_ REVIEWS

Gestational Diabetes
Beverly A. Sullivan, Scott T. Henderson, and Julie M. Davis

Objective: To review the detection, diagnosis, and clinical management of gestational diabetes. Data Sources: MEDLlNE, Gestation·
al Diabetes Guideline Review, 1968-1998. Study Selection: By the author. Data Extraction: By the author. Data Synthesis: Gesta·
tional diabetes is a common complication of pregnancy, occurring in 2% to 6% of pregnancies. Uncontrolled gestational diabetes is
associated with increased infant morbidity and mortality, macrosomia, and cesarean deliveries, and is a strong marker for the future
development of maternal diabetes mellitus. Women with risk factors for gestational diabetes should be screened for glucose intoler·
ance at 24 to 28 weeks' gestation. If a screening plasma glucose concentration is 140 mg/dL or greater one hour after a 50 gram oral
glucose load, then a diagnostic 100 gram, three·hour oral glucose tolerance test should be performed. Medical nutrition therapy is the
cornerstone of management and must be designed to meet individual needs. Self-monitoring of blood glucose should be taught to
and performed by all women with gestational diabetes. Insulin, which does not readily cross the placental barrier, is the drug therapy
of choice in women failing medical nutrition therapy. Conclusion: Pharmacists can optimize overall care by educating, monitoring,
and intervening or assisting the patient in the management of gestational diabetes.
JAm Pharm Assoc. 1998;38:364-371.

Most pregnancies are uncomplicated and result in normal, Background

healthy outcomes for both mother and child. For some women,
however, serious problems during pregnancy require a higher
level of monitoring by physicians and pharmacists and more
extensive interactions with health care providers. Gestational dia-
betes is such a disorder, and pharmacists skilled in pharmaceuti-
cal care can have a positive influence on outcomes in these
patients.
This review discusses current concepts relative to the detec-
tion, diagnosis, and clinical management of gestational diabetes.
To help the pharmacist contribute to optimal outcomes in
patients with the condition, a case study is presented to place the
concepts discussed within a relevant clinical context.
Received December 17, 1997, and in revised form March 17, 1998.
Accepted for publication April 6, 1998.
See related drug treatment protocol on page 307.
Beverly A. Sullivan, PharmD, is associate professor of pharmacy prac-
tice, School of Pharmacy; Scott T. Henderson, MD, is assistant profes-
sor of family practice, Family Practice Residency Program; Julie M.
Davis, RD, is temporary assistant lecturer, Family Practice Residency
Program, University of Wyoming, Laramie.
Correspondence: Beverly A. Sullivan, Box 3375, School of Pharmacy,
University of Wyoming, Laramie, WY 82071-3375. Fax: (307) 766-2953.
E-mail: barnone@uwyo.edu
Diabetes is a common medical complication of pregnancy. I
Women with this condition can be classified as having either
pregestational (10% of cases) or gestational (90% of cases) dia·
betes. Women who were diabetic before becoming pregnant
have pregestational diabetes. Gestational diabetes primarily aris·
es during the second half of pregnancy and is characterized by
carbohydrate intolerance of variable severity.!
Poorly controlled pregestational diabetes is associated with
progressive maternal end-organ damage; increased ketosis; con·
genital malformations such as central nervous system defects,
anencephalus, and cardiac and renal anomalies; and obstetric
complications such as stillbirth, macrosomia (birth weight
greater than 4 kg), and delayed lung maturation.
Fortunately, outcomes in gestational diabetes are generally
less dramatic, and are directly related to the successful control of
the condition. Macrosomia, dystocia (dysfunctional labor
attributed to birth canal abnormalities, fetal abnormalities, or
weak or abnormal uterine contractions), birth trauma, and neona·
tal metabolic complications are the most frequently encountered
complications.
The severity of gestational diabetes ranges from mild intoler·
ance (readily managed by diet) to frank life-threatening diabetes
(requiring aggressive insulin therapy). Reported prevalence of

364 Journal of the American PhannaceuticaJ Association May/June 1998 Vol.38,NO.J

 Gestational Diabetes REVIEWS

gestational diabetes ranges from 0.15 to 12.3% of pregnancies,

depending on the screening methods, diagnostic criteria, and the Learning Objectives
geographic, ethnic, and racial differences among the patients
screened. 2 Gestational diabetes occurs in 2% to 6% of pregnan- After reading this article, the pharmacist should be able to:
cies, making it a common complication of pregnancy. 3,4 • Describe the pathophysiology of gestational diabetes
and how it differs from normal pregnancy.
• Discuss risk factors associated with developing gesta-
Pathophysiology tional diabetes.
• List short- and long-term maternal and infant conse-
Normal, Nonpregnant Women. In the normal nonpregnant, quences of gestational diabetes.
nondiabetic woman, plasma glucose concentrations are main-
• Describe current recommendations for the screening
tained within a narrow limit (approximately 40 to 160 mgldL)
and diagnosis of gestational diabetes.
through the interaction of insulin, glucagon, growth hormone,
• Discuss the clinical management of gestational dia-
somatostatin, epinephrine, glucocorticosteroids, and thyroid hor-
betes, including the role of medical nutrition, therapy, self
mone. s Fine-tuning of glucose concentrations ensures a constant
supply of energy to the vital organs and prevents the damaging monitoring of blood glucose, drug therapy, exercise, and
consequences of hyperglycemia to normal tissues. goals of treatment.
I Following a meal, carbohydrates are broken down .to glucose, • Discuss the role of the pharmacist in the pharmaceutical
and proteins are broken down to amino acids in the gastrointesti- care of the patient with gestational diabetes.
nal tract, where they are absorbed. Pancreatic beta cells respond
quickly to a carbohydrate/protein load (i.e., a meal) by releasing
insulin in an amount appropriate for facilitating the uptake of glu- glucose levels. These changes reach a nadir by the 12th week of
cose and amino acids into tissues. Insulin is essential for liver pregnancy and remain at this level until delivery. Normal preg-
storage of glycogen, prevention of glycogenolysis, increased syn- nancy is essentially a state of insulin resistance or glucose intoler-
I thesis of fatty acids, and prevention of ketone body formation. ance that is successfully overcome by increased production of
During fasting conditions, counterregulatory substances, such as maternal insulin. Interestingly, insulin requirements are greatly
glucagon, epinephrine, and thyroid hormone, facilitate the break- diminished during labor but, along with insulin levels, return to
I down of liver glycogen to glucose, stimulate the conversion of normal upon delivery.
amino acids to glucose by gluconeogenesis, and promote lipolysis Women with Gestational Diabetes. When the state of relative
in adipose tissues. insulin resistance present in all pregnancies is not overcome, ges-
CE Credit Normal Pregnant Women. tational diabetes results. 8 Several factors are potentially responsi-
In normal pregnancy, the pres- ble for development of gestational diabetes. In obese (20% or
CE Credit ence of the fetus results in more than desired body weight) women, disordered insulin secre-
To obtain two hours of altered fuel handling and uti- tion and a deficiency of insulin receptors are major contributing
continuing education credit
(0.2 CED) for completing lization. 6 ,7 Maternal metabolism factors. Compared with normal pregnant women, patients with
"Gestational Diabetes," com- is changed to provide adequate gestational diabetes have higher fasting plasma insulin levels,
plete the assessment excercise nutrition for the mother and delayed insulin response to a glucose load, and a decreased ratio
and CE registration form and
return it to APhA. A certifi-
fetus. Modifications in the lev- of insulin produced relative to the blood glucose concentration. In
cate will be awarded upon els of hormonal substances- 10% of women with gestational diabetes, the defect appears to be
aChieving a passing grade of including estrogen, proges- a general insulin deficiency. 2,9 These women tend to be of normal
70% or better. Individuals
terone, and human placental
completing this article by
May 31, 2001, can receive lactogen-result in lower glu-
credit. cose levels, promotion of fat
deposition, delayed gastric Women's Health Series

