Title: PharmaNote
Full Citation
Permanent Link: http://ufdc.ufl.edu/UF00087345/00073
 Material Information
Title: PharmaNote
Physical Description: Serial
Language: English
Creator: College of Pharmacy, University of Florida
Publisher: College of Pharmacy
Place of Publication: Gainesville, Fla.
Publication Date: May 2009
 Record Information
Bibliographic ID: UF00087345
Volume ID: VID00073
Source Institution: University of Florida
Holding Location: University of Florida
Rights Management: All rights reserved by the source institution and holding location.


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Jamie Morancy-Maurice, Pharm.D. Candidate

Gestational diabetes mellitus (GDM) is defined
as any degree of glucose intolerance that is
first recognized during pregnancy.1 It is char-
acterized by insulin levels that are not sufficient to
meet the body's demand, much like other forms of
hyperglycemia.2 In some cases, undiagnosed diabe-
tes and/or glucose intolerance that existed before
pregnancy may reveal itself during gestation; this is
termed pregestational diabetes. This article will re-
view the current strategies for identifying and treat-
ing women with GDM. It will highlight the criteria
for screening and diagnosis of GDM, and the avail-
able methods of treatment.


Diabetes complicates approximately 7% of all
pregnancies,2 resulting in over 200,000 GDM cases
annually. Usually, women return to normoglycemia
after childbirth, but 30-50% of women will develop
type 2 DM later in life. A meta-analysis by Chueng
and colleagues found the population-attributed risk
of GDM to be between 10-31%, which means that 10
-31% of parous women with diabetes would have
experienced GDM during pregnancy.3 The relative
risk of developing diabetes later in life is 6 times

higher in women who have GDM compared to those
that do not.


Insulin is secreted from the pancreatic beta-cells
in response to intracellular glucose concentrations.
The intracellular concentration of glucose is in equi-
librium with serum glucose concentrations. When
secreted, insulin binds to insulin receptors on target
cells in liver, muscle, and fat tissues. After binding,
the receptor is activated, leading to a phosphoryla-
tion cascade within the cell that ultimately leads to
translocation of the GLUT 4 glucose transporter and
increased glucose uptake.
In the muscle, insulin stimulates glycogen syn-
thesis and inhibits glycogenolysis to promote glucose
storage. In fat tissue, increase glucose uptake and
stimulation of lipoprotein lipase promote storage of
fat. In the liver, insulin stimulates glycogen synthesis
and storage.
During pregnancy, the placenta and placental
hormones create an insulin resistance that is most
pronounced in the last trimester.4 Increases in the
levels of chorionic somatomammotropin, progester-
one, cortisol, and prolactin lead to counter-regulatory


11 Fi^ ^ ^ ^ ^ ^ -tI



i ^ ^ ^ ^^ ^ ^ ^ ^ ^^ ^ ^ ^ ^^ ^ ^ ^i^^ ^ ^ ^ j

Volume 24, Issue 8 1 May 2009


Table 1. Risk factors for gestational diabetes

SFamily history of diabetes Maternal birthweight > 9 pounds or < 6 pounds

SPre-pregnancy weight > 110% IBW or BMI > 30 kg/m2 Essential hypertension or pregnancy-related hypertension

SAge > 25 years Glycosuria at first prenatal visit

SPrevious delivery of baby > 9 pounds Current use of glucocorticoids

SHistory of abnormal glucose tolerance Polycystic ovary syndrome
SMember of ethnic group with higher than background Previous unexplained stillbirth or birth of malformed child
rate of type 2 diabetes

Adapted from Jovanovic L.9

anti-insulin effects.5 This increased insulin resistance
causes an insufficient response to insulin, leading to
maternal and fetal hyperglycemia that typically
manifests as postprandial hyperglycemic episodes.
The hyperglycemic episodes contribute to acceler-
ated growth of the fetus.
As a result of surging glucose levels in the blood,
fetal hyperinsulinemia occurs. Fetal hyperinsuline-
mia promotes excessive nutrient storage, resulting in
macrosomia, or large birth weight. Complications of
macrosomia include birth trauma, increased maternal
morbidity during labor, increased risk of glucose in-
tolerance and DM in offspring and increased risk of
Other complications that can occur in neonates
born to women with GDM include neonatal hypogly-
cemia, jaundice, polycythemia, hypocalcemia, birth
injury, hyperbilirubinemia, pre-term delivery, and
need for neonatal intensive care.6'7 Risks to the
mother with uncontrolled GDM include preeclamp-
sia, polyhydramnios, birth trauma, operative deliv-
ery, and perinatal mortality.


