Baseline serum 25-hydroxy vitamin d is predictive of future glycemic status and insulin resistance: The medical Research Council ely prospective study 1990-2000.

Diabetes. 2008;57(10):2619-2625. pittas AG, lau J, hu fB, et al. Review: The role of vitamin d and calcium in type 2 diabetes. A systematic review and meta-analysis. J Clin Endocrinol Metab. 2007;92:2017-2029. pittas AG, harris ss, stark pC, et al. The effects of calcium and vitamin d supplementation on blood glucose and markers of inflammation in nondiabetic adults. Diabetes Care. 2007;30(4):980-986. pittas AG, dawson-hughes B, li T, et al. vitamin d and calcium intake in relation to type 2 diabetes in women. Diabetes Care. 2006;29(3):650656. de Boer Ih, Tinker lf, Connelly s, et al. Calcium plus vitamin d supplementation and the risk of incident diabetes in the Women's health Initiative. Diabetes Care. 2008;31(4):701-707. schwalfenberg G. vitamin d and diabetes. Improvement of glycemic control with vitamin d3 repletion. Can Fam Physician. 2008;54:864866. holick mf. vitamin d: importance in the prevention of cancers, type 1 diabetes, heart disease, and osteoporosis. Am J Clin Nutr. 2004;79:362371.

Kull m Jr, Kallikorm R, Tamm A, et al. seasonal variance of 25-(Oh) vitamin d in the general population of estonia, a northern european country. BMC Public Health. 2009;9:22.

Barger-lux mJ, heaney Rp. effects of above average summer sun exposure on serum 25-hydroxyvitamin d and calcium absorption. J Clin Endocrinol Metab. 2002;87(11):4952-4956.

Kenny Am, Biskup B, Robbins B, et al. effects of vitamin d supplementation on strength, physical function, and health perception in older, community-dwelling men. J Am Geriatr Soc. 2003;51(12):17621767.

Proprietary Statement: The authors have no commercial or proprietary interest in any drug, device, or equipment mentioned in the submitted article.

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

Uncommon but Not Rare Lynne A.Orozco, MD

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52-year-old female presented for an initial clinic visit after being referred from the emergency department (ED). In the ED she presented with dull, achy pelvic pain for a few weeks, but resolved with menstruation.

She had not been to a doctor in more than 5 years.

In a 52-year-old female with no annual preventive care and presenting with pelvic pain, my concerns include benign and malignant uterine/endometrial or ovarian tumors, pelvic adhesions, pelvic inflammatory disease and nongynecologic conditions, such as colorectal tumors and diverticular disease. I need to know more about her obstetric and gynecologic history as well as prior abdominal surgeries and gastrointestinal habits. In addition, a review of systems and medical, surgical, family and social histories as well as physical examination, including pelvic, are pertinent.

Her past medical, social, and family histories were noncontributory. Her only surgery was a tubal ligation 20 years ago. She reported steady weight gain with fatigue over the previous 20 years, while denying fevers, chills or night sweats. She reported regular bowel movements, without melena, and noted occasional headaches. She had 4 full-term vaginal deliveries without abortion or complications. She had not had a Papanicolaou (Pap) smear in 5 years. The patient never had pain with intercourse and denied any vaginal discharge. She described her most recent menstruation as “normal flow,” lasting 5 days. However, she stated that she only menstruated every 5 years during the previous 20 years since the birth of her fourth child. Her physical examination was pertinent for central obesity, elevated blood pressure (160/85 mmHg), slightly coarse facial features, a fine amount of hirsutism and posterior cervical acanthosis nigricans. Her pelvic examination revealed normal vulvovaginal, cervical and uterine anatomy. Her breast examination was likewise unremarkable.

After hearing this history, my concern shifts towards her markedly abnormal menstruation, while remembering that pelvic pain was her inciting symptom. my first consideration is that her recent menstruation was postmenopausal bleeding, not really menstruation, AUtHOr infOrmAtiOn: lynne A. Orozco, mD is a third year resident in the Department of Family Medicine at the university of Mississippi Medical Center. cOrreSPOnDinG AUtHOr: Lynne a. Orozco, 2500 n. State Street, Department of Family Medicine, university of Mississippi Medical Center, jackson, MS 39216; Telephone: 601984-7800 (office), E-mail: LOrozco@umsmed.edu

as she believes. I also think about a local hormonal problem, such as polycystic ovary syndrome. This corresponds with her physical examination and secondary amenorrhea. however, she is older than most patients with polycystic ovary syndrome and had been pregnant 4 times previously. perhaps she has a central hormonal dysregulation, such as a pituitary lesion, but this should not cause pelvic pain.

I obtained hospital records from her original ED visit. A pelvic ultrasound showed a normal endometrial stripe and nabothian cyst.

This ultrasound makes endometrial cancer less likely and explains why she had pelvic pain that resolved entirely. Thus, I again think of central hormonal dysregulation and will order a pregnancy test, leuteinizing (lh) and follicle stimulating hormones (fsh), prolactin concentration (pRl), total testosterone, estradiol and thyroid function.

I will also obtain a pap smear, mammogram and basic laboratory studies.