ru
ffi
The American
Pharmaceutical
Association is ap-
proved by the American Council
on Phannaceutica1 Education
emptying, and increased
appetite. These changes result
in an increase in insulin pro-
"Gestational Diabetes" is part of the Journal of the Ameri-
can Pharmaceutical Association's series on women's health,
funded through an educational grant from Wyeth-Ayerst
duction and secretion, while Laboratories.
as aprovider of continuing
pharmaceutical education. increasing peripheral insulin
resistance at a postinsulin
~ APhA program number is:
~ 202-000-98-097-HOl. receptor site.
The overall result is a
decrease in maternal fasting

YOI.38,No.3 May/June 1998 Journal of the American Phannaceutical Association 365

 REVIEWS Gestational Diabetes
or less-than-normal weight, and most will proceed to develop
mature-onset insulin-dependent diabetes mellitus. 10
Case Study
BV is an obese (80 kg, 5'6"), 33-year-old caucasian woman,
mother of two (G2P2), with a history of gestational diabetes dur-
ing her most recent pregnancy. BV has a significant family history
(mother, sister) of type 2 diabetes. Her children weighed 11 and 9
pounds at birth and were both delivered by cesarean section.
Discussion: What patient factors are associated with an
increased risk of gestational diabetes? BY demonstrates several
risk factors: age 25 or older, obesity, family history of diabetes in
first-degree relatives, and a neonate weighing more than
4 kg. 2,7,11,12 Other risk factors associated with gestational diabetes
include race (Hispanic American, Native American, Asian
American, African American, and Pacific Islander women have
high incidences of gestational diabetes), glycosuria, repeated uri-
nary tract infections, history of stillbirth/miscarriages, history of
gestational diabetes with a previous pregnancy, and polyhydram-
nios (excessive amniotic fluid). Although a knowledge of the fac-
tors associated with gestational diabetes is helpful in identifying
those mothers who are at greatest risk, almost 50% of women
with the disorder have no identifiable predisposing factors. 13,14
Case (continued): During her first pregnancy, BY was seen dur-
ing her first trimester by her family physician. However, she was
lost to medical follow-up until her 35th week of pregnancy, when
she experienced preterm labor (contractions with cervical changes
before 37 weeks, gestation). Failing bed rest and hydration, BV
was hospitalized for further evaluation and for administration of
parenteral tocolytic therapy (subcutaneous terbutaline). During this
hospitalization, BY was diagnosed with gestational diabetes.
Physical examination and ultrasound measurement revealed
that the fetus was large for its gestational age (macrosomic).
Terbutaline was discontinued for fear that it would complicate
glycemic control. BY was then given magnesium sulfate 6 gram
bolus dose followed by a 2 gram/h continuous infusion to control
the preterm labor. The magnesium infusion rate was increased
until contractions resolved. The patient was discharged to her
home at 36 weeks. At 38 weeks' gestation, BY had an induction
of labor because of the gestational diabetes and macrosomia.
Because of dystocia (failure to dilate the cervix), prolonged labor,
and fetal distress, the ll-pound (5 kg) boy was delivered by
cesarean section. The infant experienced profound hypoglycemia
during the first 72 hours postpartum, which was managed with
glucose and intensive blood glucose monitoring.
Discussion: What are the maternal and fetal risks of gestational
diabetes? The short-term adverse maternal consequences appear
to be small and mainly due to the increased rate of cesarean sec-
tions performed as a result of fetal macrosomia. 8 Obstetric com-
plications commonly associated with pregestational diabetes, such
as pregnancy-induced hypertension and preeclampsia, are not
366 Journal of the American Pbannaceutical Association
clearly associated with or increased in gestational diabetes. I'
Long-term follow-up suggests an increased risk of reCUITeI1Ci !
of gestational diabetes in up to 55% of subsequent pregnancies
Glucose intolerance disappears upon delivery of the infantiL I
almost all cases; however, gestational diabetes appears to ~ a .
strong marker for the future development of diabetes mellitus. '
with reported incidences of 6% to 62%, depending on the di~1
nostic criteria and duration offollow-Up.8,15 Because oflong-tenr,'
risks, the American College of Obstetricians and Gynecolo~!t
(ACOG) recommends that women with a history of gestational
diabetes be tested for glucose intolerance during the first fe~
months following delivery and thereafter on a yearly basis. 16 Tht
1998 American Diabetes Association (ADA) Clinical Practicl
Recommendations call for testing for diabetes every three yeanli
postpartum diagnostic testing for diabetes is normal, or more fre·
quently if the woman demonstrates impaired fasting glucose O!
glucose intolerance postpartum. 12
Short-term consequences in infants born to women with gesla'l
tional diabetes are less severe than in infants born to mothers wiili '
pregestational diabetes. However, some features, such as infant
macrosomia and dystocia, are common to both. Fetal macrosomia
results from an increased fetal supply of maternal glucose, amino
acids, and fatty acids and from fetal hyperinsulinemia secondary to
the maternal hyperglycemiaP Insulin-like growth factors I andlll
are also increased in the cord blood of neonates born to mothers wiili
gestational diabetes, and concentrations of insulin-like growth facto!
I have been directly correlated with birth weight in one study.18
As described in the present case, BY bore an II-pound infant
who required delivery by caesarian section because of dystocia
prolonged labor, and fetal distress. Shoulder dystocia, a complica·
tion of gestational diabetes, occurs when the mother's pubic sym·
physis obstructs the delivery of the infant's anterior shoulder ana
results partially from increased deposition of fat in the infan!',
shoulder and trunk. Even when infants of similar large birth
weights are compared, shoulder dystocia occurs more frequentlJ
in women with diabetes. 19 Because of the known risks of fetal
macrosomia and shoulder dystocia, many practitioners will offer!
delivery by cesarian section without a trial of labor in gestational
diabetes if the infant's weight is estimated to be greater than 4
kg.8 Results from a recent prospective historically controlled
study suggested that early elective delivery at 38 to 39 weeks in
high-risk patients with gestational diabetes significantly decreased I
the incidence of shoulder dystocia from 10.2% to 1.4%.20
Past studies have suggested that infant mortality is increased in
gestational diabetes, especially if the mother is 25 years or older?
obese,13 or a member of certain ethnic minorities (Asian, Hispanic.
or the Pima Indian tribe).2,22,23 However, more recent data indicate
that optimal pregestational, prenatal, and postnatal care with goo! I
glycemic control results in reduced or normal mortality rates W
infants born to mothers with gestational diabetes. 5,8.24,25
Animal and limited epidemiologic studies suggest that obesi~ [
and the development of type 2 diabetes may be long-term conse;
quences in infants born to mothers with gestational diabetes. t
May/Junel998 VOI.38,N~)1
 Gestational Diabetes REVIEWS

