Diagnosis and Classification of DiabetesMellitusAMERICAN DIABETES ASSOCIATION

DEFINITION ANDDESCRIPTION OF DIABETESMELLITUS — Diabetes mellitus is agroup of metabolic diseases characterizedby hyperglycemia resulting from defectsin insulin secretion, insulin action, orboth. The chronic hyperglycemia of dia-betes is associated with long-term dam-age, dysfunction, and failure of variousorgans, especially the eyes, kidneys,nerves, heart, and blood vessels.

Several pathogenic processes are in-volved in the development of diabetes.These range from autoimmune destruc-tion of the �-cells of the pancreas withconsequent insulin deficiency to abnor-malities that result in resistance to insulinaction. The basis of the abnormalities incarbohydrate, fat, and protein metabo-lism in diabetes is deficient action of in-sulin on target tissues. Deficient insulinaction results from inadequate insulin se-cretion and/or diminished tissue re-sponses to insulin at one or more points inthe complex pathways of hormone action.Impairment of insulin secretion and de-fects in insulin action frequently coexistin the same patient, and it is often unclearwhich abnormality, if either alone, is theprimary cause of the hyperglycemia.

Symptoms of marked hyperglycemiainclude polyuria, polydipsia, weight loss,sometimes with polyphagia, and blurredvision. Impairment of growth and suscep-tibility to certain infections may also ac-company chronic hyperglycemia. Acute,life-threatening consequences of uncon-trolled diabetes are hyperglycemia withketoacidosis or the nonketotic hyperos-molar syndrome.

Long-term complications of diabetesinclude retinopathy with potential loss ofvision; nephropathy leading to renal failure;peripheral neuropathy with risk of foot ul-cers, amputations, and Charcot joints; andautonomic neuropathy causing gastrointes-

tinal, genitourinary, and cardiovascularsymptoms and sexual dysfunction. Patientswith diabetes have an increased incidenceof atherosclerotic cardiovascular, periph-eral arterial, and cerebrovascular disease.Hypertension and abnormalities of lipopro-tein metabolism are often found in peoplewith diabetes.

The vast majority of cases of diabetesfall into two broad etiopathogenetic cate-gories (discussed in greater detail below).In one category, type 1 diabetes, the causeis an absolute deficiency of insulin secre-tion. Individuals at increased risk of de-veloping this type of diabetes can often beidentified by serological evidence of anautoimmune pathologic process occur-ring in the pancreatic islets and by geneticmarkers. In the other, much more preva-lent category, type 2 diabetes, the cause isa combination of resistance to insulin ac-tion and an inadequate compensatory in-sulin secretory response. In the lattercategory, a degree of hyperglycemia suffi-cient to cause pathologic and functionalchanges in various target tissues, butwithout clinical symptoms, may bepresent for a long period of time beforediabetes is detected. During this asymp-tomatic period, it is possible to demon-strate an abnormality in carbohydratemetabolism by measurement of plasmaglucose in the fasting state or after a chal-lenge with an oral glucose load.

The degree of hyperglycemia (if any)may change over time, depending on theextent of the underlying disease process(Fig. 1). A disease process may be presentbut may not have progressed far enoughto cause hyperglycemia. The same diseaseprocess can cause impaired fasting glu-cose (IFG) and/or impaired glucose toler-ance (IGT) without fulfilling the criteriafor the diagnosis of diabetes. In some in-dividuals with diabetes, adequate glyce-mic control can be achieved with weight

reduction, exercise, and/or oral glucose-lowering agents. These individuals there-fore do not require insulin. Otherindividuals who have some residual insu-lin secretion but require exogenous insu-lin for adequate glycemic control cansurvive without it. Individuals with ex-tensive �-cell destruction and thereforeno residual insulin secretion require insu-lin for survival. The severity of the meta-bolic abnormality can progress, regress,or stay the same. Thus, the degree of hy-perglycemia reflects the severity of the un-derlying metabolic process and itstreatment more than the nature of theprocess itself.