Her electrolytes and kidney, liver and thyroid functions were normal, as were her total testosterone, estradiol, Pap smear and mammogram. Her urine pregnancy test was negative. Her LH and FSH were low, with reference to her perimenopausal age group, at 0.106 mIU/mL and 1.6 mIU/mL, respectively. In addition, her PRL was elevated at 75.280 ng/mL. my initial tendency is to focus on her elevated pRl. despite the broad differential diagnosis for hyperprolactinemia, I first think of pituitary pathology. Other causes of hyperprolactinemia are unlikely here. she is not pregnant or postpartum. she is not breastfeeding and relays no chest wall trauma or stimulation. her laboratory studies are not consistent with primary hypothyroidism or cirrhosis. she neither abuses alcohol nor takes any medications, specifically antipsychotics or metoclopramide (Reglan). she has never had a seizure. finally, her lh and fsh are inappropriately low for a female of her age. This supports a central or pituitary cause of her elevated prolactin.1 I will conduct a directed history for symptoms of secretory or mass effect, as well as repeat her pRl. The anterior pituitary secretes 6 hormones: fsh, lh, pRl, growth hormone (Gh), adrenocorticotropic hormone (ACTh) and thyroid stimulating hormone (Tsh). secretory symptoms are caused by excess of these hormones. for example, Cushing’s disease is the constellation of symptoms caused by excess ACTh and cortisol, acromegaly is caused by excess Gh, and galactorrhea is caused by excess pRl. mass effect symptoms include january

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fiGUre 1:

axiaL Mri OF PaTiEnT in CaSE #1

headache, nausea and vomiting, visual field defects or vision changes. mass effect may also distort hormone release, as seen with diminished concentrations of ACTh, leading to adrenal insufficiency or decreased concentrations of all 6 pituitary hormones leading to panhypopituitarism.2 Her repeat PRL was 86.69 ng/mL. She did have occasional headaches, and her shoe size had enlarged by 1 1/2 sizes peripartum. She never wore rings. She denied any failure in bite closure.

She did not have a “buffalo hump” or striae. She noted decreased libido. She stated she had bilateral galactorrhea over the previous 4-5 years. This was reproducible on physical examination.

The patient does not have frank symptoms or signs of acromegaly, cortisol excess or hypermetabolism. however, she does have a secretory symptom and sign of galactorrhea. for that reason, I will order an 8 a.m. fasting cortisol, Gh, ACTh, and the free, inactive alpha subunit of gonadotropin. In addition, I think it is necessary to image her brain with a pituitary protocol mRI. Her fasting cortisol, GH, ACTH, and alpha subunit were all normal. However, her MRI did reveal a sellar mass. (Figure 1) Subsequent visual fields were normal.

With only the knowledge of “high prolactin,” the radiologist read her MRI as an 8 x 5 mm prolactinoma with a partially empty sella that was displacing the pituitary gland anteriorly and to the left. With knowledge of her exact PRL, the neurosurgeon read her MRI as a cyst in the middle of the pituitary gland, pressing the gland peripherally. The 8 x 5 mm mass was actually the pituitary gland, not a prolactinoma.

The differential diagnosis of sellar masses is broad. pituitary adenomas are the most common and can be designated based on their size, micro versus macroadenomas. They can also be designated by their cell type, and whether they are secreting (functional) or non-secreting (non-functional).3 Clonal analysis has shown that these nonfunctional pituitary adenomas are almost always benign, but are true

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SaGiTTaL Mri OF PaTiEnT in CaSE #1

neoplasms. That is, they are uniform, originating from a somatic mutation rather than polyclonal proliferation in response to a stimulatory factor.4 By the appearance of this patient’s lesion, I also think about cystic sellar masses. These include arachnoid cyst, Rathke’s cleft cyst and craniopharyngiomas, which are solid and cystic. Other considerations for sellar masses are pituitary hyperplasia, primary and metastatic malignancy such as germ cell tumors, chordomas, lymphoma or meningioma, as well as vascular lesions. less commonly found are granulomatous diseases, lymphocytic hypophysitis and histiocytosis.2 The neurosurgeon does not think this lesion is a prolactinoma because he knows her pRl is not in prolactinoma range. A prolactinoma is likely if the pRl is greater than 250 ng/ml and unlikely if less than 100 ng/ml. A pRl of greater than 200-250 ng/ml is required to cause galactorrhea, although tissue receptors vary.

A pRl less than 150 ng/ml is more likely to be the result of “stalk” effect instead of a secretory adenoma. stalk effect refers to a sellar mass compressing the infundibulum, thus blocking dopamine and its chronic inhibition of prolactin release from the pituitary.2 The patient’s pRl of 75.28 ng/ml is more consistent with a stalk effect resulting in disinhibition rather than oversecretion of pRl. her lh and fsh values are more consistent with a mass effect leading to underproduction. In spite of inadequately elevated pRl, she has breast tissue stimulation resulting in galactorrhea. I will consult an endocrinologist.

The endocrinologist hypothesized that she had a prolactinoma that had necrosed, i.e., prolactinoma apoplexy. He prescribed cabergoline (Dostinex) at 0.5 mg twice weekly. Her dose was titrated to stop the galactorrhea and normalize her PRL. Her PRL was monitored every 2 months. It fell quite rapidly to 1.0 ng/mL after 4 months of cabergoline. Interestingly, however, her galactorrhea did not fully resolve. prolactin is produced by the anterior pituitary’s lactotrophs.

dopamine is released by the hypothalamus, through the infundibulum, and acts on the d2 receptors of these lactotrophs to chronically inhibit their release. Cabergoline is a selective, long lasting d2 agonist. It functions by simulating more dopamine at the anterior pituitary’s lactotrophs d2 site, which results in more inhibition of pRl, thus decreasing pRl concentration.5 prolactinoma apoplexy explains the patient’s cyst-like mRI findings, her only moderately elevated pRl with depressed lh and fsh values, as well as her galactorrhea. That is, she possibly had a pRl above 200 ng/ml in the past, because of prolactin being secreted from a prolactinoma. The subsequent adenoma necroses led to non-secretory pRl, with residual breast tissue effects. her history and physical examination, as well as her laboratory values are imperative in interpreting her mRI. Correct diagnosis of sellar masses is important because treatment varies markedly based on secretory effects and size or mass effect.