Therefore, recognition and appropriate lifetime monitoring with in first-degree relatives; member of an ethnic minority with a high
r risk·reduction efforts may be warranted. prevalence of diabetes (Native American, Hispanic American,
Why did BV's infant experience profound hypoglycemia after African American, Asian American, or Pacific Islander).12
~irth? Postpartum hypoglycemia-both in the neonate and in the What screening procedures and criteria are commonly recom-
mother-may accompany poorly controlled gestational diabetes. It mended? A common screening procedure recommended by ACOG
occurs more often with pregestational diabetes . Infant hypo- and ADA requires that pregnant women orally ingest a 50 g glucose
i11ycemia experienced in the neonatal period is thought to result source, with plasma glucose concentration measured one hour lat-
frominfant hyperinsulinemia, which is present at birth secondary to er.12.16.28 The test may be performed in either a fasting or nonfasting
eXiXlsure to high concentrations of maternal glucose during preg- state, but fasting improves sensitivity.16.29 A plasma glucose concen-
nancy. Other fetopathic effects of poorly controlled gestational dia- tration of 140 mg/elL or more should be followed with a diagnostic
retes include hypocalcemia, polycythemia, hyperbilirubinemia, and 100 gram, three-hour oral glucose tolerance test (OGTf). At a 140
respiratory distress syndrome. 2 If a woman is hyperglycemic during mg/elL threshold on the initial test, 15% of all pregnant women
labor, strict glycemic control is needed in the infant to prevent screened will likely need the OGTI, and 90% of women with gesta-
hYlXlglycemia. Blood glucose should be measured every one to two tional diabetes will be detected by the combination of the two tests.
hmand maintained at approximately 100 mg/elL by a continuous Some clinicians have argued that the trigger value for the OGrr
infusion or intermittent injection of glucose and insulin.5 should be 130 mg/elL; although this value might detect all women
Case (continued): During her second pregnancy, BV was with gestational diabetes, decreasing the threshold to 130 mg/eIL
! screened at her initial physician office visit and her plasma glucose would also require that 25% of all women receive further diagnostic
t values were normal. She was rescreened at 24 weeks and had a testing. 16 Others have argued that this decreasing the threshold
I Jllsitive diagnostic follow-up test for gestational diabetes. Initially, results in too high of a false-positive rate (i.e., lack of specificity)
dietary measures were sufficient to manage BV's gestational dia- and would be needlessly costly to the health care system.
retes; however, repeat fasting plasma glucose was > 105 mg/eIL While the implications of gestational diabetes are clear, and meth-
, ontwo occasions. BV's condition was then managed with insulin ods for screening and diagnosis are readily available, screenirIg-
fuerapy and diet. At 38 weeks' gestation, BV delivered a 9-pound even in women at risk-is not universally performed. In a recent
(approximately 4 kg) infant girl by elective cesarian section. study of participants in the Nurses Health Study n, 17% of normal
Discussion: What are the current recommendations for the women nurses and 14% of nurses who developed gestational dia-
screening, diagnosis, and clinical management of gestational dia- betes were not screened for the disorder during their pregnancies.3o
retes? Recommendations for screening are controversial. In the What diagnostic procedures and criteria are commonly recom-
past, some studies have suggested that up to 50% of women with mended for gestational diabetes? The woman will be asked to eat
gestational diabetes do not have pre-existing risk factors. ACOG, a diet that contains at least 150 grams of carbohydrate/day for
in ils 1994 Technical Bulletin, recommended universal screening three days prior to the diagnostic OGTT. The OGTf requires that
of pregnant women at 24 to 28 weeks' gestation in clinical set- pregnant women in a fasting state ingest 100 grams of glucose.
tings where women with risk factors for gestational diabetes are Plasma glucose samples are taken fasting and at one, two, and
~n. In some very high-risk populations, such as Native Ameri- three hours. Gestational diabetes is diagnosed when two out of
cans, ACOG suggests waiving screening procedures and proceed- four of the plasma glucose levels either meet or exceed diagnostic
ingdirectly to diagnostic testing. 16 The Second and Third Interna- criteria. 12.16 In the past, criteria for abnormal OGTf levels in ges-
tional Workshop-Conference on Gestational Diabetes Mellitus tational diabetes have varied; standards frequently used in the
recommended universal screening for the disease. 26.28 United States have included the National Diabetes Data Group
Recently, however, researchers have suggested that universal (NDDG) criteria 31 and the Carpenter and Coustan crite-
SCreening is unnecessary in low-risk populations. Results from a ria.12.13.32.33 The 1998 ADA clinical practice recommendations
retrospective analysis of a predominantly low-risk population suggest the use of the diagnostic criteria of O' Sullivan and Mahan
indicate that fewer than 1% of pregnant women without risk fac- modified by Carpenter and Coustan. 12 See Table I.
tors are ultimately diagnosed with gestational diabetes. The study What management strategies are useful in gestational diabetes?
concluded that only women with identifiable risk factors need to Optimally, management should start before conception in at-risk
be screened, but a thorough history should be taken on all preg- women. Preconception counseling and monitoring in women with
nant women to determine whether they have risk factors for ges- histories of gestational diabetes have resulted in decreased macro-
tational diabetes. 27 somia, neonatal hypoglycemia, maternal weight gain, preeclamp-
The 1998 ADA Clinical Practice Recommendations state that sia, and cesarean section in subsequent pregnancies compared
SCreening should be performed between the 24th and 28th weeks of with at-risk women who received no preconception counseling
gestation only in women meeting one or more of the following risk and monitoring. 34 Planned pregnancies in women at risk for ges-
criteria: 12 25 years of age or older; younger than 25 years of age and tational diabetes should be encouraged. Low-dose oral contracep-
obese weight (20% or more above desired body weight, or body tives have been used safely in women with a prior history of the
illass index [BMI] of 27 kg/m2 or higher); family history of diabetes disorder without apparent exacerbation of glucose intolerance. 35