CLASSIFICATION OFDIABETES MELLITUS ANDOTHER CATEGORIES OFGLUCOSE REGULATION —Assigning a type of diabetes to an individ-ual often depends on the circumstancespresent at the time of diagnosis, and manydiabetic individuals do not easily fit into asingle class. For example, a person withgestational diabetes mellitus (GDM) maycontinue to be hyperglycemic after deliv-ery and may be determined to have, infact, type 2 diabetes. Alternatively, a per-son who acquires diabetes because oflarge doses of exogenous steroids may be-come normoglycemic once the glucocor-ticoids are discontinued, but then maydevelop diabetes many years later after re-current episodes of pancreatitis. Anotherexample would be a person treated withthiazides who develops diabetes yearslater. Because thiazides in themselves sel-dom cause severe hyperglycemia, such in-dividuals probably have type 2 diabetesthat is exacerbated by the drug. Thus, forthe clinician and patient, it is less importantto label the particular type of diabetes than itis to understand the pathogenesis of the hy-perglycemia and to treat it effectively.

Type 1 diabetes (�-cell destruction,usually leading to absolute insulindeficiency)Immune-mediated diabetes. This formof diabetes, which accounts for only5–10% of those with diabetes, previouslyencompassed by the terms insulin-dependent diabetes, type I diabetes, or ju-venile-onset diabetes, results from a

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The information that follows is based largely on the reports of the Expert Committee on the Diagnosis andClassification of Diabetes (Diabetes Care 20:1183–1197, 1997, and Diabetes Care 26:3160–3167, 2003).

DOI: 10.2337/dc09-S062© 2009 by the American Diabetes Association. Readers may use this article as long as the work is properly

cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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cellular-mediated autoimmune destruc-tion of the �-cells of the pancreas. Mark-ers of the immune destruction of the�-cell include islet cell autoantibodies,autoantibodies to insulin, autoantibodiesto glutamic acid decarboxylase (GAD65),and autoantibodies to the tyrosine phos-phatases IA-2 and IA-2�. One and usuallymore of these autoantibodies are presentin 85–90% of individuals when fastinghyperglycemia is initially detected. Also,the disease has strong HLA associations,with linkage to the DQA and DQB genes,and it is influenced by the DRB genes.These HLA-DR/DQ alleles can be eitherpredisposing or protective.

In this form of diabetes, the rate of�-cell destruction is quite variable, beingrapid in some individuals (mainly infantsand children) and slow in others (mainlyadults). Some patients, particularly chil-dren and adolescents, may present withketoacidosis as the first manifestation ofthe disease. Others have modest fastinghyperglycemia that can rapidly change tosevere hyperglycemia and/or ketoacidosisin the presence of infection or other stress.Still others, particularly adults, may retainresidual �-cell function sufficient to pre-vent ketoacidosis for many years; such in-dividuals eventually become dependenton insulin for survival and are at risk forketoacidosis. At this latter stage of the dis-ease, there is little or no insulin secretion,as manifested by low or undetectable lev-

els of plasma C-peptide. Immune-mediated diabetes commonly occurs inchildhood and adolescence, but it can oc-cur at any age, even in the 8th and 9thdecades of life.

Autoimmune destruction of �-cellshas multiple genetic predispositions andis also related to environmental factorsthat are still poorly defined. Although pa-tients are rarely obese when they presentwith this type of diabetes, the presence ofobesity is not incompatible with the diag-nosis. These patients are also prone toother autoimmune disorders such asGraves’ disease, Hashimoto’s thyroiditis,Addison’s disease, vitiligo, celiac sprue,autoimmune hepatitis, myasthenia gravis,and pernicious anemia.Idiopathic diabetes. Some forms of type1 diabetes have no known etiologies.Some of these patients have permanentinsulinopenia and are prone to ketoacido-sis, but have no evidence of autoimmu-nity. Although only a minority of patientswith type 1 diabetes fall into this category,of those who do, most are of African orAsian ancestry. Individuals with this formof diabetes suffer from episodic ketoaci-dosis and exhibit varying degrees of insu-lin deficiency between episodes. Thisform of diabetes is strongly inherited,lacks immunological evidence for �-cellautoimmunity, and is not HLA associated.An absolute requirement for insulin re-

placement therapy in affected patientsmay come and go.

