An estimated half of all persons with diabetes (primarily patients The diagnosis of diabetes in many nonpregnant patients is based on typi …
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 US have diabetes mellitus1 Noninsulin-dependent diabetes mellitus NIDDM or Type II diabetes accounts for 9095 of all cases of diabetes in the US, while insulin-dependent diabetes mellitus IDDM or Type I diabetes accounts for the remaining 51014 An estimated half of all persons with diabetes primarily patients with NIDDM are currently unaware of their diagnosis2 Diabetes may cause life-threatening metabolic complications, and is the seventh leading
cause of death in the US, contributing to roughly 160,000 deaths each year1,3 It is also an important risk factor for other leading causes of death such as coronary heart disease and cerebrovascular disease4 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 US6 Diabetic nephropathy is now the leading cause of end-stage renal disease in the US7 and, if current trends continue, will soon account for 50 of all patients with renal failure8 Diabetes is the leading cause of blindness in adults ages 2074 and accounts for over 8,000 new cases of blindness each year9 Infants born of diabetic women are at increased risk of fetal malformation, prematurity, spontaneous abortion, macrosomia, and metabolic derangements10,11 Compared to persons without diabetes, diabetic patients have a higher hospitalization rate, longer hospital stays, and increased ambulatory 193
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care visits3,12 The total annual economic burden of diabetes is believed to approach 100 billion in the US13 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 US population aged 6574 has diabetes2 The prevalence of NIDDM is markedly increased in Native Americans and is also higher among black and Hispanic populations3 The prevalence of NIDDM is greater than 70 in Pima Indians 55 years of age and older14 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 35 of all pregnancies and is the most common medical problem of pregnancy3,15 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 eg, clavicular fracture, shoulder dystocia, and peripheral nerve injury1619 In some series, the incidence of shoulder dystocia in infants over 4,000 g is close to 220 Women with a history of GDM are also at increased risk for developing NIDDM later in life21 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 [78 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 WHO23 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 using a 2-hour 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 diabetes22,23 The complex diagnostic criteria
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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 3524,25 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 140200 mg/dL22,23 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 disease25 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 glucose22,27 NDDG diagnostic criteria are based on extrapolations from standards for whole blood glucose originally derived by OSullivan28 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 outcomes30 Outside of North America, the diagnosis of GDM is usually based on WHO criteria using a 2-hour 75 g glucose tolerance test23 The prevalence of GDM varies considerably depending on whether WHO, NDDG, or modified criteria of Carpenter and Coustan30 are used15,31 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 3234 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 abnor-
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mal screening result A single fasting glucose above 140 mg/dL is specific for diabetes 99 but sensitivity varies widely among different populations 21753540 Using a lower threshold 123 mg/dL improves sensitivity 4088, while maintaining reasonably high specificity 97993540 A random ie, nonfasting plasma glucose greater than 140 mg/dL has a sensitivity of 45 and a specificity of 8641 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 OGTT26 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 hemoglobin A1c HbA1c and serum fructosamine as screening tests for diabetes40,4245 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 2364 and specificity of 989940,46 In a highrisk population, quantitative assays of urine glucose achieved high sensitivity 81 with high specificity 98, comparable to both fasting plasma glucose and glycosylated protein assays40 Sensitivity of all screening tests increases with the severity of hyperglycemia among the diabetic population40 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 prevalent40 In the asymptomatic general population, where the prevalence of undiagnosed diabetes is only 13, 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 evaluation47 Even a true-positive diagnosis could have adverse consequences for an asymptomatic person if it causes labeling effects 48 or difficulty obtaining insurance Screening for GDM The Third International Workshop Conference on Gestational Diabetes has recommended screening pregnant women at 2428 weeks of gestation with a 50 g 1-hour oral glucose challenge test, performed in fasting or nonfasting state27 Patients with plasma glucose of 140 mg/dL 78 mM or greater at 1 hour should undergo a diagnostic 3-
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hour OGTT There is no single