The practice of screening for GDM is controver-
sial. Some data suggest that screening is only mar-
ginally beneficial at reducing the complications asso-
ciated with GDM. The United States Preventive Ser-
vices Task Force concluded that current clinical evi-
dence is not strong enough to prove screening is
beneficial.8 However, the American Diabetes Asso-
ciation (ADA) and the American College of Obstet-
rics and Gynecology (ACOG) continue to recom-
mend screening during pregnancy.

Table 1 summarizes risk factors for developing
gestational diabetes. The ADA suggests that all preg-
nant women should be assessed for these risks at the
first prenatal visit and screening should occur at 24-
28 weeks of pregnancy.
Some data suggest that universal screening has
added benefits compared to selective screening."
However, the ADA suggests that women who pre-
sent with a low risk for diabetes do not require
screening. The criteria for exclusion from GDM
screening are listed in Table 2. A woman must meet
ALL the criteria to be excluded from screening.
Screening for diabetes during pregnancy can be
performed in two ways: a one-step approach, using a
diagnostic oral glucose tolerance test (OGTT) with-
out prior blood glucose screening; or a two-step ap-
proach, which involves screening the blood glucose
level 1 hour after a 50 g oral glucose load and then
performing the 100 g OGTT separately in women
who have plasma glucose levels > 130 or 140 mg/dL.
Using the two-step approach and the 130 mg/dL
threshold, the glucose challenge test identifies 90%

Table 2. Criteria for exclusion from GDM screening

SAge <25 years

SNormal weight before pregnancy

SMember of ethnic group that has low prevalence of DM

SNo known family history of DM in first-degree relatives

SNo history of abnormal glucose tolerance

SNo history of poor obstetrical outcome
Adapted from ADA Position Statement on Gestational Diabetes.6

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Volume 24, Issue 8 1 May 2009


of women with GDM.7 The 140 mg/dL threshold
identifies 80% of women with GDM.
The one-step approach and the second step of
the two-step approach use the 100 g OGTT. It should
be performed after an overnight fast of at least 8
hours and requires two above-threshold plasma glu-
cose levels.


The ADA and ACOG have published practice
guidelines for the management of GDM. Treatment
of GDM should be aimed at maintaining therapeutic
plasma glucose levels, reducing the risk of macro-
somia in the fetus, and lowering the risk of peri- and
postnatal complications in the mother. Table 3 lists
the threshold glucose levels suggested by several evi-
dence-based practice guidelines.

Medical Nutrition Therapy
To achieve glycemic control in diabetic patients,
clinicians suggest medical nutrition therapy (MNT),
defined as a carbohydrate-controlled meal plan that
promotes adequate nutrition with appropriate weight
gain, normoglycemia, and the absence of ketosis.12
The ADA recommends that all women with GDM
should receive nutritional counseling and individual-
ized MNT based on individual weight and height.
For women with a BMI > 30 kg/m2, a 30-33% total
caloric restriction can reduce hyperglycemia and
triglycerides without adversely increasing ketonuria.
Similarly, a reduction of carbohydrate intake to 35-
40% of total calories can decrease maternal glucose

levels and improve outcomes for the mother and fe-

Pharmacological Management
Medical nutrition therapy alone does not uni-
formly achieve adequate glycemic control, especially
in obese women and those women who have long-
standing and/or severe hyperglycemia. In these
women, MNT should be supplemented with pharma-
cological treatment. However, questions remain
whether the treatments for DM in the non-pregnant
population are safe and effective in pregnant women.
Currently, several different classes of oral drugs
are available to treat DM: insulin sensitizers, namely
the biguanides and the thiazolidinediones (TZDs);
insulin secretagogues, such as the sulfonylureas and
the meglitinides; and alpha-glucosidase inhibitors
like acarbose. Additionally, injectable medications
are available, including insulin in various forms and
newer agents like exenatide (Byetta), an incretin
mimetic, and pramlintide (Symlin), a synthetic
amylin analogue. These agents will be described and
their role in managing GDM will be discussed.