Type 2 diabetes (ranging frompredominantly insulin resistancewith relative insulin deficiency topredominantly an insulin secretorydefect with insulin resistance)This form of diabetes, which accounts for�90–95% of those with diabetes, previ-ously referred to as non-insulin-dependent diabetes, type II diabetes, oradult-onset diabetes, encompasses indi-viduals who have insulin resistance andusually have relative (rather than abso-lute) insulin deficiency At least initially,and often throughout their lifetime, theseindividuals do not need insulin treatmentto survive. There are probably many dif-ferent causes of this form of diabetes. Al-though the specific etiologies are notknown, autoimmune destruction of�-cells does not occur, and patients donot have any of the other causes of diabe-tes listed above or below.

Most patients with this form of diabe-tes are obese, and obesity itself causessome degree of insulin resistance. Patientswho are not obese by traditional weightcriteria may have an increased percentageof body fat distributed predominantly inthe abdominal region. Ketoacidosis sel-dom occurs spontaneously in this type ofdiabetes; when seen, it usually arises inassociation with the stress of another ill-

Figure 1—Disorders of glycemia: etiologic types and stages. �Even after presenting in ketoacidosis, these patients can briefly return to normogly-cemia without requiring continuous therapy (i.e., “honeymoon” remission); ��in rare instances, patients in these categories (e.g., Vacor toxicity, type1 diabetes presenting in pregnancy) may require insulin for survival.

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ness such as infection. This form of dia-betes frequently goes undiagnosed formany years because the hyperglycemiadevelops gradually and at earlier stages isoften not severe enough for the patient tonotice any of the classic symptoms of di-abetes. Nevertheless, such patients are atincreased risk of developing macrovascu-lar and microvascular complications.Whereas patients with this form of diabe-tes may have insulin levels that appearnormal or elevated, the higher blood glu-cose levels in these diabetic patientswould be expected to result in evenhigher insulin values had their �-cellfunction been normal. Thus, insulin se-cretion is defective in these patients andinsufficient to compensate for insulin re-sistance. Insulin resistance may improvewith weight reduction and/or pharmaco-logical treatment of hyperglycemia but isseldom restored to normal. The risk ofdeveloping this form of diabetes increaseswith age, obesity, and lack of physical ac-tivity. It occurs more frequently inwomen with prior GDM and in individu-als with hypertension or dyslipidemia,and its frequency varies in different racial/ethnic subgroups. It is often associatedwith a strong genetic predisposition,more so than is the autoimmune form oftype 1 diabetes. However, the genetics ofthis form of diabetes are complex and notclearly defined.

Other specific types of diabetesGenetic defects of the �-cell. Severalforms of diabetes are associated with mo-nogenetic defects in �-cell function.These forms of diabetes are frequentlycharacterized by onset of hyperglycemiaat an early age (generally before age 25years). They are referred to as maturity-onset diabetes of the young (MODY) andare characterized by impaired insulin se-cretion with minimal or no defects in in-sulin action. They are inherited in anautosomal dominant pattern. Abnormali-ties at six genetic loci on different chro-mosomes have been identified to date.The most common form is associatedwith mutations on chromosome 12 in ahepatic transcription factor referred to ashepatocyte nuclear factor (HNF)-1�. Asecond form is associated with mutationsin the glucokinase gene on chromosome7p and results in a defective glucokinasemolecule. Glucokinase converts glucoseto glucose-6-phosphate, the metabolismof which, in turn, stimulates insulin secre-tion by the �-cell. Thus, glucokinaseserves as the “glucose sensor” for the

�-cell. Because of defects in the glucoki-nase gene, increased plasma levels of glu-cose are necessary to elicit normal levelsof insulin secretion. The less commonforms result from mutations in other tran-scription factors, including HNF-4�,HNF-1�, insulin promoter factor (IPF)-1,and NeuroD1.

Point mutations in mitochondrialDNA have been found to be associatedwith diabetes mellitus and deafness Themost common mutation occurs at posi-tion 3243 in the tRNA leucine gene, lead-ing to an A-to-G transition. An identicallesion occurs in the MELAS syndrome(mitochondrial myopathy, encephalopa-thy, lactic acidosis, and stroke-like syn-drome); however, diabetes is not part ofthis syndrome, suggesting different phe-notypic expressions of this genetic lesion.