threshold that accurately separates normal from abnormal results on the glucose challenge test, however27 Estimates of sensitivity of screening under this protocol range from 71 to 83 with a specificity of 788730,49,50 Sensitivity is increased by using a lower threshold for a positive screen30,51 and by testing in the fasting state49 A large prospective study of nearly 4,300 pregnant women reported that using higher cutpoints 142149 mg/dL and adjusting for time since last meal could reduce the misclassification of patients based on initial screening tests52 Reproducibility of the 1 hour glucose challenge test is only fair,53 but it improves with advancing gestational age54 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 OGTT52 The elevations in plasma glucose in GDM are less pronounced than in IDDM or NIDDM As a result, neither serum glycosylated proteins51,5558 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 insulin61 Islet cell autoantibodies and insulin autoantibodies are present 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 03 to 40 and the chance of developing IDDM in antibody-positive individuals is estimated to be less than 1064 The potential value of immune markers is greater in high-risk individuals ie, 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 IDDM62,63,65 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
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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 912 years before clinical diagnosis, and that the microvascular changes may precede overt symptoms in many patients66 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 neuropathy5,6872 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 patients73,74 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 NIDDM75 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 retinopathy76 More definitive results may come from the UK 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 insulin77 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 hypoglycemia78 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 patients79,80 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
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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 control79,82 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 criticized83 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 14 of subjects each year78 The majority of individuals in the US who have disordered glucose metabolism have IGT84 Untreated, most persons with IGT do not develop diabetes, but the reported cumulative incidence of diabetes at 10 years has varied from 15 to 6125 Progression to diabetes is highest in some Native American populations 85 There is little direct evidence of a benefit of detecting and treating IGT86,87 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 diabetes9092 Gestational Diabetes GDM is associated with increased risk of fetal macrosomia, birth trauma, neonatal hypoglycemia, and perinatal mortality9396 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 populations97,98 Because women screened for GDM are more likely to be at high risk, such studies cannot reliably exclude a benefit of screening98 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 GDM99 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 5100 Several randomized controlled trials have demonstrated that diet and insulin compared to diet alone results in improved glucose control and re-
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duced incidence of macrosomia in women with GDM94,101,102 Macrosomia was not significantly reduced in a fourth trial, but 15 of the women assigned to diet therapy received insulin because glucose control was inadequate103 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 17104 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 outcome101,104 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 intervention96 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,95,97,105107 none of these studies employed an appropriate control group The use of historical controls ie, 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 27 and those treated with diet alone 32104 Moreover, in trials conducted after 1975, there were no perinatal deaths in treated or control groups100,104 In one trial, insulin treatment was associated with lower rates of neonatal jaundice and
nonsignificant reductions in admissions to the neonatal ICU108 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-forgestational age infants than nondiabetic controls109 Degrees of hyperglycemia more subtle than in GDM may result in increased maternal and neonatal complication rates110112 The incidence of macrosomia and preeclampsia/eclampsia is higher in women who demonstrate at least one abnormal result among the four measurements in 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 macroso-
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mia in the general population varies from 1 to 8,93,113 and most macrosomic infants are born to women without GDM114 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 country116 Other factors such as maternal obesity, gestational weight gain, and maternal age may be more important determinants of macrosomia and adverse outcomes117 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 weight118 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 IDDM61 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 measures63,119,120 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 subjects61 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 Physicians 123 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 eg, 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 background124 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 intervention125 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