I'OI.38, No.3 May/June 1998 Journal or the American Phannaceutical Association 367
REVIEWS Gestational Diabetes
Table 1. Diagnostic Criteria for Gestational Diabetes
FoliolNing a 100-gram Oral Glucose Tolerance Test
Time After Glucose
Administration Plasma Glucose Concentration
(hrs) (mg/dL)
0* 105
1 190
2 165
3 145
* Fasting state.
Adapted from Reference 12.
Clinical Management of
Gestational Diabetes
Medical Nutrition Therapy
Medical nutrition therapy is the cornerstone of management of
gestational diabetes. Although most cases can be successfully man-
aged by diet alone, definitive studies and universally agreed-upon
nutritional guidelines are not available. 36 Issues such as optimal
daily caloric intake, ideal gestational weight gain, carbohydrate dis-
tribution, ideal meal patterns, and role of caloric restriction in gesta-
tional diabetes are controversial. 36,37 Dietary decisions will vary
depending on institutional norms of practice, severity of the dis-
ease, ongoing maternal weight gain, maternal activity level,
lifestyle, and motivation for dietary change. Dietary management
must be individualized to provide adequate calories for maternal
and fetal health while minimizing the risks of hyperglycemia and
ketonemia. Registered dietitians, certified diabetes educators
(CDEs), and pharmacists trained in the dietary management of ges-
tational diabetes can provide valuable assistance in educating, mon-
itoring, and motivating the pregnant woman with this condition.
Some sources suggest that initial daily caloric requirements
should vary based on each patient's present weight compared
with ideal body weight (lEW) (Table 2).16,36,37 For example, in
the above case, BV weighed 85 kg or 187 pounds at 24 weeks'
gestation during her second pregnancy. This is 144% of her mw
(IBW = 100 pounds + 5 pounds for every inch> 5 feet = 130
pounds) or a BMI (weight [kg]/[height in meters]2) of 30.
According to Table 2, BV's daily caloric intake should have been
Table 2. Daily Caloric Requirements in Gestational
Diabetes
Present Weight as % of IBW Daily Caloric Requirement
(kcal/kg of present weight)
< 80% (underweight) 30-40
80-120% 30-38
120-150% (overweight/obese) 24
IBW = Ideal body we·lght.
Adapted from Reference 16.
368 Journal of the American Phannaceutical Association
2,040 kcallday.
Researchers have studied the efficacy and safety of calon.
restriction in gestational diabetes. 38-42 Limited studies suggest ilia
hypocaloric diets may result in decreased maternal weight gain
decreased fetal macrosomia, and normalization of plasma glu
cose; however, ketone production may occur if calories air
restricted too severely.41 Clinicians have been reluctant to lin1
caloric intake in pregnant women because of the increased risk c;
"starvation ketosis" and the possibility of damaging effects on ilii
developing fetus. Ketosis may be fetopathic or teratogenic in
humans, although this is controversial. 8 Therefore, in women willi
gestational diabetes on calorie-restricted diets, urinary ketonel
should be monitored along with blood glucose concentrations37
Recommended weight gain during pregnancy is generall!
based on prepregnancy BMI (Table 3).36,38 In BV's case, her
prepregnancy weight was 84 kg and she was approximately 161
meters tall; therefore, her BMI was 30. From Table 3, her gesta·
tional weight gain should be at least 15 pounds by term.
ADA has traditionally recommended that patients with dia·
betes obtain 10% to 20% of calories from protein, with the
remaining caloric requirements obtained from carbohydrates ana
fats in proportions individualized to meet treatment goalS.43 For
many nonpregnant diabetic patients, a diet low in fat « 30%) ana
protein is desirable to minimize cardiovascular risk and nephropa·
thy. Gestational diabetes, however, is a short-term problem; there·
fore, restriction of fat and protein is not necessary to prevent long·
term complications.
Recommendations for meal patterns (frequency, proportions
content) vary depending on the clinical site; there are no defini
tive data to indicate whether maternal or fetal outcomes diffel
according to the meal pattern. Frequent snacks have been recom·
mended on the basis of evidence suggesting that small, frequent
meals result in lower overall insulin concentration and improved
glucose tolerance. 44 At the very least, small, frequent meals are
compatible with the later stages of pregnancy because of
decreased stomach capacity and decreased gastric emptying.
The California "Sweet Success" program recommends that
women with gestational diabetes eat three meals and three or
more snacks per day, with 38% to 45% of calories obtained from
carbohydrate, 20% to 25% from protein, and 30% to 40% from
fat. 36,45 The recommended daily caloric distribution of carbohy·
drate is 10% to 15% at breakfast, 5% to 10% at the morning
snack, 20% to 30% at lunch, 5% to 10% at the afternoon snack,
30% to 40% at dinner, and 5% to 10% at the evening snack
Breakfast carbohydrate calories are minimized, because glucose
tolerance is frequently worse in the early moming hours. 36
Exercise
Exercise is important in ensuring psychological and physical
well-being in patients with diabetes, but it may also have an impor·
tant role in increasing the sensitivity of body tissues to insulin and
increasing glucose utilization. 46 Several studies suggest that a care·
May/June 1998 Vol. 38, NO,.1