Genetic abnormalities that result inthe inability to convert proinsulin to in-sulin have been identified in a few fami-lies, and such traits are inherited in anautosomal dominant pattern. The result-ant glucose intolerance is mild. Similarly,the production of mutant insulin mole-cules with resultant impaired receptorbinding has also been identified in a fewfamilies and is associated with an autoso-mal inheritance and only mildly impairedor even normal glucose metabolism.Genetic defects in insulin action.There are unusual causes of diabetes thatresult from genetically determined abnor-malities of insulin action. The metabolicabnormalities associated with mutationsof the insulin receptor may range fromhyperinsulinemia and modest hypergly-cemia to severe diabetes. Some individu-als with these mutations may haveacanthosis nigricans. Women may be vir-ilized and have enlarged, cystic ovaries. Inthe past, this syndrome was termed type Ainsulin resistance. Leprechaunism andthe Rabson-Mendenhall syndrome aretwo pediatric syndromes that have muta-tions in the insulin receptor gene withsubsequent alterations in insulin receptorfunction and extreme insulin resistance.The former has characteristic facial fea-tures and is usually fatal in infancy, whilethe latter is associated with abnormalitiesof teeth and nails and pineal glandhyperplasia.

Alterations in the structure and func-tion of the insulin receptor cannot bedemonstrated in patients with insulin-resistant lipoatrophic diabetes. Therefore,it is assumed that the lesion(s) must residein the postreceptor signal transductionpathways.

Diseases of the exocrine pancreas. Anyprocess that diffusely injures the pancreascan cause diabetes. Acquired processesinclude pancreatitis, trauma, infection,pancreatectomy, and pancreatic carci-noma. With the exception of that causedby cancer, damage to the pancreas mustbe extensive for diabetes to occur; adre-nocarcinomas that involve only a smallportion of the pancreas have been associ-ated with diabetes. This implies a mecha-nism other than simple reduction in�-cell mass. If extensive enough, cysticfibrosis and hemochromatosis will alsodamage �-cells and impair insulin secre-tion. Fibrocalculous pancreatopathy maybe accompanied by abdominal pain radi-ating to the back and pancreatic calcifica-tions identified on X-ray examination.Pancreatic fibrosis and calcium stones inthe exocrine ducts have been found atautopsy.Endocrinopathies. Several hormones(e.g., growth hormone, cortisol, gluca-gon, epinephrine) antagonize insulin ac-tion. Excess amounts of these hormones(e.g., acromegaly, Cushing’s syndrome,glucagonoma, pheochromocytoma, re-spectively) can cause diabetes. This gen-eral ly occurs in individuals withpreexisting defects in insulin secretion,and hyperglycemia typically resolveswhen the hormone excess is resolved.

Somatostatinoma- and aldoster-onoma-induced hypokalemia can causediabetes, at least in part, by inhibiting in-sulin secretion. Hyperglycemia generallyresolves after successful removal of the tu-mor.Drug- or chemical-induced diabetes.Many drugs can impair insulin secretion.These drugs may not cause diabetes bythemselves, but they may precipitate dia-betes in individuals with insulin resis-tance. In such cases, the classification isunclear because the sequence or relativeimportance of �-cell dysfunction and in-sulin resistance is unknown. Certain tox-ins such as Vacor (a rat poison) andintravenous pentamidine can perma-nently destroy pancreatic �-cells. Suchdrug reactions fortunately are rare. Thereare also many drugs and hormones thatcan impair insulin action. Examples in-clude nicotinic acid and glucocorticoids.Patients receiving �-interferon have beenreported to develop diabetes associatedwith islet cell antibodies and, in certaininstances, severe insulin deficiency. Thelist shown in Table 1 is not all-inclusive,but reflects the more commonly recog-

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nized drug-, hormone-, or toxin-inducedforms of diabetes.Infections. Certain viruses have been as-sociated with �-cell destruction. Diabetesoccurs in patients with congenital rubella,although most of these patients have HLAand immune markers characteristic oftype 1 diabetes. In addition, coxsackievi-rus B, cytomegalovirus, adenovirus, andmumps have been implicated in inducingcertain cases of the disease.Uncommon forms of immune-medi-ated diabetes. In this category, there aretwo known conditions, and others arelikely to occur. The stiff-man syndrome isan autoimmune disorder of the centralnervous system characterized by stiffnessof the axial muscles with painful spasms.Patients usually have high titers of theGAD autoantibodies, and approximatelyone-third will develop diabetes.