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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 eg, Native Americans and those with specific risk factors age over 30, family history of diabetes, previous macrosomia, malformed or stillborn infants, hypertension, or glucosuria126,127 The CTF concluded that there was insufficient evidence to recommend for or against universal screening for GDM, but suggested close monitorin 
g of women with risk factors for GDM121 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 ie, 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 an effect 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
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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 prevented122 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
problems128 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 diabetesassociated 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, clin icians 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 bene fits 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 cer tain 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 rou tine screening for GDM C recommendation
Although a beneficial ef-
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fect of screening on perinatal morbidity has not been clearly demonstrated for any group, clinicians may decide to screen high-risk pregnant women on other grounds, including the higher burden of disease, and the poten tial 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 1hour 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 US 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 US Preventive Services Task Force by M Carrington Reid, MD, PhD, Harold C Sox, Jr, MD, Richard Comi, MD, and David Atkins, MD, MPH REFERENCES
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diabetes mellitus-United States, 19801989 MMWR 1993;42SS-2:120 13 American Diabetes Association Direct and indirect costs of diabetes in the United States in 1992 Alexandria, VA: American Diabetes Association, 1993 14 Knowler WC, Saad MS, Pettitt DJ, et al Determinants of diabetes mellitus in the Pima Indians Diabetes Care 1993;16Suppl 1:216226 15 Magee MS, Walden CE, Benedetti TJ, et al Influence of diagnostic criteria on the incidence of gestational diabetes and perinatal morbidity JAMA 1993;269:609615 16 Gross TL, Sokol RJ, Williams T, et al Shoulder dystocia: a fetal-physician risk Am J Obstet Gynecol 1987;156:14081418 17 McFarland LV, Raskin M, Daling JR, et al Erb/Duchennes palsy: a consequence of fetal macrosomia and method of delivery Obstet Gynecol 1986;68:784788 18 Modanlou HD, Dorchester WL, Thorosian A, et al Macrosomia-maternal, fetal, and neonatal implications Obstet Gynecol 1980;55:420424 19 Sandmire HF, OHalloin TJ Shoulder dystocia: its incidence and associated risk factors Int J Gynaecol Obstet 1988;26:6573
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represent discovery of preexisting glucose intolerance Diabetes Care 1988;11:402411 22 National Diabetes Data Group Classification and diagnosis of diabetes mellitus and other categories of glucose tolerance Diabetes 1979;28:10391057 23 Expert Committee on Diabetes Mellitus-World Health Organization Technical Report Series no 646 Geneva: World Health Organization, 1980 24 Home P The OGTT: gold that does not shine Diabetes Med 1988;5:313314 25 Yudkin JS, Alberti KG, McLarty DG, et al Impaired glucose tolerance Is it a risk factor for diabetes or a diagnostic ragbag? BMJ 1990;301:397402 26 American Diabetes Association Office guide to diagnosis and classification of diabetes mellitus and other categories of glucose intolerance Diabetes Care 1993;16Suppl 2:46 27 Metzger BE Summary and recommendations of the Third International Workshop Conference on Gestational Diabetes Mellitus Diabetes 1991;40Suppl 2:197201 28 OSullivan JB, Gellis SS, Dandrow RV, et al The potential diabetic and her treatment in pregnancy Obstet Gynecol 1966;27:683689 29 Sacks DA, Salim AF, Greenspoon JS, et al Do the current standards for glucose tolerance testing in pregnancy represent a valid conversion of
OSullivans original criteria? Am J Obstet Gynecol 1989;161:638641 30 Carpenter MW, Coustan DR Criteria for screening tests for gestational diabetes Am J Obstet Gynecol 1982; 144:768773 31 Li DFH, Wong VCW, OHoy KM, et al Evaluation of the WHO criteria for 75 g oral glucose tolerance test in pregnancy Br J Obstet Gynaecol 1987;94:847850 32 Canadian Task Force on the Periodic Health Examination Periodic health examination, 1992 update: 1 Screening for gestational diabetes mellitus Can Med Assoc J 1992;147:435443 33 Naylor CD Diagnosing gestational diabetes: is the gold standard valid? Diabetes Care 1989;12:565572 34 Singer DE, Coley CM, Samet JH, et al Tests of glycemia in diabetes mellitus Ann Intern Med 1989; 110:125137 35 Cockram CS, Lau JT, Chan AY, et al Assessment of glucose tolerance test criteria for diagnosis of diabetes in Chinese subjects Diabetes Care 1992;15:988990 36 Blunt BA, Barrett-Connor E, Wingard DL Evaluation of fasting plasma glucose as screening test for NIDDM in older adults Diabetes Care 1991;14:989993 37 Seikikawa A, Tominaga M, Takahashi K, et al Is examination of fructosamine levels valuable as a diagnostic test for diabetes mellitus Diabet Res Clin Pract