Historically, insulin therapy has been the treat-
ment of choice for GDM. Clinical evidence for cur-
rent insulin products demonstrates no crossing of the
human placenta and minimal risk to the fetus, mak-
ing insulin a safe option for gestational diabetes
management. 14
Human insulin is the least immunogenic of the
available insulin products, therefore it is the most
widely used for the treatment of GDM. Each pa-

Table 3. Recommended glycemic thresholds (mg/dL)1

ACOG ADA 4th Int'l Workshop CDA Thresholds in Non-
(2001) (2004) Conf. (1998) (2003) DM patients

Fasting 60-90 <105 <95 ---- 75 +/- 12

Premeal 60-105 ---- ---- 95 78 +/- 11

lhr post-prandial <130-140 <155 <140 <140 105 +/- 13

2hr post-prandial <120 <130 <120 <120 97+/- 11

Mean post-prandial 100 ---- ---- ---- 84+/- 18

Night-time 60-90 ---- ---- ---- 68+/- 10
Abbreviations: ACOG=American College of Obstetricians and Gynecologists, ADA= American Diabetes Association, CDA=Canadian Diabetes Association
Data are means +/- 1 SD

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V U1110 00UV IcllyVV


tient's dose should be individualized to meet her spe-
cific goals, and is based on the patient's current level
of glycemic control and carbohydrate intake.
Currently, the only insulin analogs FDA-
approved for GDM are isophane insulin (NPH), and
regular insulin.15 Lente insulin once carried this indi-
cation, but it is no longer available in the US. Regu-
lar and NPH insulin are used in combination to man-
age fasting and post-prandial glucose levels in GDM.
Doses typically start at 0.3-0.7 units/kg/day, but must
be individualized to each patient to achieve desired
glucose levels.
A study in women with GDM investigated the
short-term effects of insulin aspart compared to regu-
lar insulin or no insulin in controlling glucose lev-
els.16 It found that higher post-prandial insulin peaks
could be attained with insulin aspart (95.9 mcU/mL)
compared to regular insulin (84.7 mcU/mL) vs. no
insulin (72.6 mcU/mL). Additionally, insulin aspart
(Novolog) was very effective in reducing the peak
postprandial glucose concentration, resulting in a sig-
nificantly lower glucose than without insulin
(p<0.001). The difference with regular insulin com-
pared to no insulin was modest (p=0.034). The study
also found that at 3 hours post-prandial, there was a
lower demand for endogenous insulin with insulin
aspart than with regular insulin. Because elevated
post-prandial glucose levels are associated with an
increased risk of macrosomia, the study suggested
that administering insulin aspart 5 minutes before a
meal can reduce this risk.
Currently there are no published large-scale con-
trolled studies investigating the use of long-acting
insulins in GDM patients. While several small stud-
ies suggest that long-acting insulin analogs can be
effective in managing GDM,17'18 these studies have
failed to show that long-acting insulins are superior
to intermediate- or short-acting insulins, even though
they carry an increased risk of hypoglycemic epi-
sodes. Currently, long-acting insulins are used pre-
dominantly in pregnant women with pre-existing
type 1 DM. There is not enough clinical evidence to
support the use of long-acting insulin analogs includ-
ing insulin glargine (Lantus) or insulin detemir
(Lc\ cmii )in GDM.
While insulin is the cornerstone of GDM treat-
ment, the aversion to multiple daily injections has
prompted research of the oral anti-diabetes medica-
tions with regard to their efficacy and safety in preg-