Transsphenoidal resection is first line therapy for macroadenomas and (non-prolactinoma) secretory tumors, especially acromegaly and Cushing disease. dopaminergic drugs, such as cabergoline are first line therapy for prolactinomas. They shrink the adenoma and reduce pRl.6

mentioned case, i.e., Gh (or Insulin Growth factor-1), ACTh and 8 a.m. cortisol, lh and fsh, pRl, free T4 and Tsh and alpha subunit, in addition to serial mRI scans. Of note, the alpha subunit of gonadotropin can be elevated in non-secretory pituitary adenomas that otherwise lack serum hormone markers.4 In contrast, other endocrinologists recommend only a pRl for asymptomatic patients with incidentalomas. studies have shown that differences in outcomes between the evaluations are small.8 The minimal-evaluation approach is only possible after completing a thorough history and physical examination, as well as proper sellar imaging. Imaging is by pituitary protocol mRI in all cases except for suspected craniopharyngiomas, where the cystic, solid, calcified regions are best visualized by CT.9 It is important to know the size and consistency of the mass, because, as previously noted, the differential for sellar masses is quite broad. Over all, evaluating sellar masses involves assimilating history, physical examination, and hormonal and radiological data in order to guide medical, surgical and/or expectant management.

KeY WOrDS:

AmenORRheA, hypeRpROlACTInemIA, pROlACTInOmA, pITuITARy GlAnd

cOmmentArY The process of diagnosing a prolactinoma status post apoplexy was somewhat onerous and theoretical. Conversely, her medical management was straightforward. This is not always the case with sellar masses, as they often require a teamwork approach with medical, surgical, and/or expectant management. for example, a second patient presented to clinic with a history of colon and lung adenocarcinoma. his metastatic workup revealed a large pituitary mass. he had hormonal derangements and needed a tissue diagnosis, as lung cancer can metastasize to the pituitary.7 he underwent transsphenoidal resection and was managed by his primary care provider, endocrinologist and neurosurgeon.

In contrast, a third patient was found to have an idiopathic, cystic mass that was found incidentally in mRI for a stroke. It involved the sella turcica, sphenoid sinus and clivus, but she had no hormonal derangement. Because she was a frail, completely asymptomatic 82-yearold female, taking warfarin (Coumadin), her primary care provider expectantly managed her condition.

With the proliferation of brain imaging, findings in the sellar region are more frequently encountered. In fact, high-resolution mRI screening of a normal population has shown a 10 percent prevalence of sellar masses.8 many sellar masses are “incidentalomas,” i.e., micro- or macroadenomas of the pituitary. Controversy remains over the current recommendations for their management. some endocrinologists recommend the extensive biochemical screening outlined in the afore-

referenceS 1.

2.

3.

4.

5.

6.

7.

8.

9.

Groff TR, shulkin Bl, utiger Rd, Talbert lm. Amenorrheagalactorrhea, hyperprolactinemia, and suprasellar pituitary enlargement as presenting features of primary hypothyroidism. Obstet Gynecol.1984; (3 suppl):86s-89s. pituitary Adenoma’s, Craniopharyngiomas, Rathke’s Cleft Cyst, Colloid Cyst. In: Greenberg m. Handbook of Neurosurgery, 6th ed. new york, ny: Theime; 2006: 438-457. freda pu, post Kd. differential diagnosis of sellar masses. Endocrinol Metab Clin North Am. 1999;28(1):81-117.

Alexander Jm, Biller Bm, Bikkal h, Zervas nT, Arnold A, Klibanski A. Clinically nonfunctioning pituitary tumors are monoclonal in origin. J Clin Invest.1990; 86:336-340.

Colao A, di sarno A, Cappabianca p, di somma C, pivonello R, lombardi G. Withdrawal of long-term cabergoline therapy for tumoral and nontumoral hyperprolactinemia. N Engl J Med. 2003; 349(21):2023-2033.

Kuwayama A, Kageyama n, nakaneT, Watanabe m, Kanie n. Anterior pituitary function after transsphenoidal selective adenomectomy in patients with Cushing's disease. J Clin Endocrinol Metab.

1981;53(1):165-173. fassett dR, Couldwell WT. metastases to the pituitary gland. neurosurg focus. 2004;16(4):e8.

King JT, Justice AC, Aron dC. management of incidental pituitary microadenomas: a cost-effectiveness analysis. J Clin Endocrinol Metab.

1997; 82(11):3625-3632. pressman Bd. pituitary imaging. In: melmed s. The pituitary.

Cambridge: Blackwell scientific publications;1995:681-684.

Clinical Problem-solving is a monthly feature of the Journal of the Mississippi State Medical Association. Clinical Problem-solving manuscripts are case-based and portray the sequential process of clinical decision-making when the physician is faced with a diagnostic dilemma. Cases may be unusual presentations of common diseases or common presentations of unusual diseases. patient problems must be based on actual patients from your practice, not contrived patients, and the problem must be solvable. Cases with interesting and educational differential diagnoses are most appropriate. patient information is presented in segments (indicated in boldface type in the manuscript). The clinician then shares with the reader (regular type) how the new information is synthesized and the rationale for critical decisions. The decision making process continues as new information emerges until there is resolution of the problem. Authors from all medical and surgical specialties are encouraged to submit manuscripts for consideration in this monthly feature. manuscripts and requests for Instructions to Authors should be addressed to dr. Replogle at department of family medicine, 2500 n. state st., Jackson, ms 39216.

Review Committee: Chris R. Arthur, PhD; Diane K. Beebe, MD; Judy Gearhart, MD; Shannon D. Pittman, MD; William H. Replogle, PhD january

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Mississippi state Medical association P.O. Box 2548 • Ridgeland, Mississippi 39158-2548 • 408 West Parkway Place 39157 • (601) 853-6733 • Fax (601) 853-6746 • 1-800-898-0251

January 1, 2010 The Mississippi State Medical Association (MSMA) has collaborated with the Mississippi State Department of Health (MSDH) to issue the second annual Public Health Report Card grading the quality of health of Mississippians and the adequacy of health programs to improve the health status of our population. Our intent is to help Mississippians reduce risky health behaviors and show them how to work with their physician to meet health goals.