fully monitored exercise program combined with proper diet
enhances glycemic control in women with gestational diabetes.47 ,48
Appropriate exercise should involve the upper-body muscles and
place little mechanical stress on the trunk region and lower body.49
According to ACOG guidelines, exercise compatible with pregnan-
cy should be encouraged in women habituated to exercise before
pregnancy, whether or not they have gestational diabetes. 16
Self-Monitoring of Blood Glucose
Concentrations
Successful management of gestational diabetes requires close
monitoring of blood glucose. 8 ,12,16 Frequency of monitoring
depends on the severity of the diabetes and the cooperation and
motivation of the patient. At a minimum, patients should have a fast-
ing and a two-hour postprandial measurement weekly, preferably at
aclinical laboratory. Optimally, a woman should also monitor her
blood glucose at home four to eight times per day until blood glu-
cose content is consistently normal. A common regimen for check-
ingblood glucose levels includes a morning fasting measurement
~ong with levels taken one or two hours after eating. A decrease in
fetal macrosomia has been reported in women who have been
instructed how to modify their therapy in response to changes in
their blood glucose. 50 Improved neonatal outcomes, such as
decreased macrosomia and decreased hypoglycemia, have been
reported in women with insulin-treated gestational diabetes who
monitored fasting and postprandial glucose levels compared with
women who monitored fasting and preprandial glucose levels. S1
Whole blood concentrations determined using home blood glu-
cose meters are usually lower than plasma glucose samples
obtained in a laboratory. In general, whole blood determinations
are 85%of plasma concentrations.46 In other words, a sample of
whole blood that reads 85 mg/dL on a home glucometer usually
reads higher if the sample was from plasma.
Drug Therapy
Insulin therapy should be considered in women failing dietary
intervention with fasting plasma glucose concentrations of 105
mg/dL or higher and two-hour postprandial concentrations of 120
mg/dL or more (or one-hour postprandial concentrations of 140
mg/dLorhigher).12,16 Women who present with excessively high
concentrations (> 200 mg/dL) of plasma glucose are likely to fail
dietary therapy and are frequently started on insulin therapy soon
after diagnosis.
Human insulin is the drug of choice in gestational and preges-
~tional diabetes and has been shown to decrease macrosomia.9 It
I, aprotein of approximately 6,000 daltons, and only negligible
amOunts cross the placenta and reach the fetal circulation. Oral
'Ulfonylureas, which can cross the placenta and disturb fetal
metabolism, are contraindicated in pregnancy.52
Other agents, such as metforrnin and troglitazone, also may
Closs the placenta and affect fetal metabolism, and are therefore
101.38, No.3 May/June 1998
Gestational Diabetes REVIEWS
Table 3. Desirable Weight Gain in Gestational Diabetes
Prepregnancy Prepregnancy Pregnancy Weight Gain
%oflBW (BMI) (lb)
<90% < 19.8 2S-40
IBW 19.8 25-35
> 120% 26-29 15-25
> 135% > 29 At least 15
BMI = Body mass index ; IBW = Ideal body weight.
Adapted from References 36, 38.
not recommended.
Acarbose, a new alpha-glucosidase inhibitor, is minimally
absorbed from the gastrointestinal tract; therefore, the risk of fetal
exposure is small. s3 Acarbose delays the absorption of dietary
sugars and diminishes peak concentrations of glucose, thereby
contributing to overall glycemic control. Its role in gestational
diabetes, if any, has not been determined.
Insulin lispro (Humalog-Eli Lilly and Company), a recently
marketed synthetic insulin analogue, when administered subcuta-
neously, has a faster onset of action and shorter duration of action
compared with other human regular insulins. 54,ss Because the
pharmacokinetics of this new insulin more closely reflect the
appearance and disappearance of glucose with the administration
of a meal, the risk of postprandial hyperglycemia or postprandial
hypoglycemia is lessened. Unfortunately, the utility of lispro in
gestational diabetes has yet to be determined.
Case (continued): After failing diet therapy alone, BY was
started on an insulin regimen of 27 U NPH insulinl13 U regular
insulin every morning 30 minutes before breakfast and 10 U NPH
insulinllO U regular insulin every afternoon 30 minutes before
dinner. Fasting and two-hour postprandial plasma glucose con-
centrations were 100 mg/dL and 135 mg/dL, respectively, after
one week of therapy.
Discussion: How is insulin dosed in gestational diabetes?
Obese pregnant women are treated with insulin doses and regi-
mens similar to obese nonpregnant patients with type 2 diabetes
mellitus. These patients often have normal amounts of endoge-
nous insulin, but they require large doses of exogenous insulin to
overcome insulin resistance. If BY were thin, then a relative
paucity of endogenous insulin would be suspected and low doses
of insulin would be carefully titrated.
Insulin dosing is initiated in many regimens; the decision as to
which regimen to try depends on the severity of the disorder, the
motivation and education of the patient, and the availability of close
follow-up from health care providers. Insulin therapy can be initiat-
ed based on weight; a common starting dosage is 0.7 U/kg. 5,11 BV
is receiving a total dose of insulin 60 U, two-thirds as a 2: I ratio of
neutral protamine Hagedorn (NPH)/regular insulin in the morning