Metformin increases the body's sensitivity to in-
sulin without directly stimulating insulin secretion. It
acts by decreasing hepatic gluconeogenesis produc-
tion, decreasing intestinal absorption of glucose, and
increasing peripheral glucose uptake and utilization
in the muscle and fat tissues via increased cell mem-
brane glucose transport.19
Metformin is the first-line treatment of type 2
DM in non-pregnant states.20 It significantly lowers
HbAlc, has favorable effects on the lipid profile, is
associated with less weight gain than with other oral
agents, and is useful in treating the insulin resistance
in polycystic ovarian syndrome (PCOS).
Metformin was investigated for the management
of GDM in the Metformin in Gestational Diabetes
(MiG) trial.21 The study compared the effects of met-
formin versus insulin in 751 women with GDM
(more than one fasting glucose of > 97.2 mg/dL or
more than one 2hr-postprandial glucose of > 120.6
mg/dL). The metformin group received 500 mg once
or twice daily, up to a maximum daily dose of 2500
mg, to achieve glycemic control of fasting glucose <
99 mg/dL or a 2-hour postprandial level < 126 mg/
The median daily dose that achieved glycemic
control in the metformin group was 2500 mg. Forty-
six percent of the women in the metformin group
were given insulin supplementation to achieve rec-
ommended glucose levels. At the end of the study,
there was no significant difference between the two
groups in the primary outcome, a composite of neo-
natal complications that included neonatal hypogly-
cemia (2 blood glucose readings < 46.8 mg/dL), res-
piratory distress that required at least 4 hours of oxy-
gen support, birth trauma, pre-mature birth (<37
weeks), and 5-minute APGAR scores <7 points. The
secondary outcomes measured were birth weight and
anthropometric measures, maternal hypertensive
complications, and maternal glycemic control up to 6
-8 weeks postpartum. The study also found no sig-
nificant difference in these outcomes.
Investigators also assessed the patients' accept-
ability of their respective treatment assignments us-
ing a questionnaire at 2 weeks post-partum. Seventy-
six percent of the women in the metformin group
said they would choose metformin again in a subse-
quent pregnancy, whereas 27% would prefer insulin
in a subsequent pregnancy. More women in the insu-
lin group rated taking the medication as the most dif-


Volume 24, Issue 8 1 May 2009


ficult part of the treatment.
The MiG trial demonstrated that metformin is a
safe alternative to insulin for the management of
GDM. While roughly half of the patients on met-
formin required insulin, it is important to note that
these patients generally had higher baseline glucose
levels and/or were significantly obese. Therefore, in
patients with milder hyperglycemia, metformin is a
reasonable initial option for treating GDM, offering
more ease of use with no additional risk of maternal
or neonatal complications.21

For more information on metformin in GDM, a recent
comprehensive review is available in the latest issue
of Annals of Pharmacotherapy:

Wensel TM. Ann Pharmacother 2009;43 [Epub]. DOI

Sulfonylureas act by stimulating pancreatic islet
cells to secrete insulin. Several studies have investi-
gated sulfonylureas in pregnancy. Older studies sug-
gested that treatment with sulfonylureas could in-
crease the fetal anomaly rate and neonatal hypogly-
cemia.22'23 These studies primarily investigated the
first-generation sulfonylureas including chlorpropa-
mide (Diabenese ) and tolbutamide (Orinase),
which cross the maternal placenta and lead to neona-
tal complications. The second-generation sulfony-
lureas, however, have minimal human placental
Langer and colleagues compared glyburide and
insulin in 404 pregnant women between 11 and 33
weeks gestation.25 Glyburide at a starting dose of 2.5
mg orally in the morning was titrated weekly to
achieve glycemic control, to a maximum dose of 20
mg. The authors reported no significant differences
between the two treatment groups in rates of macro-
somia (birth weight of 4000 g or more), lung compli-
cations, hypoglycemia, neonatal intensive care unit
admission, or fetal anomalies. In addition, they ob-
served similar levels of glucose control in both
groups, with the exception of 8 patients in the gly-
buride group requiring insulin to achieve target glu-
cose levels (90 mg/dL fasting and 100 mg/dL post-
A smaller study by Bertini and colleagues com-
pared insulin, glyburide, and acarbose in 70 pa-
tients.26 Patients in the glyburide group were given a
starting dose of 5 mg in the morning, increasing

every 7 days until achieving glucose control with
maximum dosage of 20 mg per day. The investiga-
tion found a higher rate of large for gestational age
(LGA) fetuses in the glyburide group compared to
the acarbose and insulin groups (p=0.073). Also, the
rate of neonatal hypoglycemia was higher in the gly-
buride group (33.3%; p=0.006), but the babies were
well-managed on their mothers' milk. Neonatal cap-
illary glucose levels did not differ significantly at
one, three, and six hours after birth. The investiga-
tion acknowledged that while insulin is a more effec-
tive choice in managing GDM, glyburide is an ac-
ceptable alternative when considering ease of use
and costs.