The Public Health Report Card promotes healthy lifestyle choices as a personal responsibility. If Mississippians would do only four things — engage in regular physical activity, eat a healthy diet, not smoke, and avoid becoming obese — they could slash their risk of diabetes, heart attack, stroke or cancer by 80 percent. Centers for Disease Control researchers found that less than 10 percent of people followed in the multiyear study actually lived their lives this way.

As “Physicians Who Care for Mississippi,” MSMA members are working to reduce infant mortality, improve access to care for all, halt childhood obesity, prevent substance abuse and stop underage drinking. MSMA takes public health seriously publishing this annual Public Health Report Card, circulating news and updates about H1N1 influenza, reducing health disparities, preparing for disaster response, and promoting healthy lifestyle choices.

And, we put our money where our mouth is.

• MSMA helped push through two cigarette tax increases last year.

• It was MSMA that insisted the Legislature put physicians in charge of the Board of Health.

• MSMA is addressing the workforce shortage with the Rural Physicians Scholarship Program and funding to increase medical school classes to 120 students each year.

• MSMA works closely with Medicaid and the State Legislature to ensure Medicaid patients have access to quality medical care.

• MSMA works hard to protect and improve the tort climate in Mississippi to make this state a great place to practice medicine.

• As the voice of medicine in Mississippi, our MSMA promotes physicians’ expertise and the positive impact of physicians on public policy.

• MSMA encourages the development of policies and mechanisms to assure the continuity, coordination and continuous availability of patient care, including professional preventive care and early-detection screening services in the most effective yet cost-efficient manner.

Physicians know all too well that taking steps now to improve key lifestyle behaviors can help prevent and manage unhealthy conditions.

Living a healthy lifestyle greatly reduces risk of chronic diseases and can help reduce health care costs for the individual and our state. Our MSMA and the Mississippi State Department of Health hope the Public Health Report Card will encourage Mississippians to partner with their physician to make lasting changes in these key health behaviors to live a longer, healthier life.

d Easterling, dy Easterling MD Randy MSMA President

MISSISSIPPI STATE DEPARTMENT OF HEALTH

• PrESiDEnT’S PaGE •

Have a Good Night

T

his “president’s page” will arrive at your home or office long after my 58th Christmas has come and gone. We will well be into the year 2010, all be on our well meaning but rarely maintained diets, and remembrances of recent and past Christmases will still be dancing like sugarplums in our heads. It is my prayer that your holidays were full of family, friends, and the warmth and well-being that comes only from looking back on years past with the satisfaction of a life and job well done.

rAnDY eASterlinG, mD 2009-10 mSmA PreSiDent

While I am rarely disappointed at Christmas, (After all, what can you give someone who has everything: a loving wife, wonderful children, a comfortable home, family and friends I love, and patients I care for? my cup runneth over!) there was one gift that was conspicuously absent from under my tree on Christmas morning.

Actually, it was not a gift that was missing, but a well-earned payment for almost a decade of service to the most vulnerable in our society, the elderly. A gift is something you receive out of love, not something you have earned.

I am referring of course to a permanent fix to the sGR (sustainable growth rate). Congress is optimistically going to be benevolent enough to stop the projected 21.5% across the board cuts for physicians in 2010; but, in their infinite wisdom they failed (as they have for the last decade) to enact a permanent fix to the flawed government formula.

A quick lesson in sGR 101 is in order. The sustainable growth rate (sGR) was created in 1997 as a target rate of growth in medicare part B spending for physician and nonphysician practitioners’ services (nurses, physical therapists, physician assistants, etc.). The sGR is used to establish payment updates and is one of several factors that are in play when setting medicare physician payment rates each year. The formula looked good on paper, and, I believe, was a well-meaning effort by the federal government to give us docs our due. however, like so many things the united states government undertakes, it has been a dismal disaster. simply put, in the past eight years the formula designed to provide regular physician payment updates to keep up with inflation (the cost of running your practice) has resulted in an overall increase of 6.2%. for those of you who are arithmetically challenged, this represents an average annual increase 0.775%. Remember: the cost of running your practice has gone up anywhere from 3% to 6% each year. What can I say? I guess that is the proverbial “close enough for government work.” While physicians have bathed in the excess of an average annual increase of 0.775% for the past eight years, it would serve us well to remember that a number of specialties (cardiology, radiology, anesthesiology, ophthalmology, the list goes on) have suffered significant overall decreases in reimbursement. As is true with most negative economic news, insufficient medicare payment formulas affect mississippi physicians even more so than the rest of the nation. for example, our beloved magnolia state has an above-average proportion of medicare patients at 15% of the general population. mississippi has the highest proportion of disabled beneficiaries on medicare of any state at 24%. On top of that, to add “insult to injury,” with just twelve practicing physicians for 1,000 beneficiaries, mississippi has the lowest ratio of physicians to medicare recipients of any state in the union. don’t let me get on a rant! Research has shown that 32% of mississippi residents live in a primary care shortage area and more than 18% of our state’s population reported that they did not see a doctor in the past 12 months due to cost. physician work force data has revealed that 43% of mississippi practicing physicians are over 50 years of age. surveys have spoken loudly, many of our older docs (50 and above) have already begun the process of cutting back on the number of medicare patients they tend to. This trend is even more dramatic in primary care, the first line of defense against death and disease. january

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I really did not expect the gift of an sGR fix to be neatly wrapped under my tree in Bovina. After all, what is Christmas without anticipation and dreams of things yet to come? What was the most disappointing of all was not that Congress “again” refused to keep their promise to the elderly and disabled, but that our own two homegrown united states senators (one medicare-aged and the other with medicareaged parents) voted once again not to fix the problem. Both senators Cochran and Wicker have been educated time and time again on the plight that mississippi physicians face while taking care of the elderly. numerous phone calls, letters, and emails have evidently fallen on deaf ears.

