Part C. Metabolic, Nutritional, and Environmental Disorders

19.  Screening for Diabetes Mellitus

RECOMMENDATION

There is insufficient evidence to recommend for or against routine

screening for diabetes mellitus in asymptomatic adults. There is also

insufficient evidence to recommend for or against universal screening for

gestational diabetes. Although the benefit of early detection has not been

established for any group, clinicians may decide to screen selected

persons at high risk of diabetes on other grounds (see Clinical

Intervention). Screening with immune markers to identify persons at risk

for developing insulin-dependent diabetes is not recommended in the

general population.

Burden of Suffering

Approximately 14 million persons in the U.S. have diabetes mellitus.1 Non-

insulin-

dependent diabetes mellitus (NIDDM) or Type II diabetes accounts for 90-

95% of all cases of diabetes in the U.S., while insulin-dependent diabetes

mellitus (IDDM) or Type I diabetes accounts for the remaining 5-10%.1-4

An estimated half of all persons with diabetes (primarily patients with

NIDDM) are currently unaware of their diagnosis.2 Diabetes may cause

life-threatening metabolic complications, and is the seventh leading

cause of death in the U.S., contributing to roughly 160,000 deaths each

year.1,3 It is also an important risk factor for other leading causes of

death such as coronary heart disease and cerebrovascular disease.4

Diabetes is the most common cause of polyneuropathy, with approximately

50% of diabetics affected within 25 years of diagnosis,5 and is

responsible for over 50% of the 120,000 annual nontraumatic amputations

in the U.S.6 Diabetic nephropathy is now the leading cause of end-stage

renal disease in the U.S.7 and, if current trends continue, will soon

account for 50% of all patients with renal failure.8 Diabetes is the leading

cause of blindness in adults ages 20-74 and accounts for over 8,000 new

cases of blindness each year.9 Infants born of diabetic women are at

increased risk of fetal malformation, prematurity, spontaneous abortion,

macrosomia, and metabolic derangements.10,11 Compared to persons

without diabetes, diabetic patients have a higher hospitalization rate,

longer hospital stays, and increased ambulatory care visits.3,12 The total

annual economic burden of diabetes is believed to approach $100 billion in

the U.S.13

The onset of NIDDM is usually after age 30, and the prevalence steadily

increases with advancing age. It is estimated that nearly 20% of the U.S.

population aged 65-74 has diabetes.2 The prevalence of NIDDM is markedly

increased in Native Americans and is also higher among black and Hispanic

populations.3 The prevalence of NIDDM is greater than 70% in Pima Indians

55 years of age and older.14 Other risk factors for diabetes include family

history, obesity, and a previous history of gestational diabetes or

impaired glucose tolerance. IDDM has an earlier onset (usually before age

30), a much shorter asymptomatic period, and a more severe clinical

course than NIDDM. 

Gestational diabetes mellitus (GDM), the development of glucose

intolerance during pregnancy, occurs in 3-5% of all pregnancies and is the

most common medical problem of pregnancy.3,15 Risk factors for GDM

include obesity, increased maternal age, hypertension, glucosuria, a

family history of diabetes, and a history of a macrosomic, stillborn, or

congenitally malformed infant. GDM is a risk factor for fetal macrosomia

and is associated with other neonatal complications, such as

hyperbilirubinemia and hypoglycemia. Macrosomia-most commonly defined

as birth weight above 4,000 or 4,500 g-is not itself a morbid condition

but is associated with increased risk of operative delivery (cesarean

section or vacuum or forceps delivery) and birth trauma (e.g., clavicular

fracture, shoulder dystocia, and peripheral nerve injury).16-19 In some

series, the incidence of shoulder dystocia in infants over 4,000 g is close

to 2%.20 Women with a history of GDM are also at increased risk for

developing NIDDM later in life.21

Accuracy of Screening Tests

The diagnosis of diabetes in many nonpregnant patients is based on typical

symptoms (polyuria, polydypsia) in association with clear elevation of

glucose (fasting plasma glucose > 140 mg/dL [7.8 mM]). Many

asymptomatic persons, however, may have abnormal glucose metabolism

and be at increased risk for complications of diabetes.