Anti–insulin receptor antibodies cancause diabetes by binding to the insulinreceptor, thereby blocking the binding ofinsulin to its receptor in target tissues.However, in some cases, these antibodiescan act as an insulin agonist after bindingto the receptor and can thereby cause hy-poglycemia. Anti–insulin receptor anti-bodies are occasionally found in patientswith systemic lupus erythematosus andother autoimmune diseases. As in otherstates of extreme insulin resistance, pa-tients with anti–insulin receptor antibod-ies often have acanthosis nigricans. In thepast, this syndrome was termed type Binsulin resistance.Other genetic syndromes sometimesassociated with diabetes. Many geneticsyndromes are accompanied by an in-creased incidence of diabetes mellitus.These include the chromosomal abnor-ma l i t i e s o f Down ’ s syndrome ,Klinefelter’s syndrome, and Turner’s syn-drome. Wolfram’s syndrome is an autoso-mal recessive disorder characterized byinsulin-deficient diabetes and the absenceof �-cells at autopsy. Additional manifes-tations include diabetes insipidus, hypo-gonadism, optic atrophy, and neuraldeafness. Other syndromes are listed inTable 1.

Gestational diabetes mellitus (GDM)GDM is defined as any degree of glucoseintolerance with onset or first recognitionduring pregnancy. The definition appliesregardless of whether insulin or only dietmodification is used for treatment orwhether the condition persists after preg-nancy. It does not exclude the possibilitythat unrecognized glucose intolerance may

Table 1—Etiologic classification of diabetes mellitus

I. Type 1 diabetes (�-cell destruction, usually leading to absolute insulin deficiency)A. Immune mediatedB. Idiopathic

II. Type 2 diabetes (may range from predominantly insulin resistance with relative insulin deficiency to apredominantly secretory defect with insulin resistance)

III. Other specific typesA. Genetic defects of �-cell function

1. Chromosome 12, HNF-1� (MODY3)2. Chromosome 7, glucokinase (MODY2)3. Chromosome 20, HNF-4� (MODY1)4. Chromosome 13, insulin promoter factor-1 (IPF-1; MODY4)5. Chromosome 17, HNF-1� (MODY5)6. Chromosome 2, NeuroD1 (MODY6)7. Mitochondrial DNA8. Others

B. Genetic defects in insulin action1. Type A insulin resistance2. Leprechaunism3. Rabson-Mendenhall syndrome4. Lipoatrophic diabetes5. Others

C. Diseases of the exocrine pancreas1. Pancreatitis2. Trauma/pancreatectomy3. Neoplasia4. Cystic fibrosis5. Hemochromatosis6. Fibrocalculous pancreatopathy7. Others

D. Endocrinopathies1. Acromegaly2. Cushing’s syndrome3. Glucagonoma4. Pheochromocytoma5. Hyperthyroidism6. Somatostatinoma7. Aldosteronoma8. Others

E. Drug- or chemical-induced1. Vacor2. Pentamidine3. Nicotinic acid4. Glucocorticoids5. Thyroid hormone6. Diazoxide7. �-adrenergic agonists8. Thiazides9. Dilantin10. �-Interferon11. Others

F. Infections1. Congenital rubella2. Cytomegalovirus3. Others

G. Uncommon forms of immune-mediated diabetes1. “Stiff-man” syndrome2. Anti–insulin receptor antibodies3. Others

H. Other genetic syndromes sometimes associated with diabetes1. Down’s syndrome2. Klinefelter’s syndrome3. Turner’s syndrome4. Wolfram’s syndrome5. Friedreich’s ataxia6. Huntington’s chorea7. Laurence-Moon-Biedl syndrome8. Myotonic dystrophy9. Porphyria10. Prader-Willi syndrome11. Others

IV. Gestational diabetes mellitus (GDM)

Patients with any form of diabetes may require insulin treatment at some stage of their disease. Such use ofinsulin does not, of itself, classify the patient.

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have antedated or begun concomitantlywith the pregnancy. GDM complicates�4% of all pregnancies in the U.S., result-ing in �135,000 cases annually. The prev-alence may range from 1 to 14% ofpregnancies, depending on the populationstudied. GDM represents nearly 90% of allpregnancies complicated by diabetes.