While waving the banner of “fiscal responsibility,” they continue to “kick the can down the road” which results in subsequent steeper cuts and incrementally escalating the cost of a permanent solution. A permanent fix to the sGR in 2005 would have cost around $50 billion. At the end of 2010 that price tag will be well over $300 billion. Am I missing something? how is that fiscally responsible?

Well, in spite of the aforementioned disappointment of Christmas 2009, while I take down the tree and pack up the ornaments, I find myself looking forward to Christmas 2010. Remember that is what the season is all about: wishing, dreaming, anticipation, and looking forward to! As the year rolls around remember: I will be making a list and checking it twice, to see who in Washington has been naughty or nice.

While there will be speeches to give and issues to weigh, I will be counting the votes as santa loads his sleigh.

In 12 months from now as saint nick flies out of sight, I pray the elderly in mississippi will have had a good night. yours in helping make mississippi healthier,

Randy Easterling, MD President, Mississippi State Medical Association

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2010

Let Us SHOWCASE Your ARTWORK

by donating it to the Silent Auction to be held at Annual Session Silent Auction Annual Session June 3-6, 2010 Natchez, Mississippi Benefiting the University of MS Medical Center AMA Foundation Scholars Fund ! !# % !

MSMA & MSMA ALLIANCE ALL types artwork welcome: photography, paintings, pottery, ceramics, woodwork, jewelry, sculpture, etc.

Contact Amy Gammel, AMA Foundation Chair, at fivegammels@bellsouth.net or Barbara Shelton at bshelton@msmaonline.com

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• EDiTOriaL •

Start to Finish “All the forces in the world,” said French writer Victor Hugo, “are not so powerful as an idea whose time has come.”

This fortuitous opening line literally jumped out at me from this morning’s sunday school lesson. now all I had to do was to come up with an editorial which expounded appropriately on this provocative idea. What a switch…getting started is usually the kicker!

The passionate opinion of my esteemed friend dr. lamar Weems in the december Journal MSMA notwithstanding, my gut reaction to an idea whose time had come was “deunification.” With the distinction as the last holdout, there is little doubt in my mind that we have more than recouped our investment over the years as a unified medical association…both financially and politically. however, when it appeared that “this ain’t yo’ mama’s AmA,” the deunification handwriting seemed to emblazon itself indelibly on the prescription pad, especially as it related to the very survival of our own mississippi state medical Association.

With the historic vote cast in special session last fall by our msmA delegates, it is now the responsibility of eveRy member to ensure that this decision was not in vain. younger physicians of every persuasion must join us of the “Old Guard” on the local, component society, state, and national levels as we continue to practice, learn, educate, lobby, testify, and even twist a few arms to preserve the integrity of our special calling. To paraphrase our illustrious and never-at-a-loss-for-words msmA president, dr. Randy easterling, do whatever you will with the AmA, but neveR forsake your mississippi state medical Association! now that I think about it, this whole notion of deunification was brought about by another idea whose time may (or may not) have come—healthcare reform. As I write, today’s newspaper carries an article which begins, “senate democratic liberals are seeking expansion of two large federal programs, medicare and medicaid, in exchange for dropping a government-sold insurance option from health care legislation sought by president Barack Obama… At its core, the legislation is designed to expand coverage to more than 30 million who lack it, while curbing controversial insurance industry practices and generally restraining the growth of medical spending.”

What do yOu think? Best wishes to you and your families for a happy and healthful new year!

—Stanley Hartness, MD Associate Editor

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

you can submit your letter via email to Kevers@msmAonline.com or mail to the Journal office at msmA headquarters: p.O. Box 2548, Ridgeland, ms 39158-2548.

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• PHySiCianS’ BOOKSHELF • The Color Atlas of Family Medicine.

By Richard P. Usatine, Mindy Ann Smith, E. J. Mayeauz Jr., Heidi Chumley, and James Tysinger.

1108 page hardback, $99 New York, NY, McGraw Hill Publishing, 2008.

m

edicine requires that a physician possess the ability to both identify the cause of their patient’s illness and, secondly, offer sound treatment. Those who dedicate their lives to the art of medicine will attest that for those maladies that present with corporal signs one can expect to encounter an assortment of physical manifestations within the scope of an individual disease. It is generally true then that the diversity of a particular disease may not be fully appreciated until at last, one has witnessed the manifestations.

The Color Atlas of Family Medicine offers an excellent method for physicians, and medical students alike, to augment their knowledge of disease presentation, assessment, diagnosis, and clinical treatments.

This book is a wonderful visual guide, offering 1500 full-color photographs of common disease processes, paralleled by superb content and structure.

The authors organized the text into seventeen broad-topic “parts,” with subdivided “sections” and subject-specific “Chapters.”

The topic page for each part greets us with the title and the legend for the strength of Recommendation (sOR) ratings, which are located throughout each chapter for the pertinent treatment recommendations. part 1 simply contains Chapter 1, which familiarizes the reader with how to use this pictorial atlas as a conduit to “patient Care, learning, and Teaching.” The five Chapters of part 2 serve as a gentle, yet fact-filled reminder to the reader of the tenets of family medicine, i.e. the “essence of family medicine.” The subsequent fifteen parts are primarily categorized by organ system, but also separately highlight such topics as, part 3: physical and sexual Abuse; part 11: Women’s health; part 15: Infectious diseases; and part 18: substance Abuse.