Diagnosis of Diabetes in Asymptomatic Persons. The National Diabetes

Data Group (NDDG)22 and World Health Organization (WHO)23 have issued

similar criteria for diagnosing diabetes in asymptomatic persons, based

on elevated fasting plasma glucose (>140 mg/dL) or an abnormal plasma or

serum glucose following an 75 g oral glucose tolerance test (OGTT). NDDG

criteria for a positive OGTT (> 200 mg/dL at 2 hours and before 2 hours)

differ slightly from WHO criteria (glucose > 200 mg/dL at 2 hours alone).

Abnormal glucose measurements on more than one occasion are required

for a diagnosis of diabetes.22,23 The complex diagnostic criteria reflect

both the difficulty in distinguishing diabetic from nondiabetic patients on

the basis of a single measurement, and the substantial test-retest

variability of the OGTT. The coefficient of variation for OGTT ranges from

20% to 35%.24,25 To improve reliability of the OGTT in nonpregnant

adults, the American Diabetes Association (ADA) recommends that

patients eat an unrestricted diet for 3 days preceding the test and fast

overnight before the test.26

Both the NDDG and WHO recognize an intermediate form of disordered

glucose metabolism, impaired glucose tolerance (IGT), based on

intermediate results of the OGTT (140-200 mg/dL).22,23 Patients with

IGT are at increased risk of developing frank diabetes, but rates of

progression are highly variable. IGT is also a risk factor for

cardiovascular disease.25 A significant number of individuals diagnosed

with IGT revert to normal on repeat testing,25 and the treatment

implications of IGT alone are uncertain.

Diagnosis of Gestational Diabetes. The diagnosis of GDM is traditionally

based on two or more abnormal values during a 3-hour glucose tolerance

test using 100 g glucose.22,27 NDDG diagnostic criteria are based on

extrapolations from standards for whole blood glucose originally derived

by O'Sullivan28 to identify mothers at risk of developing diabetes in long-

term follow-up. The conversion factor used to develop criteria for plasma

glucose measurements may have been incorrect, however,29 and others

have proposed modified criteria with lower thresholds as more sensitive

predictors of adverse pregnancy outcomes.30 Outside of North America,

the diagnosis of GDM is usually based on WHO criteria using a 2-hour 75 g

glucose tolerance test.23 The prevalence of GDM varies considerably

depending on whether WHO, NDDG, or modified criteria of Carpenter and

Coustan30 are used.15,31 In addition to poorly standardized criteria for a

positive OGTT in pregnancy, the lack of studies on the reproducibility of

the 100 g glucose tolerance test contributes to ongoing controversy over

the diagnosis of GDM.32-34

Because diagnostic glucose tolerance testing is too time-consuming and

expensive for routine screening, various blood or urine tests have been

examined for their ability to identify three distinct at-risk populations

among asymptomatic persons: persons with undiagnosed NIDDM, pregnant

women with GDM, and individuals at high risk of developing IDDM. 

Screening for Non-Insulin-Dependent Diabetes. The most commonly used

screening tests for NIDDM include measurement of serum or plasma

glucose in fasting or postprandial specimens, measurement of

glycosylated proteins in blood, and detection of glucose in urine. The

sensitivity and specificity of the fasting plasma glucose (compared to

diagnostic oral glucose tolerance testing) depends on the threshold set to

define an abnormal screening result. A single fasting glucose above 140

mg/dL is specific for diabetes (>99%) but sensitivity varies widely among

different populations (21-75%).35-40 Using a lower threshold (>123

mg/dL) improves sensitivity (40-88%), while maintaining reasonably high

specificity (97-99%).35-40 A random (i.e., nonfasting) plasma glucose

greater than 140 mg/dL has a sensitivity of 45% and a specificity of

86%.41 The ADA recommends that a fasting plasma glucose greater than

115 mg/dL, or a random glucose greater than 160 mg/dL, be considered a

positive screen to be confirmed with OGTT.26 

The nonenzymatic attachment of glucose to circulating proteins, primarily

hemoglobin and albumin, reflects overall metabolic control in diabetic

populations. A number of studies have evaluated HbA1c and serum

fructosamine as screening tests for diabetes.40,42-45 Test

characteristics are more variable than fasting plasma glucose, with

sensitivity ranging from 15% to 93% and specificity from 84% to 99%.