and one-third as a I: I ratio of NPHiregular insulin before the
evening meal. At 85 kg, this is a daily dose of 0.7 U/kg. Patients
with gestational diabetes who require insulin usually can be man-
aged with a split dose of insulin per day; an intensive regimen of
Journal of the American Phannaceutical Association 369
 REVIEWS Gestational Diabetes
Table 4. Goals for Glycemic Control in Pregnancy Complicated by Diabetes Mellitus
Glucose Concentrations (mg/dL)
Time Period ACOG*,t
Fasting 60-90
Pre-meal 60-105
l-hr postprandial 130-140
2-hr postprandial 120 or less
2-6am 60-90
ACOG = American College of Obstetrics and Gynecology; ADA = American
* From Reference 16.
t Plasma glucose values.
:j: From Reference 8.
# Acceptable values for patients on intensive insulin therapy.
II Blood glucose values.
three or more doses per day is rarely needed,5.16
Has BV reached a therapeutic goal in terms of glycemic con-
trol? ADA and ACOG have proposed goals for glycemic control
during pregnancy, As illustrated in Table 4, thresholds for
glycemic control during pregnancy are generally lower than even
"acceptable" thresholds in nonpregnant diabetic patients. Accord-
ing to established goals, BV has not achieved an adequate degree
of glycemic control. If diet is stable and no other confounding
variables, such as hypoglycemia, can be identified, BV may
require an increase in her insulin dose.
Insulin requirements in gestational diabetes may change dra-
matically at the time of labor and delivery. During labor, insulin
requirements often decrease markedly. Delivery is the definitive
"cure" for gestational diabetes in most cases, and most women
become normoglycemic in the immediate postpartum period.
Role of the Pharmacist
Pharmacists are becoming increasingly involved in the educa-
tion and monitoring of patients with diabetes. Educational oppor-
tunities and certification avenues are paving the way to reim-
bursement for such services. Certificate programs, such as those
sponsored by the American Pharmaceutical Association and vari-
ous schools of pharmacy (e.g., University of Tennessee, Purdue
University), provide the foundation for establishing these ser-
vices. Many pharmacists have become CDEs through the Nation-
al Certification Board for Diabetes Educators.
The pharmacist in professional practice is in a strong position
to offer key interventions for patients with gestational diabetes.
Specific educational materials for patients and pharmacists can be
obtained through sources such as ADA, the American Associa-
tion of Diabetes Educators, as well as on the Internet (e.g.,
www.niddk.nih.gov). Finally, pharmacists interested in the case
management of patients with diabetes should contact other phar-
macists with experience in this area. 56
The pharmacist can optimize overall care by educating the
patient with gestational diabetes, as well as by monitoring and
intervening when necessary in the management of this disorder.
Patient education should include information about the disease
370 Journal of the American Pharmareu1icaJ Association
-)
ADAu Nonpregnantil,1I
60-90 70-140
60-105 70-130
110-130 100-180
90-120 80-150
60-120 70-120
Diabetes Association.
process, its management with medical nutrition therapy and
insulin, goals of therapy, self-monitoring of blood glucose.
administration of and dosage adjustment of insulin, adverse
effects/interactions of medications, and expected outcomes. The i
pharmacist should monitor patients for adverse effects, drug and
disease interactions, medication and diet adherence, goals, and I
outcomes of therapy.
In addition, by working closely with the patient and with other I
health care providers, the pharmacist can help with the develop· \
ment and implementation of an individualized care plan. Phanna'l
cists can help patients adhere to their care plan by assisting them
with insulin dosage adjustments to improve glycemic control and'
by being accessible, reliable sources of information and support.
Conclusion
Armed with the proper knowledge and tools, the pharmacist is I
in an excellent position to participate fully on the health care team I
for the patient with gestational diabetes, greatly increasing the
likelihood of optimal outcomes in both mother and child.
References
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1973;4(884):89-93.
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3. Barss VA. Diabetes and pregnancy. Med Clin North Am. ,
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New York, NY: Wiley-Liss; 1995: chap 1.
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PJ, Hammond CB, et al., eds. Danforth's Obstetrics and GynecologY.
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9. Freinkel N, Metzer BE, Phelps RL, et al. Heterogeneity of maternal age,
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18. Insulin-like growth factors I and II peptide and messenger RNA levels
in macrosomic infants of diabetic pregnancies. J Soc Gynecol Invest.
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20. Lurie S, Insler U, Hagay ZJ. Induction of labor at 38 to 39 weeks of ges-
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natal mortality rate. Am J Obstet Gynecol. 1972;116:901-4
22. Pettitt OJ, Knowler WC, Baird HR, et al. Gestational diabetes: infant and
maternal complications of pregnancy in relation to third trimester glu-
cose intolerance in Pima Indians. Diabet Care. 1980;3:458-64.