The wide-ranging imagery of this text is captivating and informative, but as the reader delves deeper into the book they will find evidence-based medicine at the core of the content. Beginning with part 3, each Chapter starts with a relevant patient story, followed sequentially by sections on epidemiology, etiology and pathophysiology, diagnosis, differential diagnosis, management, patient education, and follow-up. This pattern of organization makes the book very user friendly. each page is divided into two columns of text, with associated photos on the right. At the very end of each Chapter the authors offer the reader helpful internet links for patients and providers alike, supplemental journal articles for physicians, and finally the evidence-based references. If you need quickly to look up a particular subject, start with the Topic Index inside the front hardcover. This reference book is a pleasure to explore.

In the “typical” reference book to patient care, carefully crafted descriptions of human pathology are often used to paint an image in the mind of the reader. however, in medicine, words alone seldom stand in fully for the entity of interest, and too infrequently does the photography in the standard pathology text capture the variety of disease presentations. The Color Atlas of Family Medicine uses a spectrum of examples for each diagnostic condition and proceeds to back up the imagery with strong clinical knowledge. The Color Atlas of Family Medicine is a wonderful visual guidebook of clinical medicine, offering the reader both common and rare presentations of highly prevalent diseases found in active medical practice.

—Snow Marika Petersen, MD, MPH Class of 2011 Tulane University School of Medicine & School of Public Health and Tropical Medicine january

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â&#x20AC;˘ MSDH â&#x20AC;˘ Mississippi Reportable Disease Statistics

October 2009

* Totals include reports from Department of Corrections and those not reported from a specific district NA - Not available (temporarily) for the most current mmr figures, visit the mississippi State Department of Health web site: www.HealthymS.com january

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• MSDH •

In Memoriam State Health Officer Ed Thompson, Jr., MD, MPH 1947-2009

m

ississippi and the nation have lost a “medical statesman”

and public health champion with the passing of dr. ed Thompson, Jr. dr. Thompson peacefully died after a

long battle with cancer, december 1, 2009 in the comfort of his home, and with his wife by his side. he is survived by his wife marsha; sons mark

during the October 2009 mississippi state Board of health meeting, the Board unanimously adopted a resolution requesting that the legislature name the new public health laboratory the “f. e. Thompson, Jr. public health laboratory.”

“The loss of dr. ed Thompson is a great tragedy for our state. We’ve

Thompson of Atlanta, matthew Thompson of memphis, as well as his son

lost a gifted and extraordinary leader in his prime, who still had much to

matthew pollock of Jackson and daughter morgan pollock of nashville.

contribute. his seasoned leadership of the department during two critical time

his career was driven by his devotion to mississippians and passion for health care. dr. Thompson served as state health Officer for the mississippi state department of health (msdh) from 1993 to 2002 and was

periods should be remembered with appreciation by the state’s citizens,” said mississippi state Board of health Chairman dr. lucius “luke” lampton. “ed Thompson gave us back our department of health,” dr. lampton

named Interim state health Officer in July 2007. he was later reappointed to

said. “he restored order, integrity, and competence at a department in chaos,

the permanent position of state health Officer in december 2007. dr.

and within a short time, the department reasserted itself as a vital and

Thompson also served as state epidemiologist from 1983 to 1993.

respected state agency. The Board and dr. Thompson prepared for this sad

he received his medical degree from the university of mississippi school of medicine, his masters of public health from Johns hopkins university school of hygiene and public health, and was board certified in preventive medicine.

day and the department will continue to operate smoothly, despite this irreplaceable loss.” “he was literally the face of public health in mississippi and, in large measure, across the nation,” said msmA president dr. Randy easterling.

he was also a past president of the Council of state and Territorial

“With a limited budget, he was able to take on all the health problems in the

epidemiologists and the Association of state and Territorial health Officials

poorest state in the country. It took a real passion for the sickest of the sick

(AsThO). This year, the national Association of local Boards of health

and the poorest of the poor to accomplish that.”

recognized him as the “outstanding state health officer in the united states.”

Ripley family physician and msmA past president dr. dwalia south

In 2008 he received AsThO’s presidential meritorious service Award in

said Thompson had a gift not just for diagnosing difficult public health

recognition of his exemplary service.

problems, but for finding solutions. “The grand thing about ed was that he

Among his accomplishments, dr. Thompson was selected to serve as

didn’t just point this widely known shortcoming out to the media and poor-

deputy director for the Centers for disease Control in Atlanta. he was

mouth about how bad our public health was,” dr. south said. “he got in there

CdC’s Chief of public health practice. dr. Thompson served on numerous

and literally ‘hands on the wheel’ did something about it. he could navigate

CdC advisory committees, the department of health and human services’

the halls of the legislature as well as he could the laboratory.”

secretary’s Council on public health preparedness, including the Anti-

he frequently testified before Congress on important public health

terrorism preparedness Task force. his distinguished career also included

issues. even in that formal environment he was down to earth, once quoting

service as professor and Chairman of the department of preventive medicine

Three dog night, “that ain’t the way that it works.”

at the university of mississippi school of medicine and professor of medicine in the Infectious disease division.

Tupelo family physician dr. ed hill, who serves on the mississippi state Board of health, said dr. Thompson was a giant in the field of public

Another great joy was sailing. dr. Thompson was 2009 Commodore

health as a teacher, epidemiologist, manager and administrator. “he had the

of the Jackson yacht Club. he set great courses for regattas and loved the

uncanny gift of being able to calm the fears and anxieties of any audience,

being on the water. It gave him time to reflect and relax with friends and

large or small, and conveyed a profound sense of trust,” said dr. hill, who

family.

held public health meetings around mississippi with dr. Thompson in the early 1980s to talk about hIv-AIds.

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Gov. haley Barbour noted that dr. Thompson’s “medical expertise and counsel were highly respected” nationally. state Rep. steve holland and sen. hob Bryan, chairmen of their respective public health committees, agreed, saying in a statement that Thompson’s “vast knowledge of public health put him at the forefront of health care leadership in mississippi and nationally. We have lost a stalwart leader, a dear friend and an outstanding mississippian.”

s eye view on medicine follow MSMA on

!