Presence of glucose in the urine is fairly specific but less sensitive than

most blood tests for NIDDM. In population-based screening using

semiquantitative urine dipstick, a "trace positive" dipstick result or

greater has a reported sensitivity of 23-64% and specificity of 98-

99%.40,46 In a high-risk population, quantitative assays of urine glucose

achieved high sensitivity (81%) with high specificity (98%), comparable to

both fasting plasma glucose and glycosylated protein assays.40

Sensitivity of all screening tests increases with the severity of

hyperglycemia among the diabetic population.40 Both the sensitivity and

positive predictive value of screening tests will be highest in high-risk

populations such as Native Americans and African Americans, where

undiagnosed diabetes and severe hyperglycemia are more prevalent.40 In

the asymptomatic general population, where the prevalence of undiagnosed

diabetes is only 1-3%, a greater proportion of diabetic patients may be

missed by screening, and many persons with a positive screening test will

not have diabetes. Screening asymptomatic persons may have some

harmful effects, including an increase in false-positive diagnoses; in a

review of 112 patients being treated for diabetes in a general practice,

nine (8%) patients, all without classic symptoms, were found not to have

diabetes on further evaluation.47 Even a true-positive diagnosis could

have adverse consequences for an asymptomatic person if it causes

"labeling" effects48 or difficulty obtaining insurance. 

Screening for GDM. The Third International Workshop Conference on

Gestational Diabetes has recommended screening pregnant women at 24-

28 weeks of gestation with a 50 g 1-hour oral glucose challenge test,

performed in fasting or nonfasting state.27 Patients with plasma glucose

of 140 mg/dL (7.8 mM) or greater at 1 hour should undergo a diagnostic 3-

hour OGTT. There is no single threshold that accurately separates normal

from abnormal results on the glucose challenge test, however.27

Estimates of sensitivity of screening under this protocol range from 71%

to 83% with a specificity of 78%-87%.30,49,50 Sensitivity is increased by

using a lower threshold for a positive screen30,51 and by testing in the

fasting state.49 A large prospective study of nearly 4,300 pregnant

women reported that using higher cutpoints (142-149 mg/dL) and

adjusting for time since last meal could reduce the misclassification of

patients based on initial screening tests.52 Reproducibility of the 1 hour

glucose challenge test is only fair,53 but it improves with advancing

gestational age.54 In an unselected pregnant population (prevalence of

GDM approximately 3%), fewer than one in five women with a positive

glucose challenge test will meet criteria for gestational diabetes on a

full OGTT.52 

The elevations in plasma glucose in GDM are less pronounced than in IDDM

or NIDDM. As a result, neither serum glycosylated proteins51,55-58 nor

urine glucose34 are sufficiently sensitive for detecting GDM. In addition,

glucosuria is common among nondiabetic pregnant women. Random blood

glucose has been advocated as a simpler and less costly screening test for

GDM59,60 but its test performance has not been fully evaluated. A large

prospective study is comparing fasting and random plasma glucose to oral

glucose challenge for detecting GDM and for predicting adverse perinatal

outcomes.52

Screening for Patients at Risk for IDDM. A growing body of evidence

indicates that IDDM is a genetically linked autoimmune disorder, in which

progressive destruction of insulin-producing pancreatic islet cells

eventually leads to complete dependence on exogenous insulin.61 Islet cell

autoantibodies and insulin autoantibodies are pres- ent in the majority of

patients with newly diagnosed IDDM,62 and may precede the onset of

clinical symptoms by months to years. Immunoassays for islet cell

antibodies remain difficult to standardize,63 however, and appear to be of

limited value for screening in the general population. In individuals

without a family history of IDDM, the prevalence of islet cell

autoantibodies ranges from 0.3% to 4.0% and the chance of developing IDDM

in antibody-positive individuals is estimated to be less than 10%.64 The

potential value of immune markers is greater in high-risk individuals (i.e.,

first-degree relatives of affected patients). Several studies report that a

combination of immune markers and measures of insulin responsiveness

can identify a population at very high risk (up to 70%) of developing

IDDM.62,63,65 This high risk may make such persons appropriate

candidates for experimental interventions to reduce the risk of

progression to IDDM. Only 10% of all cases of IDDM, however, occur in

persons with a positive family history.