Acarbose (Precose) is an oligosaccharide that
inhibits carbohydrate absorption from the gut to re-
duce post-prandial glucose levels. Because it is asso-
ciated with a reduced risk of placental transfer and is
not systemically absorbed, acarbose has been of sig-
nificant interest for use in GDM.
At an initial dose of 50 mg before main meals,
titrated by 50 mg/day to a maximum total dose of
300mg/day, acarbose treatment resulted in fewer
cases of hypoglycemia than glyburide (5.3% vs
33.3%; p=0.006), but required insulin treatment in a
larger proportion of patients compared to glyburide
(42.1% vs 20.8%).26 The investigators suggested that
acarbose may be an option in GDM patients wishing
to delay the need for insulin injections.

Other Therapies
Other oral options for treating diabetes outside
the setting of pregnancy include the thiazolidin-
ediones, meglitinides, and the newer class DPP-IV
inhibitor, sitagliptin (Januvia). For many of these
options, animal studies have illustrated placental
transfer with no teratogenic effects. However, there
have not been adequate human studies looking at the
effects of these drugs in pregnancy. These agents
should not be used in the treatment of GDM unless
the benefits of therapy clearly outweigh the potential
risks, and when other better-studied options have
been exhausted.
In cases when monotherapy does not achieve op-
timal glucose control, combination therapy may be
considered. Combination therapy offers the opportu-
nity to decrease doses on individual agents and to
decrease the side effect profile. Currently, the Re-

Phraoe oue2, su IMy20

Volume 24, Issue 8 1 May 2009


Table 4. Average retail costs of selected GDM medications


Insulin NPH
Novolin N 100u/ml 10ml vial 57.81
Novolin Penfill 100u/ml 5 pens x 3ml 133.28
Humulin N 100/ml 10ml vial 54.00
Regular Insulin
Novolin R 100u/ml 10ml vial 57.81
Humulin R 100u/ml 10ml vial 54.00
500mg tablet 30 tablets 12.99
1000mg tablet 30 tablets 17.99
2.5mg tablet 30 tablets 12.99
5mg tablet 30 tablets 11.99
50mg tablet 100 tablets 87.99
100mg tablet 100 tablets 89.99
Adopted from www.drugstore.com Prescription Price Checker.28

gional Obstetrical Consultants group in Tennessee is complications in the mother and neonate. The ADA
investigating the use of Glucovance, a combination recommends that all pregnant women be screened for
of glyburide and metformin, with a starting dose of the risk of GDM at 24-28 weeks gestation, and that
1.25/250 mg twice daily.27 Until this and other study women at risk be screened using the one-step or two-
results are available, there is limited data to routinely step glucose challenge test.
recommend combination oral therapy in gestational Insulin continues to be the standard of treatment
diabetes. for GDM. In patients in whom glycemic control is
not achieved by medical nutrition therapy, NPH or
COST regular insulin can be used to achieve normoglyce-
mia and reduce the risk of maternal and neonatal
Table 4 summarizes the average retail price of complications. Insulin aspart is pregnancy category
the agents discussed in this article. Using these B and has favorable data supporting its use in GDM,
prices, the cost of treating a patient with metformin but awaits approval.
2500 mg daily would be $61.96 (two 100 mg tablets Oral options for treating GDM include met-
and one 500mg tablet each day) or $64.95 (500 mg formin, glyburide, and acarbose. Metformin, at a
tablets only) for 30 days. Glyburide would cost dose of 2500 mg daily, achieves normoglycemia in
$12.99-44.95, depending on the dose. Insulin prices women with GDM. It is a more widely accepted dos-
vary by brand and dose. age form and can be used in patients who are averse
to multiple insulin injections. Glyburide is used to
manage GDM at a starting dose of 2.5 mg daily ti-
SUMMARY treated to a maximum dose of 20 mg daily. Acarbose,
in small studies, is somewhat effective in treating
Tight control of plasma glucose is important dur- GDM. No definitive conclusions can be drawn about
ing pregnancy to reduce the risk of GDM and its its use in GDM; it is an area of research that requires

ri ia i -W^ **1UiL v^I I, 1 no I Ay f rAnn

V U1110 00UW IcllyVV

0rilma illtU L

further exploration. Other oral antidiabetic agents
should not be used for the management of GDM
unless a thorough risk:benefit evaluation is made and
other better-studied options are exhausted.