Deterioration of glucose tolerance oc-curs normally during pregnancy, particu-larly in the 3rd trimester.

Impaired glucose tolerance (IGT)and impaired fasting glucose (IFG)The Expert Committee (1,2) recognizedan intermediate group of subjects whoseglucose levels, although not meeting cri-teria for diabetes, are nevertheless toohigh to be considered normal. This groupis defined as having fasting plasma glu-cose (FPG) levels �100 mg/dl (5.6mmol/l) but �126 mg/dl (7.0 mmol/l) or2-h values in the oral glucose tolerancetest (OGTT) of �140 mg/dl (7.8 mmol/l)but �200 mg/dl (11.1 mmol/l). Thus, thecategories of FPG values are as follows:

● FPG �100 mg/dl (5.6 mmol/l) � nor-mal fasting glucose;

● FPG 100–125 mg/dl (5.6–6.9 mmol/l) � IFG (impaired fasting glucose);

● FPG �126 mg/dl (7.0 mmol/l) � pro-visional diagnosis of diabetes (the diag-nosis must be confirmed, as describedbelow).

The corresponding categories when theOGTT is used are the following:

● 2-h postload glucose �140 mg/dl (7.8mmol/l) � normal glucose tolerance;

● 2-h postload glucose 140–199 mg/dl(7.8–11.1 mmol/l) � IGT (impairedglucose tolerance);

● 2-h postload glucose �200 mg/dl (11.1

mmol/l) � provisional diagnosis of di-abetes (the diagnosis must be con-firmed, as described below).

Patients with IFG and/or IGT are nowreferred to as having “pre-diabetes” indi-cating the relatively high risk for develop-ment of diabetes in these patients. In theabsence of pregnancy, IFG and IGT arenot clinical entities in their own right butrather risk factors for future diabetes aswell as cardiovascular disease. They canbe observed as intermediate stages in anyof the disease processes listed in Table 1.IFG and IGT are associated with the met-abolic syndrome, which includes obesity(especially abdominal or visceral obesity),dyslipidemia of the high-triglycerideand/or low-HDL type, and hypertension.It is worth mentioning that medical nutri-tion therapy aimed at producing 5–10%loss of body weight, exercise, and certainpharmacological agents have been vari-ably demonstrated to prevent or delay thedevelopment of diabetes in people withIGT; the potential impact of such inter-ventions to reduce cardiovascular risk hasnot been examined to date.

Note that many individuals with IGTare euglycemic in their daily lives. Indi-viduals with IFG or IGT may have normalor near normal glycated hemoglobin lev-els. Individuals with IGT often manifesthyperglycemia only when challengedwith the oral glucose load used in thestandardized OGTT.

DIAGNOSTIC CRITERIA FORDIABETES MELLITUS — The cri-teria for the diagnosis of diabetes areshown in Table 2. Three ways to diagnosediabetes are possible, and each, in the ab-sence of unequivocal hyperglycemia,must be confirmed, on a subsequent day,by any one of the three methods given in

Table 2. The use of the hemoglobin A1c(A1C) for the diagnosis of diabetes is notrecommended at this time.

Diagnosis of GDMThe criteria for abnormal glucose toler-ance in pregnancy are those of Carpenterand Coustan (3). Recommendations fromthe American Diabetes Association’sFourth Internat ional Workshop-Conference on Gestational Diabetes Mel-litus held in March 1997 support the useof the Carpenter/Coustan diagnostic cri-teria as well as the alternative use of a di-agnostic 75-g 2-h OGTT. These criteriaare summarized below.Testing for gestational diabetes. Previ-ous recommendations included screeningfor GDM performed in all pregnancies.However, there are certain factors thatplace women at lower risk for the devel-opment of glucose intolerance duringpregnancy, and it is likely not cost-effective to screen such patients. Pregnantwomen who fulfill all of these criterianeed not be screened for GDM.