Effectiveness of Early Detection

Asymptomatic NIDDM. Up to 20% of patients with newly diagnosed NIDDM

already have early retinopathy, suggesting that the onset of diabetes may

be many years (estimated 9-12 years) before clinical diagnosis, and that

the microvascular changes may precede overt symptoms in many

patients.66 Earlier detection through screening might provide an

opportunity to reduce the progression of microvascular or macrovascular

disease due to asymptomatic hyperglycemia. Animal models of diabetes

suggest that hyperglycemia is the underlying cause of microvascular

complications,67 and numerous epidemiologic studies confirm that the

degree of hyperglycemia and duration of disease are associated with

microvascular complications such as nephropathy, retinopathy, and

neuropathy.5,68-72 Direct evidence that improving glucose control

reduces the incidence of these complications has only recently become

available, and only for patients with IDDM. In the Diabetes Control and

Complications Trial (DCCT), over 1,400 subjects with IDDM were

randomized to intensive insulin therapy versus conventional treatment.

Intensive insulin therapy improved average blood glucose, significantly

reduced progression of existing retinopathy, and significantly lowered the

incidence of retinopathy, neuropathy, and nephropathy in all patients.73,74 

The DCCT study is generally regarded as providing strong evidence of the

role of hyperglycemia in diabetic microvascular disease, but questions

remain about extrapolating its results to the management of patients with

NIDDM.75 The incidence of microvascular complications is lower in NIDDM

than IDDM, and the largest controlled trial to date of treatment of NIDDM

(the University Group Diabetes Program study) found no effect of improved

glucose control with insulin or drug therapy on retinopathy.76 More

definitive results may come from the U.K. Prospective Diabetes Study

(UKPDS), which randomized 2,520 patients with newly diagnosed NIDDM 

controlled with diet to diet alone, or additional therapy with

chlorpropamide, glibenclamide, metformin, or insulin.77 Three-year

results indicated that patients receiving drug or insulin therapy had

significantly better glucose control but greater weight gain and more

frequent episodes of hypoglycemia.78 Data on other clinical outcomes are

not yet available.

 Patients with diabetes are at significantly increased risk for coronary

heart disease, stroke, and peripheral vascular disease; cardiovascular

diseases combined account for the majority of deaths in diabetic patients.

