804
U N I T 9
Endocrine System
or removal of pancreatic tissue and with other endocrine
diseases, such as acromegaly, Cushing syndrome, or
pheochromocytoma. Endocrine disorders that produce
hyperglycemia do so by increasing the hepatic produc-
tion of glucose or decreasing the cellular use of glucose.
Several specific types of diabetes are associated with
single gene defects in beta cell function. These specific
types of diabetes, which resemble type 2 diabetes but
occur at an earlier age (usually before 25 years of age),
were formerly referred to as
maturity-onset diabetes of
the young
(MODY).
3
Cystic fibrosis–related diabetes
(CFRD) is now recognized as the most common com-
plication of cystic fibrosis. Glucose abnormalities are
especially common in children younger than 10 years
old. The pathophysiology of CFRD is poorly under-
stood, but insulin deficiency is the major factor (possibly
related to pancreatic scarring).
11
Several diuretics—thiazide and loop diuretics—can
elevate blood glucose. These diuretics increase potas-
sium loss, which is thought to impair beta cell release
of insulin. Other drugs and therapies known to cause
hyperglycemia include diazoxide, glucocorticoids, oral
contraceptives, antipsychotic agents, and total paren-
teral nutrition (i.e., hyperalimentation). Drug-related
increases in blood glucose usually are reversed after
the drug has been discontinued. A newly recognized
form of diabetes, new-onset diabetes after transplant
(NODAT), is a common complication after tissue or
organ transplant and occurs in 15% to 30% of recipi-
ents. Several drugs are thought to be important in the
pathophysiology of this condition including glucocor-
ticoids (which can increase insulin resistance) and cer-
tain immunosuppressants such as cyclosporine (which
are beta-cell toxic).
11
The advent of potent antiretro-
viral therapy (especially protease inhibitors) for the
treatment of human immunodeficiency virus (HIV)
infection has significantly improved survival in these
conditions. However, these people are now developing
metabolic derangements with features similar to those
seen in the metabolic syndrome (see Chart 33-1).
25
In addition, changes in fat distribution (peripheral
lipoatrophy and visceral obesity), sometimes referred
to as
lipodystrophy,
often occur (see Chapter 16).
These people should be aggressively treated to prevent
cardiovascular complications resulting from the abnor-
mal risk factors.
Gestational Diabetes
Gestational diabetes mellitus (GDM) is defined as glu-
cose intolerance that develops during pregnancy and
is not clearly overt diabetes (either type 1 or type 2).
11
It occurs in 3% to 7% of pregnancies in the United
States and is growing in prevalence.
26,27
The hyperglyce-
mia varies in severity from glucose concentrations that
would be diagnostic of diabetes apart from pregnancy to
concentrations that are asymptomatic and only slightly
above normal.
27
Factors that indicate a high risk for
GDM include glycosuria, strong family history of type
2 diabetes, severe obesity, polycystic ovary disease, and
prior history of GDM or delivery of a previous large-
for-gestational-age infant.
All pregnant women should undergo risk assessment
for diabetes during their first prenatal visit to determine
the need for additional screening tests. Women who
are younger than 25 years of age; were of normal body
weight before pregnancy; have no family history of dia-
betes, prior history of GDM or large-for-gestational age
infant, or presence of glycosuria; and are not members
of a high-risk ethnic/racial group (e.g., Hispanic, Native
American, Asian, African American) may not need to
be screened.
11,26,27
Women at high risk for GDM should
undergo glucose testing as soon as possible. An FPG
greater than or equal to 126 mg/dL; or a casual plasma
glucose greater than or equal to 200 mg/dL; or a A1C
greater or equal to 6.5% meets the threshold for diag-
nosis of diabetes mellitus and should be confirmed on a
subsequent day as soon as possible.
11
Women of average
or low risk, including those not found to have diabetes
early in pregnancy, should undergo GDM testing at 24 to
28 weeks of gestation using a 50-g OGTT. This screen-
ing test consists of 50 g of glucose given without regard
to the last meal, followed in 1 hour by a venous blood
sample for glucose concentration. If the plasma glucose
level is greater than 140 mg/dL (7.8 mmol/L), a 100-g
3-hour OGTT is indicated to establish the diagnosis of
GDM.
27
If the plasma glucose measured 3 hours after
the test is greater or equal to 140 mg/dL (7.8 mmol/L),
a diagnosis of GDM is made.
27
Diagnosis and careful medical management are essen-
tial because women with GDM are at higher risk for
complications of pregnancy, mortality, and fetal abnor-
malities.
3
Fetal abnormalities include macrosomia (i.e.,
large body size), hypoglycemia, hypocalcemia, polycy-
themia, and hyperbilirubinemia.
Treatment of GDM includes close observation of
mother and fetus because even mild hyperglycemia has
been shown to be detrimental to the fetus.
26,27
Maternal
fasting and postprandial blood glucose levels should be
measured regularly. The mother’s diet should provide
the necessary nutrients for maternal and fetal health,
CHART 33-1
NCEP ATP III Criteria for a Diagnosis of
Metabolic Syndrome
Three or more of the following:
■■
Abdominal obesity: waist circumference >35 inches
(88 cm) in women or >40 inches (102 cm) in men
■■
Triglycerides:
≥
150 mg/dL (1.7 mmol/L)
■■
High-density lipoproteins (HDL): <50 mg/dL
(1.3 mmol/L) in women or <40 mg/dL (1.0 mmol/L) in
men
■■
Blood pressure: >130/85 mm Hg
■■
Fasting plasma glucose: >100 mg/dL (5.6 mmol/L)
Developed from Grundy SM. Panel Chair.Third Report of
the National Cholesterol Education Program (NCEP) Expert
Panel on Detection, Evaluation, andTreatment of High
Blood Cholesterol in Adults (AdultTreatment Panel III). NIH
Publication No. 01–3670. Bethesda, MD: National Institutes of
Health; 2001.