State Epidemiologist and Deputy State Health Officer for Medicine and Science Dr. Mary Currier Appointed Interim State Health Officer

I

n an emergency mississippi state Board of health meeting held

on december 1, 2009 state epidemiologist and deputy state health Officer for medicine and science dr. mary Currier was

unanimously appointed Interim state health Officer effective immediately.

The Board resolution naming dr. Currier Interim state health Officer states that dr. Currier will have the full authority of the state health Officer position, as provided by law, until such time as the Board takes further action.

The Board will discuss the process of searching for a permanent replacement at its regularly scheduled January meeting. dr. Currier said the agency has been extremely fortunate to have had the leadership of dr. ed Thompson for the past two and a half years. “public health was his passion; we at the agency, and the state as a whole, benefited from his knowledge and wisdom. he was my mentor, I will miss him greatly.

Through dr. Thompson’s leadership, msdh has made significant strides in addressing several key health concerns such as infant mortality, sexually transmitted diseases and increasing the number of public health field staff. he also played a key role in obtaining funding and starting the current construction of the new public health laboratory,” dr. Currier said.

Mark Your Calendar! the 142nd Annual session of the MsMA house of delegates and Medical Affairs Forum 2010 will be held

* ) ( ' ( & %$ # $ " ! $ ! $ ! $ $! ' # ( $ ( ( $ %! $ i & %$ ( # %$ ! $ %$ som %! ( ) $ $! &' ($! $ )($ ! $T you stay in touch h no matter where you # '( $ $ is%$ now no ! $ ! # $ v # $ * witter $ # ! $ ) ' ( ( $ inut( % $ ! $# $ %( $ $ a # $ fre ' (($ Twitter account for ! ' %( " $ $ "$ visit www twitter ! $# $% $ your name, email # ' ( %$ # $ ! "($ )! ($ (' $ ! ! # " $ % # # ' $ ( $ essa ( %# $ ' # ( %$ # " $ ce ( $ y! &' ($ s ( $ $ ) $ Twitt witter ! $# $# $ $ ! $ ! $ )($ ! ""! $ ( $ # ($ h (' ! $# $" $ ! ""! $ ( $ ! $ )($ $ !

MSMA1

June 3-6, 2010 in natchez.

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CALL FOR ENTRIES

Seeking Nominations for the 2010 MSMA Award for Community Service The Annual Physician Award for Community Service, sponsored by Mississippi State Medical Association, is designed to provide recognition to members of the association who are actively engaged in the practice of medicine, for the many and varied services above and beyond the call of duty which they render to their respective communities.

Each recipient of the award is nominated by his or her component society and selection is made by the members of the Council on Public Information. The intent of the program is to honor only living persons, and to honor no person more than once. Presentation is made at the + 44!+ ) $ 88,.4& 5# ,98 + 775* .+ ,.54 7 5!7 8 5# 8)8&+ ,87 %8 30 75* .8,0 9+ 7 $ + 40 $ 8$ 1837 " 53,90 5# ,9.7 2.7,.4&!. 7982 + " + 32 , .7 05!3 75* .8,0 7 3876547.1.).,0 ,5 788 ,9+ , ,980 + 38 nominated. A nomination form is avaiable on the MSMA Web site. All nominations should be submitted to the Mississippi State Medical Association by May 1, 2010.

The award is a handsome plaque " 9.* 9 # 8+ ,! 387 + * + 7, 1354 8 $ 82+ )).54 : 98 $ 82+ )).54 7 287.& 4 symbolizes the close relationship between medicine and the community. A $500 contribution is also made by the association to a civic organization designated by the award recipient.

Nominations should be submitted in writing. Since the award is for outstanding community service it is important that all accomplishments of the nominee in this regard be presented in detail. The Council on Public Information encourages you to seek the assistance of your local MSMA Alliance in preparing the written nomination and supporting materials.

Nomination supporting documents may include all or some of the following: a narrative about the person and his community involvement, newspaper clippings, letters of support from community leaders, newspaper or magazine articles written about the person, photographs and 5,983 $ + ,83.+ )7 ,9+ , 795" ,98 6907.* .+ 4 7 * 5$ $ !4. ,0 .4%5) %8 $ 84, Nominations should be sent to MSMA, P.O. Box 2548, Ridgeland, MS 39158-2548, as soon as 6577.1)8' 1!, 45 )+ ,83 ,9+ 4 / + 0 ' 53 # !3 ,983 .4# 53$ + ,.54 * 54,+ * , + 384 %8 37' .38* ,53 5# 5$ $ !4. * + ,.547' 53 ' 53 %8 37 / - / ( 54).48* 5$

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• una VOCE •

Canine Behavior

I

will admit that I’m not an expert on dogs. I’ve always had at least one dog around if I was here in the united states. I’ve even trained a few bird dogs, but I don’t sit around much and think about what dogs think about. Recently, at a family get-together, I had the chance to learn a lot about both human and canine behavior that I never r. Scott Anderson, mD knew before during a conversation that I had with an eight-year-old.

Because the nature of this conversation is potentially embarrassing, the identity of the specific eight-year-old is a secret. It’s a secret, which to avoid being in “deep trouble with somebody that’s going to be nine soon,” I must carry with me to my grave. In fact, to avoid any possibility of the specific eight-year-old being identified, I should probably assume the posture of our military when discussing nuclear weapons by saying, “I can neither confirm nor deny the presence of an eight-year-old, of any type or description, as having been a part of this conversation.”

The promise of anonymity that I made when I asked if I could write about our conversation was secured by that most sacred of vows, a “pinky swear.” And, everybody knows what happens to somebody that breaks a “pinky promise.”