The risk of cardiovascular disease, however, is not clearly associated

with either disease duration or degree of glycemic control. The rate of

increase in coronary heart disease risk over time is similar in patients

with NIDDM and in nondiabetic patients.79,80 In 8-year follow-up of

almost 500 diabetic men and women, disease duration was associated

with risk of ischemic heart disease in patients with IDDM but not in those

with NIDDM,81 and there was no correlation between cerebrovascular and

peripheral vascular events and diabetes duration. Detecting such an

association may be complicated by difficulty in accurately ascertaining

the onset of diabetes in patients with NIDDM. Insulin resistance and

hyperinsulinemia may be more important determinants of macrovascular

complications than degree of glucose control.79,82 In the UGDP study,

neither cardiovascular disease nor mortality was reduced by improved

glucose control in the intervention groups,76 but the interpretation of

these findings has been criticized.83 Drug therapy for NIDDM carries the

risk of hypoglycemia. In the UKPDS study, the annual incidence of

hypoglycemia was 28% for patients on glibenclamide, and 33% for those on

insulin; episodes requiring medical therapy occurred in 1.4% of subjects

each year.78

The majority of individuals in the U.S. who have disordered glucose

metabolism have IGT.84 Untreated, most persons with IGT do not develop

diabetes, but the reported cumulative incidence of diabetes at 10 years

has varied from 15% to 61%.25 Progression to diabetes is highest in some

Native American populations.85 There is little direct evidence of a benefit

of detecting and treating IGT.86,87 Prospective studies of interventions

to prevent progression to frank diabetes in patients with IGT have

produced conflicting results. One trial of dietary and pharmacologic

treatment88 and a nonrandomized trial of diet and physical activity

training89 each reported a reduced incidence of diabetes, whereas other

prospective studies have reported no effect on the rate of progression to

diabetes.90-92

Gestational Diabetes. GDM is associated with increased risk of fetal

macrosomia, birth trauma, neonatal hypoglycemia, and perinatal

mortality.93-96 No properly controlled trial has examined the benefit of

universal or selective screening compared to routine care without

screening. In two retrospective analyses, no significant difference in

macrosomia or in birth trauma was found in women screened for GDM

compared to unscreened control populations.97,98 Because women

screened for GDM are more likely to be at high risk, such studies cannot

reliably exclude a benefit of screening.98

The clearest benefit of screening is the potential for treatment to reduce

the incidence of fetal macrosomia in women with GDM. Although modified

diet can reduce hyperglycemia in GDM, only one controlled trial has

examined the effect of dietary therapy on clinical outcomes in GDM.99 A

total of 158 women with mild GDM (positive by NDDG criteria but not WHO

criteria) were randomized to diet treatment or no therapy; there were no

significant differences in perinatal outcomes, although slightly fewer

infants over 4,000 g were born to diet-treated mothers (3 vs. 5).100

Several randomized controlled trials have demonstrated that diet and

insulin (compared to diet alone) results in improved glucose control and

reduced incidence of macrosomia in women with GDM.94,101,102

Macrosomia was not significantly reduced in a fourth trial, but 15% of the

women assigned to diet therapy received insulin because glucose control

was inadequate.103 An overview of four randomized trials estimated that

treatment of GDM with diet and insulin, compared to diet alone, reduced

the incidence of macrosomia by two thirds (6% vs. 17%).104 Despite a

reduction in macrosomia, there were no significant differences in rates of

cesarean section, forceps delivery, or birth trauma between treated and

control groups in any of the prospective trials, however. There was only

one reported instance of shoulder dystocia among 140 births in the two

trials reporting this outcome.101,104 In a retrospective analysis of 445

gestational diabetics, women who received both insulin and dietary

treatment had significantly lower rates of birth trauma and operative

delivery than women who received dietary treatment alone or no

intervention.96 Since treatment was not randomly assigned, factors other

than treatment may have contributed to the differences in outcomes. 

The benefit of improved glucose control on other outcomes in GDM,

including perinatal mortality, remains uncertain. Although several case

series have reported marked improvements in perinatal death rates with

treatment of GDM,95,97,105-107 none of these studies employed an

appropriate control group. The use of historical controls (i.e., outcomes of

prior pregnancies) or general population controls is likely to exaggerate

the apparent benefits of treatment. In an overview of five randomized

trials, there was no significant difference in perinatal mortality among

women treated with diet and insulin (2.7%) and those treated with diet

alone (3.2%).104 Moreover, in trials conducted after 1975, there were no

perinatal deaths in treated or control groups.100,104 In one trial, insulin

treatment was associated with lower rates of neonatal jaundice and

nonsignificant reductions in admissions to the neonatal ICU.108 At the

same time, treatment of GDM may have adverse effects for some women.

In one retrospective analysis, women with GDM who maintained tight

glucose control (mean glucose < 87 mg/dL) had a higher incidence of

small-for-gestational age infants than nondiabetic controls.109 

Degrees of hyperglycemia more subtle than in GDM may result in increased

maternal and neonatal complication rates.110-112 The incidence of

macrosomia and preeclampsia/eclampsia is higher in women who

demonstrate at least one abnormal result among the four points on a

glucose tolerance test. The prevalence of mildly hyperglycemic pregnant

women who do not meet the criteria for GDM but are at increased risk

during pregnancy is unknown.