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24. Kalkoff AK. Therapeutic results of insulin therapy in gestational dia-
betes mellitus. Diabetes. 1985; 34(S2):97-100.
25. Beischer NA. Wein p, Sheedy MT, et al. Identification and treatment of
women with hyperglycemia diagnosed during pregnancy can signifi-
cantly reduce perinatal mortality rates. Aust N Z J Obste Gynecol.
1996;36:239-47.
26. Freinkel N, Gabbe SG, Hadden R, et al. Summary and recommenda-
tions of the second international workshop-conference on gestational
diabetes mellitus. Diabetes.1985;34:12H.
27. Helton MR, Arndt J, Kebede M, et al. Do low risk prenatal patients real-
ly need a screening glucose challenge test? J Fam Pract.
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28. Metzger BE. Summary and recommendations ofthe third international
workshop-conference on gestational diabetes mellitus. Diabetes.
1991;4O(S2):197-201 .
29. Coustan DR, Widness JA, Carpenter MW, et al. Should the fifty-gram,
one hour plasma glucose screening test for gestational diabetes be
administered in the fasting or fed state? Am J Obstet Gynecol.
1986;154:1031-5.
~. Solomon CG, Willett WC, Rich-Edwards, et al. Variability in diagnostic
evaluation and criteria for gestational diabetes. Diabetes Care.
1996;19: 12~.
31. National Diabetes Data Group. Classification and diagnosis of diabetes
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1979;28:1039-57.
32. Kaufmann RC, Schleyhahn BA. Huffman DG, et al. Gestational diabetes
diagnostic criteria: long-term maternal follow-up . Am J Obstet
Gynecol. 1995;172:621-5.
33. Rust OA, Bofill JA, Andrew ME, et al: Lowering the threshold for the
diagnosis of gestational diabetes . Am J Obstet Gynecol.
1996;175(4Pt1 ):961-5.
Vol. 38, No.3 May/June 1998
Gestational Diabetes REVIEWS
34. Goldman JA. Dicker D, Feldberg A. et al. Preconceptional diabetes
counseling in gestational diabetes. In: Weiss PAM, Coustan DR, eds.
Gestational Diabetes. Wien, NY: Springer-Verlag. 1988; chap.1.
35. Kjos SL, Shoupe D, Douyan S, et al. Effect of low-dose oral contracep-
tives on carbohydrate and lipid metabolism in women with recent ges-
tational diabetes: Results of a controlled, randomized, prospective
study. Am J Obstet Gynecol. 1990;163:1822-7.
36. Gunderson EP. Intensive nutrition therapy for gestational diabetes:
Rationale and current issues. Diabetes Care. 1997;20(2):2-7.
37. Mulford MI, Jovanovic-Peterson L, Peterson CM. Alternative therapies
for the management of gestational diabetes. Clin Perinatol. 1993;20:630.
38. Jovanovic-Peterson L. Nutritional management of the obese gestation-
al diabetic pregnant woman. J Am Coli Nutr. 1992;11:25~2 .
39. Phelps RL, Metzger BE. Caloric restriction in gestational diabetes:
When and how much? J Am Coli Nutr. 1992; 11 :246-50.
40. Knopp RH, Magee MS, Raisys V, et al. Metabolic effects of hypocaloric
diets in management of gestational diabetes . Diabetes.
1991 ;4O(S2):165-71.
41 . Dornhorst A, Nicholls JSD, Probst F, et al. Calorie restriction for treat-
ment of gestational diabetes. Diabetes. 1991;4O(S2):161-4.
42. Committee on Nutritional Status During Pregnancy and Lactation,
Food and Nutrition Board, Institute of Medicine, National Academy of
Sciences. Nutrition During Pregnancy. Washington, DC: National
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43. American Diabetes Association . Nutrition recommendations and prin-
ciples for people with diabetes position statement. Diabetes Care.
1994;17:519-22.
44. Jenkins DJA, Wolever TMS, Vuksan V, et al. Nibbling versus gorging:
metabolic advantages of increased meal frequency. N Engl J Med.
1989;321 ( 14):929-34.
45. State of California, Maternal and Child Health Branch, Department of
Health Services. Sweet Success: Guidelines for Care. Rev ed. San Fran-
cisco: California Diabetes and Pregnancy Program; 1992.
46. Koda-Kimble MA, Carlisle BA. Diabetes mellitus. In: Young LY, Koda-
Kimble MA. eds. Applied Therapeutics: The Clinical Use of Drugs. 6th
ed. Vancouver, Wash: Applied Therapeutics, Inc; 1995: chap. 48.
47. Javanovic-Peterson L, Durak EP, Peterson C. Randomized trial of diet
versus diet plus cardiovascular conditioning on glucose levels in gesta-
tional diabetes. Am J Obstet Gynecol. 1989;161 :415-9.
48. Bung P, Artal R, Khodiguian N, et al. Exercise in gestational diabetes.
An optional therapeutic approach. Diabetes. 1991;4O(S2):182-5.
49. Durak EP, Jovanovic-Peterson L, Peterson CM. Comparative evaluation
of uterine response to exercise on five aerobic machines. Am J Obstet
Gynecol. 1990;162:754.
50. Goldberg JD, Franklin B, Lasser 0, et al. Gestational diabetes: impact of
home glucose monitoring on neonatal birth weight. Am J Obstet
Gynecol.1986;154:546-50.
51 . De Veciana M, Major CA, Morgan MA, et al. Postprandial versus
preprandial blood glucose monitoring in women with gestational dia-
betes mellitus requiring insulin therapy . N Engl J Med.
1995;333:1237-41.
52. Briggs GG. Teratogenicity and drugs in breast milk. In: Young LY,
Koda-Kimble MA. eds. Applied Therapeutics: The Clinical Use of
Drugs. 6th ed. Vancouver, Wash: Applied Therapeutics, Inc; 1995: chap
45.
53. Drug Facts and Comparisons. Acarbose. Facts and Comparisons, St.
Louis: 1996; 129a-12ge.
54. Humalog Package Insert. Indianapolis, Ind: Eli Lilly and Company; June
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55. Lispro, a rapid-onset insulin. Med Lett. 1996;38:96-7.
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Journal of the American Phannaceutical Association 371
 REVIEWS Gestational Diabetes