Actually, I didn’t, but I wanted to convey the fact that I had a grasp of the serious nature of our agreement, so I shook my head solemnly and affirmed that I would never want to risk that. I could only assume that it must be something horrible in the mind of an eight-year-old child, like having to go to school in your underwear or having to kiss the teacher. (for those of you who are married to a teacher, remember, I’m qualifying this by saying “in the mind of an eight-year-old child,” as I don’t wish to offend anyone. I’m sure that kissing your wife would be far from horrible and probably be quite wonderful, not that I’m saying that I want to kiss your wife, but you get my point.)

As it turned out I was wrong and the consequences were of a far graver nature. I surveyed my children on the subject, and they looked at me as if I had asked them what the purpose of a television set was.

The answer was universal, “nobody will ever trust you again…duh.”

This to me is significantly worse than going to school in your underwear, and certainly worse than kissing a teacher.

This extremely delicate conversation began with a simple statement. “If I was a dog, I’d tell all the other dogs to sniff my butt,” the child said without a preamble while lying on the floor and looking up at the ceiling fan. “you better hush up and stop being rude. you’re going to get in trouble,” I responded from the couch. “no. I was thinking about this, and I’m serious.”

“Okay then,” I said, still suspicious, “What makes you say that?” “see there are three kinds of dogs.”

“There are lots of kinds of dogs,” I corrected.

“I’m not talking about collies, and poodles, or any of that stuff. I’m talking about how they act.” “different dogs act different ways,” I offered.

“I mean when dogs meet each other they act one of three ways.”

“Okay,” I replied, expectantly.

“The first kind of dog runs up and barks and growls and acts all mean. It’s like he’s saying, ‘I’m the boss, you better do what I say or I’m going to bite you all up’.” “so you don’t want to be the boss dog?” I asked, truly curious at this point. “naaah, the other dogs don’t really like him. It’s like they’re stuck with him and they just try to get away from him as soon as they can.”

“But he’s the alpha male, that’s what they call him. he’s the dog that all the other dogs have to listen to,” I instructed.

“They don’t listen to him. They just run off and go somewhere else. They go and are with dogs they like.”

“But the alpha males are the toughest dogs in the pack. They’re the bravest . . .” I started.

“They aren’t really. They’re afraid some other dog is tougher so they don’t want to take a chance. They stand in their own yard and act january

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tough, and growl.”

“Okay, so what are the other kinds of dogs?” I asked.

“The second kind of dog is the kind I’d hate to be. he’s the scared little dog; he just falls over on his back, with his belly up in the air. he’s saying, ‘don’t eat me. you can if you want, but I wish you wouldn’t.’ sometimes they even pee on themselves.”

“Well nobody wants to be that kind of a dog,” I reinforced, “so what’s the last kind?”

“The last kind of dog is the kind of dog I’d be. he just walks up like he is sticking out his paw to shake hands with the other dogs. he just lets the other dogs sniff at him. he’s saying, ‘What’s up?

Guess what I had for dinner last night?’ he’s the dog all the other dogs like.” “so, he’s just laid back,” I replied “no, he’s really the brave one. he’s not afraid of the other dogs. he just lets them come right up to him. If they act bad or bite at him or something then he might get mad, but most of the time he just acts nice and friendly. so if I was a dog, I’d just tell all the other dogs, ‘you can sniff my butt.’”

I took a sip of my coffee and thought about it for a moment.

“It’s just the butt smelling that...” I started.

“That’s not the right way to say it. humans might have to get that close to smell. A dog can smell you from across the room. It’s not smelling. dogs sniff.” for some reason, I found that even more disquieting. “If I were a dog, I think I’d stick to smelling them from across the room.

It would be a whole lot more sanitary.” “dogs don’t care about stuff being sanitary. They drink out of the toilet. Their favorite things to do are to roll in cow poop, or eat something dead that they found alongside the road. you got to think like a dog, to see what kind of dog you’d be.”

I guessed that I’d never know what kind of dog I’d be, because if I was a dog I wouldn’t be capable of rational thought or to make a decision based on reason. “see you’re a people doctor.…”

I nodded. “people get to tell you what’s bothering them, right?” “most of the time,” I replied.

“Well, see, dogs can’t talk.”

“At least, not any dogs I know,” I answered. “so, if I’m going to be a veterinarian I’ve got to know how dogs think; otherwise, how am I going to know what’s wrong with them?”

“Good point.”

The conversation taught me a couple of things. first, never underestimate an eight-year-old; they see things that we adults are too busy for. second, canine behavior is not too much different from

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1-800-962-2230 human behavior. A little more disgusting, maybe, but it’s not that different. how many of us hasn’t seen someone so obsequious that you didn’t automatically think of a submissive dog lying on its back, hoping that the big dog doesn’t bite it to pieces? Anybody that has watched a televised football game with all of the pre-game posturing, not much different from barking and growling, has seen the other side of that coin. most of us aren’t all that comfortable with either of these kinds of behaviors. We do our best to get away from people who act like that so we can go and hang out with folks we like. I guess my young friend hit the nail on the head. The bravest thing any of us can do is be open to each other, get close to each other, and take a chance on each other. The mechanisms of social interaction differ, but the principles are the same. so if you want to know what kind of dog I am, I have to say, I’m the kind of dog that still thinks the whole butt-sniffing thing is disgusting, but I will shake your paw.

—R. Scott Anderson, MD

[R. Scott Anderson, MD, a radiation oncologist, is medical director of the Anderson Regional Cancer Center in Meridian, and vice chair of the MSMA Board of Trustees. Additionally, he is an accomplished oil-painter and also dabbles in the motion-picture industry as a screenwriter and helped form P-32, an entertainment funding entity. “Una Voce” (With One Voice) is a column in the JMSMA designed by Dr. Dwalia S. South, MSMA past president and chair of the Committee on Publications. “Una Voce” features the selected prose of MSMA members. If you are a writer and would like to submit your work for consideration please send us your contribution or contact one of the editors.]—ED.

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