Although treatment of GDM can reduce macrosomia, the impact of

widespread screening and treatment on the overall incidence of

macrosomia and dystocia may be quite small. The reported incidence of

macrosomia in the general population varies from 1% to 8%,93,113 and

most macrosomic infants are born to women without GDM.114 Gestational

diabetes was responsible for only 5% of infants over 4,500 g in one

study,115 and it is estimated to account for only 5% of shoulder dystocia

cases in this country.116 Other factors such as maternal obesity,

gestational weight gain, and maternal age may be more important

determinants of macrosomia and adverse outcomes.117 In a prospective

study of GDM controlled with diet, the only significant predictor of birth

weight was maternal weight at delivery; plasma glucose levels were poor

predictors of birth weight.118

Persons at Risk for IDDM. Earlier diagnosis of IDDM could be of

considerable benefit if treatment could arrest the disease process before

severe insulinopenia and hyperglycemia had developed. A number of recent

trials have examined whether immunosuppressive agents can delay

disease progression in patients with new-onset IDDM.61 Although some

patients have experienced prolonged remissions, the benefit has not been

sustained in most patients, and the serious adverse effects of

immunosuppressive agents are likely to preclude their use in completely

asymptomatic persons. There have been several promising small trials of

other interventions to prevent IDDM in high-risk asymptomatic persons,

enrolling individuals identified by autoantibodies levels and other

physiologic measures.63,119,120 Multicenter randomized clinical trials

are currently underway to determine whether prophylactic regimens of

insulin or nicotinamide can prevent progression to IDDM in such high-risk

subjects.61

Recommendations of Other Groups

The Canadian Task Force on the Periodic Health Examination (CTF),121 the

American College of Physicians (ACP),122 and the American Academy of

Family Physicians123 recommend against routine screening for diabetes

among asymptomatic nonpregnant adults; each of these organizations

concluded that selective screening may be reasonable among individuals at

high risk of developing diabetes (e.g., older obese persons, those with a

strong family history). AAFP policy is currently under review. The ADA

recommends screening all individuals with a careful history and

measuring fasting glucose on those with identified risk factors for

developing diabetes, including obesity, family history, history of GDM,

selected medical conditions, or selected ethnic background.124 A 1994

report of the WHO concluded that population screening for NIDDM was not

justified, but that opportunistic screening of high-risk persons may be

useful to permit earlier intervention.125

The ACP,122 the ADA,124 and the Third International Workshop

Conference on Gestational Diabetes27 recommend universal screening for

GDM in pregnant women between weeks 24 and 28 using a 1-hour glucose

tolerance test. The American College of Obstetricians and Gynecologists

and the American Academy of Pediatrics do not recommend universal

screening in pregnancy but strongly recommend screening pregnant women

in certain high-prevalence populations (e.g., Native Americans) and those

with specific risk factors (age over 30, family history of diabetes,

previous macrosomia, malformed or stillborn infants, hypertension, or

glucosuria).126,127 The CTF concluded that there was insufficient

evidence to recommend for or against universal screening for GDM, but

suggested close monitoring of women with risk factors for GDM.121

Discussion

Screening for diabetes in asymptomatic adults suffers from two

important limitations: the lack of a practical screening test that is both

sensitive and specific, and insufficient evidence that detection of

diabetes in the asymptomatic period significantly improves long-term

outcomes. Even if improving glucose control can reduce long-term

complications of NIDDM, many other factors must be considered in

determining the likely benefits and risks of screening in asymptomatic

persons: efficacy of diet or medications in reducing glucose levels;

compliance of asymptomatic persons with lifestyle advice; possible risks

of drug or insulin therapy; inconvenience and costs of screening, follow-

up, and treatment; and the potential adverse effects of screening (false-

positive diagnoses, "labeling" of asymptomatic persons). Targeting

screening to high-risk groups (certain ethnic populations, older

overweight subjects) and emphasizing interventions that are inexpensive

and safe (exercise, prudent diet, and weight loss) are likely to minimize

the potential adverse effects of screening. Since most of these

interventions are recommended for all adults, the additional benefit of

screening to promote lifestyle interventions remains uncertain. If the

ongoing UKPDS trial demonstrates important clinical benefits from more

intensive interventions (i.e., drug or insulin therapy) in patients with

minimally symptomatic NIDDM, this would provide stronger support for

screening for diabetes among asymptomatic adults. 