This low-risk group compriseswomen who

● are �25 years of age● are a normal body weight● have no family history (i.e., first-degree

relative) of diabetes● have no history of abnormal glucose

metabolism● have no history of poor obstetric out-

come● are not members of an ethnic/racial

group with a high prevalence of diabe-tes (e.g., Hispanic American, NativeAmerican, Asian American, AfricanAmerican, Pacific Islander)

Risk assessment for GDM should beundertaken at the first prenatal visit.Women with clinical characteristics con-sistent with a high risk of GDM (markedobesity, personal history of GDM, glyco-suria, or a strong family history of diabe-tes) should undergo glucose testing (seebelow) as soon as feasible. If they arefound not to have GDM at that initialscreening, they should be retested be-tween 24 and 28 weeks of gestation.Women of average risk should have test-ing undertaken at 24 –28 weeks ofgestation.

A fasting plasma glucose level �126mg/dl (7.0 mmol/l) or a casual plasmaglucose �200 mg/dl (11.1 mmol/l) meetsthe threshold for the diagnosis of diabe-tes. In the absence of unequivocal hyper-

Table 2—Criteria for the diagnosis of diabetes

1. FPG �126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for atleast 8 h.*

OR2. Symptoms of hyperglycemia and a casual plasma glucose �200 mg/dl (11.1

mmol/l). Casual is defined as any time of day without regard to time since lastmeal. The classic symptoms of hyperglycemia include polyuria, polydipsia, andunexplained weight loss.

OR3. 2-h plasma glucose �200 mg/dl (11.1 mmol/l) during an OGTT. The test

should be performed as described by the World Health Organization, using aglucose load containing the equivalent of 75 g anhydrous glucose dissolved inwater.*

*In the absence of unequivocal hyperglycemia, these criteria should be confirmed by repeat testing on adifferent day.

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S66 DIABETES CARE, VOLUME 32, SUPPLEMENT 1, JANUARY 2009

glycemia, the diagnosis must beconfirmed on a subsequent day. Confir-mation of the diagnosis precludes theneed for any glucose challenge. In the ab-sence of this degree of hyperglycemia,

evaluation for GDM in women with aver-age or high-risk characteristics should fol-low one of two approaches.One-step approach. Perform a diagnos-tic OGTT without prior plasma or serumglucose screening. The one-step approachmay be cost-effective in high-risk patientsor populations (e.g., some Native-American groups).Two-step approach. Perform an initialscreening by measuring the plasma or se-rum glucose concentration 1 h after a50-g oral glucose load (glucose challengetest [GCT]) and perform a diagnosticOGTT on that subset of women exceedingthe glucose threshold value on the GCT.When the two-step approach is used, aglucose threshold value �140 mg/dl (7.8mmol/l) identifies �80% of women withGDM, and the yield is further increased to90% by using a cutoff of �130 mg/dl (7.2mmol/l).

With either approach, the diagnosisof GDM is based on an OGTT. Diagnosticcriteria for the 100-g OGTT are derivedfrom the original work of O’Sullivan andMahan (4) modified by Carpenter and

Coustan (3) and are shown in the top ofTable 3. Alternatively, the diagnosis canbe made using a 75-g glucose load and theglucose threshold values listed for fasting,1 h, and 2 h (Table 2, bottom); however,this test is not as well validated as the100-g OGTT.

References1. The Expert Committee on the Diagnosis

and Classification of Diabetes Mellitus:Report of the Expert Committee on theDiagnosis and Classification of DiabetesMellitus. Diabetes Care 20:1183–1197,1997

2. The Expert Committee on the Diagnosisand Classification of Diabetes Mellitus:Follow-up report on the diagnosis of dia-betes mellitus. Diabetes Care 26:3160–3167, 2003

3. Carpenter MW, Coustan DR: Criteria forscreening tests for gestational diabetes.Am J Obstet Gynecol 144:768–773, 1982

4. O’Sullivan JB, Mahan CM: Criteria for theoral glucose tolerance test in pregnancy.Diabetes 13:278, 1964

Table 3—Diagnosis of GDM with a 100-g or75-g glucose load

mg/dl mmol/l

100-g glucose loadFasting 95 5.31-h 180 10.02-h 155 8.63-h 140 7.8

75-g glucose loadFasting 95 5.31-h 180 10.02-h 155 8.6

Two or more of the venous plasma concentrationsmust be met or exceeded for a positive diagnosis.The test should be done in the morning after anovernight fast of between 8 and 14 h and after at least3 days of unrestricted diet (�150 g carbohydrate perday) and unlimited physical activity. The subjectshould remain seated and should not smokethroughout the test.

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