1. Proceedings of the 4th International Workshop-
Conference on Gestational Diabetes Mellitus. Chi-
cago, Illinois, USA. 14-16. March 1997. Diabetes
Care 1998;21:B1.
2. Metzger B, Buchanan T, Coustan D, De Leiva A,
Dunger D, Hadden D, et al. Summary and Recom-
mendations of the Fifth International Workshop-
Conference on Gestational Diabetes Mellitus. Dia-
betes Care 2007 Jul;30: S252-60.
3. Cheung N, Bythe K. Population Health Signifi-
cance of Gestational Diabetes. Diabetes Care
4. Dahlgren J. Pregnancy and Insulin Resistance. Me-
tab Syndr Relat Disord 2006;4(2): 149-52.
5. Funk JL. Disorders of the Endocrine Pancreas. In:
McPhee SJ, Ganong WF, editors. Pathophysiology
of Disease: An Introduction to Clinical Medicine,
5th Ed. Available from: http://
6. American Diabetes Association. Position State-
ment: Managing Gestational Diabetes. Diabetes
Care 2003;26(1):S103-5.
7. HAPO Study Cooperative Research Group. Hyper-
glycemia and Adverse Pregnancy Outcomes. N
Engl J Med 2008;358(19): 1991-2002.
8. U.S. Preventive Services Task Force. Screening for
Gestational Diabetes Mellitus: U.S. Preventive Ser-
vices Task Force Recommendation Statement. Ann
Intern Med 2008;148(10):759-65.
9. Jovanovic L. Screening and diagnosis of gesta-
tional diabetes mellitus. UpToDate Online. Avail-
able at http://www.utdol.com/online/content/
t o p i c d o ?
topicKey=pregcomp/28647&selectedTitle= 141 &s
10. Cosson E, Benchimol M, Carbillon L, et.al. Univer-
sal rather than selective screening for gestational
diabetes mellitus may improve fetal outcomes.
Diabetes Metab 2006;32(2): 140-6.
11. Yogev Y, Hod M. Goals of Metabolic Management
of Gestational Diabetes: Is it all about the sugar?
Diabetes Care 2007;30:S180-7.

12. Medical Nutrition Therapy, Evidence-Based
Guides for Practice: Nutrition Practice. Guidelines
for Gestational Diabetes Mellitus (CD-ROM). Chi-
cago, IL, American Dietetic Association, 2001.
13. Franz MJ, Monk A, Barry B, et al. Effectiveness of
medical nutrition therapy provided by dietitians in
the management of non-insulin dependent diabetes
mellitus: a randomized, controlled clinical trial. J
Am Diet Assoc 1995;95:1009-17.
14. Coustan D. Pharmacological Management of Ges-
tational Diabetes: An overview. Diabetes Care
15. Gold Standard, Inc. Isophane Insulin (NPH) Mono-
graph. Clinical Pharmacology [database online].
Available at : h t t p : / /
www.clinicalpharmacology.com. Accessed: March
16. Pettitt D, Ospina P, Kolaczynski J, Jovanovic L.
Comparison of an Insulin Analog, Insulin Aspart,
and Regular Human Insulin With No Insulin in
Gestational Diabetes Mellitus. Diabetes Care
2003 ;26(1):183-6.
17. Graves D, White J, Kirk J. The Use of Insulin
Glargine With Gestational Diabetes Mellitus. Dia-
betes Care 2006;29(2):471-2.
18. Price N, Bartlett C, Gillmer M. Use of insulin
glargine during pregnancy: a case-control pilot
study. BJOG 2007;114(4):453-7.
19. Gold Standard, Inc. Metformin Monograph. Clini-
cal Pharmacology [database online]. Available at:
http://www.clinicalpharmacology.com. Accessed:
March 13, 2009.
20. Nathan DM, Buse JB, Davidson MB, et al. Man-
agement of Hyperglycemia in Type 2 Diabetes: A
Consensus Algorithm for the Initiation and Adjust-
ment of Therapy. Diabetes Care 2006;29(8): 1963-
21. Rowan JA, Hague WM, Gao W, et al. Metformin
versus Insulin for the Treatment of Gestational Dia-
betes. N Engl J Med 2008;358(19):2003-15.
22. Kemball ML, McIver C, Milner RDG, et al. Neona-
tal hypoglycaemia in infants of diabetic mothers
given sulphonylurea drugs in pregnancy. Arch Dis
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23. Lebovitz HE. Insulin secretagogues: old and new.
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24. Elliott BD, Langer O, Schenker S, Johnson RF.
Insignificant transfer of glyburide occurs across the
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parison of Glyburide and Insulin in Women with
Gestational Diabetes Mellitus. N Engl J Med