The value of widespread screening for GDM is also unproven. Important

questions remain about the diagnostic gold standard, the optimal

screening test, and the appropriate management of GDM. Although there is

good evidence that insulin treatment can reduce the incidence of

macrosomia in GDM, evidence of a benefit on clinically important perinatal

outcomes (birth trauma, operative delivery, neonatal metabolic

derangements, or perinatal mortality) is much weaker. The high risk

associated with GDM in earlier cohorts primarily reflects adverse

outcomes in women who were older, overweight, or otherwise at

increased risk. Universal screening is likely to have only a small impact

on the overall incidence of macrosomia and birth trauma and may subject

many low-risk women to the inconvenience, costs and possible risks of

follow-up testing, dietary restriction, or insulin management. A 1988

study estimated that universal screening would cost $8,000 per case of

macrosomia prevented.122 By one estimate, however, up to 10,000 women

would need to be screened to prevent 50 cases of macrosomia, 6 cases of

shoulder dystocia, and 1 case of shoulder girdle injury (few of which

cause lasting problems).128 Targeting screening to women with risk

factors for GDM (including older age), with emphasis on dietary

management of GDM, is likely to minimize the adverse effects and costs of

screening. Direct evidence of a benefit of screening on important clinical

outcomes is not available for any group, however.

Immune markers are not sufficiently specific to recommend their use in

the general population at this time. Screening persons with a family

history of IDDM using immune markers and physiologic measurements can

identify a small number of persons at very high risk of developing IDDM.

Patients with a family history account for only 10% of all cases of IDDM,

however, and trials of interventions to prevent IDDM in high-risk patients

have not yet been completed.

Primary prevention may be a more effective means to reduce diabetes-

associated morbidity than widespread screening. Diet, exercise, and

weight reduction can safely improve glucose tolerance and are likely to

have independent benefits on other important chronic diseases (see

Chapters 55 and 56). Whether diabetes screening improves compliance

with generally recommended lifestyle interventions has not been

determined. 

CLINICAL INTERVENTION

There is insufficient evidence to recommend for or against routine

screening for NIDDM in nonpregnant adults ("C" recommendation). Although

evidence of a benefit of early detection is not available for any group,

clinicians may decide to screen selected persons at high risk of NIDDM on

other grounds, including the increased predictive value of a positive test

in individuals with risk factors and the potential (although unproven)

benefits of reducing asymptomatic hyperglycemia through diet and

exercise. Individuals at higher risk of diabetes include obese men and

women over 40, patients with a strong family history of diabetes, and

members of certain ethnic groups (Native Americans, Hispanics, African

Americans). In persons without risk factors, screening for asymptomatic

disease is much less likely to be of benefit, due to the low burden of

disease and the poor predictive value of screening tests in low-risk

persons. Measurement of fasting plasma glucose is recommended by

experts as the screening test of choice; the frequency of screening is left

to clinical discretion.

There is also insufficient evidence to recommend for or against routine

screening for GDM ("C" recommendation). Although a clear benefit of

screening on perinatal morbidity has not been demonstrated for any group,

clinicians may decide to screen high-risk pregnant women on other

grounds, including the higher burden of disease, and the potential clinical

benefits from reducing macrosomia due to GDM. Risk factors for GDM

include obesity, older maternal age, a family history of diabetes, and a

history of macrosomia, fetal malformation, or fetal death. The 1-hour 50

g glucose challenge test, with confirmation of abnormal results with a 3-

hour 100 g oral glucose tolerance test, is the screening test recommended

by expert panels in the U.S. 

Screening with immune markers to identify asymptomatic individuals at

risk for developing IDDM is not recommended in the general population ("D"

recommendation).

The draft update of this chapter was prepared for the U.S. Preventive

Services Task Force by M. Carrington Reid, MD, PhD, Harold C. Sox, Jr., MD,

Richard Comi, MD, and David Atkins, MD, MPH.

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