1990;8:187192 38 Swai ABM, Harrison K, Chuwa LM, et al Screening for diabetes: does measurement of serum fructosamine help? Diabet Med 1988;5:648652 39 Hanson RI, Nelson RG, McCance DR, et al Comparison of screening tests for non-insulin dependent diabetes mellitus Arch Intern Med 1993;153:21332140 40 Modan M, Harris MI Fasting plasma glucose in screening for NIDDM in the US and Israel Diabetes Care 1994;17:436439 41 Bourn D, Mann J Screening for noninsulin dependent diabetes mellitus and impaired glucose tolerance in a Dunedin general practice-is it worth it? NZ Med J 1992;105:208210 42 Croxson SC, Absalom S, Burden AC Fructosamine in diabetes screening of the elderly Ann Clin Biochem 1991;28:279282 43 Guillausseau PJ, Charles MA, Paolaggi F, et al Comparison of HbA1 and fructosamine in diagnosis of glucose-tolerance abnormalities Diabetes Care 1990;13:898900 44 Forrest RD, Jackson CA, Gould BJ, et al Four assay methods for glycated hemoglobin compared as screening tests for diabetes mellitus: the Islington diabetes survey Clin Chem 1988;34:145148 45 Little RR, England JD, Wiedmeyer H, et al Relationship of glycosylated hemoglobin to oral glucose tolerance Diabetes 1988;37:6064 46
Anderson DKG, Lundblad E, Svardsudd K A model for early diagnosis of type II diabetes mellitus in primary health care Diabetes Med 1993;10:167173 47 Patchett P, Roberts D Diabetic patients who do not have diabetes: investigation of register of diabetic patients in general practice BMJ 1994;308:12251226 48 Haynes RB, Sackett DL, Taylor DW, et al Increased absenteeism after detection and labelling of hypertensive patients N Engl J Med 1978;299:741744
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49 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;154:10311035 50 OSullivan JB, Mahan CM Criteria for the oral glucose tolerance test in pregnancy Diabetes 1964;13:278285 51 Roberts AB, Baker JR, Metcalf P, et al Fructosamine compared with a glucose load as a screening test for gestational diabetes Obstet Gynecol 1990;76:773775 52 Sermer M, Naylor CD, Gare DJ, et al Impact of time since last meal on the gestational glucose challenge test The Toronto Tri-Hospital Gestational Diabetes Project Am J Obstet Gynecol 1994;171: 607616 53 Sacks DA, Abu-Fadil S,
Greenspoon JS, et al How reliable is the fifty-gram one-hour glucose screening test? Am J Obstet Gynecol 1989;161:642645 54 Espinosa de los Monteros A, Carino N, Ramirez A The reproducibility of the 50-gram, 1-hour glucose screen for diabetes in pregnancy Obstet Gynecol 1993;82:515518 55 Menon U, Ranjan M, Jasper P, et al Evaluation of plasma fructosamine as a screening test for gestational diabetes Aust NZ J Obstet Gynaecol 1991;31:2526 56 Corcoy R, Cerqueira MJ, Pedreno J, et al Serum fructosamine is not a useful screening test for gestational diabetes Eur J Obstet Gynecol Reprod Biol 1990;38:217220 57 Comtois R, Desjarlais F, Nguyen M, et al Clinical usefulness of estimation of serum fructosamine concentration as screening test for gestational diabetes Am J Obstet Gynecol 1989;160:651654 58 Cefalu WT, Prather KL, Chester DL, et al Total serum glycosylated proteins in detection and monitoring of gestational diabetes Diabetes Care 1990;13:872875 59 Lind T Antenatal screening using random blood glucose values Diabetes 1985;34Suppl 2:1720 60 Hatem M, Dennis KJ A random plasma glucose method for screening abnormal glucose tolerance in pregnancy Br J Obstet Gynaecol 1987;94:213216 61
Atkinson MA, Maclaren NK The pathogenesis of insulin-dependent diabetes mellitus N Engl J Med 1994;331:14281444 62 Riley WJ, Maclaren NK, Krischer J, et al A prospective study of the development of diabetes in relatives of patients with insulin-dependent diabetes N Engl J Med 1990;323:11671172 63 Eisenbarth GS, Verge CF, Allen H, et al The design of trials for prevention of IDDM Diabetes 1993;42:941946 64 Bingley PJ, Bonifacio E, Shattock M, et al Can islet cell antibodies predict IDDM in the general population? Diabetes Care 1993;16:4550 65 Bonifacio E, Bingley PJ, Shattock M, et al Quantification of islet-cell antibodies and prediction of insulin-dependent diabetes Lancet 1990;335:147149 66 Harris MI, Klein R, Welbourn TA, et al Onset of NIDDM occurs at least 47 years before clinical diagnosis Diabetes Care 1992;15:815819 67 Brownlee M Glycation and diabetic complications Diabetes 1994;43:836841 68 Takazakura E, Nakamoto Y, Hayakawa H, et al Onset and progression of diabetic glomerulosclerosis: a prospective study based on serial renal biopsies Diabetes 1975;24:19 69 Miki E, Fukuda M, Kuzuya T, et al Relation of the course of retinopathy to control of diabetes, age, and
therapeutic agents in diabetic Japanese patients Diabetes 1969;18:773780 70 Chase HP, Jackson WE, Hoops SL, et al Glucose control and the renal and retinal complications of insulin-dependent diabetes mellitus JAMA 1989;261:11551160 71 Reichard P, Berglund B, Britz A, et al Intensified conventional insulin treatment retards the microvascular complications of insulin-dependent diabetes mellitus IDDM: the Stockholm Diabetes Intervention Study SDIS after 5 years J Intern Med 1991;230:101108 72 Dahl-Jorgensen K, Bjoro T, Kierulf P, et al Long term glycemic control and kidney function in insulindependent diabetes mellitus Kidney Int 1992;41:920923 73 Diabetes Control and Complications Trial Research Group The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus N Engl J Med 1993;329:977986 74 The Diabetes Control and Complications Trial The effect of intensive diabetes therapy on the development and progression of neuropathy Ann Intern Med 1995;122:561568 75 Lasker RD The Diabetes Control and Complications Trial Implications for policy and practice N Engl J Med 1993;329:10351036
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Diabetes Mellitus
207
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Source:ahrq.gov