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26. Bertini AM, Silva JC, Taborda W, et al. Perinatal
outcomes and the use of oral hypoglycemic agents.
J Perinat Med 2005;33(6):519-23.
27. ClinicalTrials.gov. Bethesda (MD): National Li-
brary of Medicine (US). Identifier NCT00371306,
Comparison of Glucovance to Insulin for Diabetes
During Pregnancy; Sep 1, 2006. Available at:
NCT00371306. Accessed cited Mar 26, 2009.
28. Drugstore.com. Online Prescription Price Finder.
Accessed April 17, 2009. Available at http://
default.asp?trx= lZ5015.


SGoliimumab iSimponi Ccmict'i r Orii BiD- i
tech, Inc

In April, 2009, the FDA granted approval for a
new monoclonal antibody, golimumab, for the $
treatment of moderate-to-severe rheumatoid arthri-
tis, ankylosing spondylitis, and active psoriatic ar-
thritis. Golimumab is injected subcutaneously on a
Monthly basis and is approved in combination with $
methotrexate in rheumatoid arthritis and active pso-
riatic arthritis. However, it may also be used as
monotherapy in active psoriatic arthritis and anky-
losing spondylitis.
As with other tumor necrosis factor alpha in-
hibitors, golimumab has been associated with an
iiiC i-scL d iik >\ l tubicutIlosis ,I d lotlh IIn\t i\c
I Iun'e.il inIl. ion' .l.'
* /

New indication for tigecycline

On March 20, 2009, the FDA approved a tige-
cycline for use in community-acquired bacterial
pneumonia (CABP) caused by susceptible strains
of S. pneumoniae, H. influenzae, or Legionella
Spneumophila. The approval was based on the re-
Ssults of two randomized trials showing non-
Sinferiority to levofloxacin 500 mg dosed once or
Twice daily. Dosing for CABP is equivalent to pre-
vious indications (100 mg loading dose then 50 mg
every 12 hours).

% ........................ e ......................................


% S ine Inluiienza Update

As of April 29, 2009, 91 cases of Swine influ-
enza, an influenza A (H1N1) strain, have been
confirmed in the U.S. Although most cases in the
U.S. and elsewhere have resulted in clinically mild
disease, at least 1 death in Texas and > 150 deaths
in Mexico have been attributed to this virus. Sub-
sequently, the FDA has authorized Emergency Use
SAuthorization (EUA) for the influenza antivirals,
oseltamivir and zanamivir. The EUA temporarily
lifts restrictions on the use of these antivirals and
Sallows a variety of healthcare workers as well as
volunteers to dispense these medications.
S The CDC is recommending that nasopharyngeal
Sswabs/aspirates be collected from patients with sus-
Spected swine influenza infection and transported to
state public health departments for confirmatory
Analysis. In addition, recommendations for the use
of each of influenza antivirals can be found on the
CDC website available at:


The PharmaNote is Published by:
The Department of Pharmacy
Services, UF Family Practice Medical
Group, Departments of Community
Health and Family Medicine and
Pharmacotherapy and Translational
University of Florida

John G. Gums Editor
PharmD, FCCP

R. Whit Curry, MD Associate Editor

Steven M. Smith Assistant Editor

Phraoe oue2, su IMy20

Volume 24, Issue 8 i May 2009


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