Assessment Questions 8. Optimally, women with gestational diabetes should self-monitor

blood glucose concentrations: .
a. Once per week fasting and at two hours postprandial.
Instructions: For each question, blacken the letter on the answer sheet b. Four to eight times per day with fasting and one or two hOIll1
corresponding to the answer you select as being the correct one. Please post-meal levels taken until blood glucose consistently nor·
malizes.
review all your answers to be sure that you have blackened the prop-
c. Three times per week.
er spaces. There is only one correct answer to each question. d. Once per day.

1. Gestational diabetes is defined as:
a. Carbohydrate intolerance of variable severity that occurs dur-
ing pregnancy.
b. Carbohydrate intolerance of variable severity that occurs pri-
marily during the second half of pregnancy.
c. Carbohydrate intolerance of variable severity that begins dur-
ing the first half of pregnancy.. .
d. Diabetes that precedes pregnancy and 1S aggravated by 1t.
2. A difference between gestational diabetes and nonnal pregnancy is:
a. Glucose intolerance is overcome by an increase in insulin
production. . c. Assisting with dosage therapy adjustment.
b. Insulin response to a glucose load 1S delayed. . d. All of the above alternatives are correct.
c. The amount of insulin produced relative to the concentratlOn
of blood glucose is diminished.
d. Alternatives b and c are both correct.
3. Which of the following is a risk factor in increasing the risk of ges-
tational diabetes?
a. 25 years of age or more.
b. Less than 25 years of age and obese.
c. Race/ethnic group (Native American, Asian American,
African American, Hispanic American, Pacific Islander).
d. All the above alternatives are correct.
4. Which of the following is not a potential maternal consequence of
gestational diabetes?
a. Recurrence of gestational diabetes in a subsequent pregnancy.
b. Increased risk of developing diabetes mellitus.
c. A significant increase in infant mortality.
d. Increased risk of cesarean section.
5. The diagnosis of gestational diabetes does not involve which of the
following?
a. Performance of a fasting plasma glucose followed by a 100 g,
three-hour oral glucose tolerance test (OGIT) with plasma
levels taken at one, two, and three hours after administration.
b. Two of four levels exceeding Carpenter and Coustan modi-
fied criteria.
c. One of four levels exceeding Carpenter and Coustan modified
criteria.
d. A fasting plasma glucose (FPG) level> 105 mgldL and a two-
hour FPG > 165 mgldL from a 100 gm OGIT.
6. When should the management of gestational diabetes start in an at-
risk woman?
a. Before conception.
b. After conception.
c. When gestational diabetes is diagnosed.
d. When complications arise.
7. All women with gestational diabetes on calorie-restricted diets
should:
a. Self-monitor blood glucose.
b. Monitor urinary ketones.
c. Monitor urinary protein.
d. Alternatives a and b are both correct.
9. The drug therapy of choice in gestational diabetes is:
a. Sulfonylureas.
b. Acarbose.
c. Insulin.
d. Troglitazone.
10. The role of the pharmacist in gestational diabetes includes which of
the following?
a. Monitoring for patient outcomes (efficacy, adverse effects,
compliance, quality of life).
b. Patient education.
11. Pregestational diabetes is
a. Early pregnancy, prior to 24 weeks gestation, in the woman
with gestational diabetes.
b. Glucose intolerance, prior to 24 weeks gestation, in the worn·
an with gestational diabetes.
c. Diabetes occurring in women before they become pregnant.
d. Diabetes occurring immediately postdelivery.
12. Gestational diabetes
a Is extremely rare, occurring in fewer than 0.004% of pregnancies.
b. Is a common complication of pregnancy, occurring in 2% to
6% of pregnancies.
c. Occurs in almost all obese pregnant women. ..
d. Should be suspected in all women who are underwe1ght pnor
to pregnancy.
13. According to ADA 1998 Clinical Practice Recommendations, how
frequently should women with gestational diabetes be tested for dla·
betes postpartum if initial diagnostic testing for diabetes is nonnal?
a. Every three years.
b. Every six months.
c. After age 45.
d. With sudden weight gain.
14. Hypoglycemia in the newborn should be managed with
a. Constant infusion of glucose.
b. Intermittent or continuous infusion of insulin to maintain
blood glucose around 100 mgldL.
c. Intensive blood glucose monitoring every one to two hours.
d. All of the above alternatives are correct.
15. The California Sweet Success Program recommends that women
with gestational diabetes eat
a. Three square meals a day with 60% of calories from carb?hY"
drate, 20% of calories from protein, and 20% of calories trom
fat.
b. Three meals with three snacks a day with 38% to 45% of
calories from carbohydrate, 20% to 25% from protein, and
30% to 40% from fat.
c. Three square meals a day with 60% of calories from fat, 20%
of calories from protein, and 20% of calories from carbohy- .
drate.
d. Three meals with three snacks a day with 38% to 45% of
I
calories from fat, 20% to 25% from carbohydrate, and 30% to
45% from protein.

372 Journal of the American Pharmaceutical Association May/June 1998 Vol.38,~O.J I

 Gestational Diabetes REVIEWS

16, Breakfast carbohydrate intake usually should be minimized because Instructions

a. Breakfast is hard for most people to eat.
b. Patients with diabetes require high protein intake in the early
morning hours. . To receive two hours of continuing education credit (0.2 CEU) for suc-
c. Glucose intolerance is frequently worse in the early morning cessful completion of this program, you must:
hours. 1. Complete the answer sheet and type or print your name,
d. Glucose intolerance is frequently worse at midday. address, and Social Security number in the space provided.

17, Acarefully monitored exercise program in women with gestational
diabetes may
a. Help ensure psychological and physical well-being.
b. Increase tissue sensitivity to insulin and increase glucose uti-
lization.
c. Enhance glycemic control.
d. All of the above alternatives are correct.
2. Mail your completed answer sheet with the correct handling
fee ($5 for APhA members; $15 for nonmembers; no additional charge for
current 12-exam continuing education program members) to:
Processing DesklEducation
American Pharmaceutical Association
2215 Constitution Ave., NW
Washington, DC 20037-2985

18, Aplasma glucose concentration of 126 mg/dL roughly corresponds Certificates will be issued to those who score 70% or higher. Those who
to a whole blood glucose concentration of score below 70% will be notified, and no credit will be recorded. Allow
a. 107 mg/dL. four weeks for processing.
b. 145 mg/dL. Expiration date: May 31,2001
c. 126 mg/dL.
d. 140 mg/dL.
Answer Sheet
19, Thresholds for glycemic control during pregnancy are usually
a. Lower than acceptable thresholds in nonpregnant women 1. @ ® © @ ® 11. @ ® © @ ®
with diabetes. 2. @ ® © @ ® 12. @ ® © @ ®
b. Higher than acceptable thresholds in nonpregnant women 3. @ ® © @ ® 13. @ ® © @ ®
with diabetes.
c. About the same acceptable thresholds in nonpregnant women
4. @ ® © @ ® 14. @ ® © @ ®
with diabetes.
5. @ ® © @ ® 15. @ ® © @ ®
d. None of the above alternatives are correct. 6. @ ® © @ ® 16. @ ® © @ ®
7. @ ® © @ ® 17. @ ® © @ ®
20, In the woman with gestational diabetes, insulin requirements during 8. @ ® © @ ® 18. @ ® © @ ®
labor frequently 9. @ ® © @ ® 19. @ ® © @ ®
a. Increase dramatically.
b. Decrease dramatically.
10. @ ® © @ ® 20. @ ® © @ ®
c. Remain the same.
d. Alternative a or c is correct. Gestational Diabetes

APhA provider number for this program is: 202-000-98-097-HOl .

Make checks payable to "APhA":
o $5 fee enclosed (member rate).
o $15 fee enclosed (nonmember rate).
D $45 12-exam continuing education program fee enclosed.
o $45 12-exam continuing education program fee paid earlier.
Name __________________________________________

Address,________________________________________

City _ _ _ _ _ _ _ _ _ _ _ State ZIP _ _ _ __

Social Security # _ _ _ _ _ _ _ _ _ _ _ _ _ __

I hereby certify that I have taken this test: (signature)

Program Evaluation
Excellent Poor
Overall quality 5 4 3 2 1
Relevance to practice 5 4 3 2
Value of content 5 4 3 2
Agree Disagree
Important to pharmacists 5 4 3 2 1
Increased my knowledge 5 4 3 2
Achieved stated objectives 5 4 3 2
Did not promote particular
product or company 5 4 3 2
It took me hours and minutes to read this article and
complete the assessment questions.

VO
L38
,No.3 May/June 1998 Journal of the American Pharmaceutical Association 373