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P O S I T I O N S T A T E M E N T

Diagnosis and Classification of Diabetes
Mellitus
AMERICAN DIABETES ASSOCIATION but may not have progressed far enough
to cause hyperglycemia. The same disease
process can cause impaired fasting glu-
cose (IFG) and/or impaired glucose toler-
DEFINITION AND vision; nephropathy leading to renal failure; ance (IGT) without fulfilling the criteria
DESCRIPTION OF DIABETES peripheral neuropathy with risk of foot ul- for the diagnosis of diabetes. In some in-
MELLITUS — Diabetes mellitus is a cers, amputations, and Charcot joints; and dividuals with diabetes, adequate glyce-
group of metabolic diseases characterized autonomic neuropathy causing gastrointes- mic control can be achieved with weight
by hyperglycemia resulting from defects tinal, genitourinary, and cardiovascular reduction, exercise, and/or oral glucose-
in insulin secretion, insulin action, or symptoms and sexual dysfunction. Patients lowering agents. These individuals there-
both. The chronic hyperglycemia of dia- with diabetes have an increased incidence fore do not require insulin. Other
betes is associated with long-term dam- of atherosclerotic cardiovascular, periph- individuals who have some residual insu-
age, dysfunction, and failure of various eral arterial, and cerebrovascular disease. lin secretion but require exogenous insu-
organs, especially the eyes, kidneys, Hypertension and abnormalities of lipopro- lin for adequate glycemic control can
nerves, heart, and blood vessels. tein metabolism are often found in people survive without it. Individuals with ex-
Several pathogenic processes are in- with diabetes. tensive ␤-cell destruction and therefore
volved in the development of diabetes. The vast majority of cases of diabetes no residual insulin secretion require insu-
These range from autoimmune destruc- fall into two broad etiopathogenetic cate- lin for survival. The severity of the meta-
tion of the ␤-cells of the pancreas with gories (discussed in greater detail below). bolic abnormality can progress, regress,
consequent insulin deficiency to abnor- In one category, type 1 diabetes, the cause or stay the same. Thus, the degree of hy-
malities that result in resistance to insulin is an absolute deficiency of insulin secre- perglycemia reflects the severity of the un-
action. The basis of the abnormalities in tion. Individuals at increased risk of de- derlying metabolic process and its
carbohydrate, fat, and protein metabo- veloping this type of diabetes can often be treatment more than the nature of the
lism in diabetes is deficient action of in- identified by serological evidence of an process itself.
sulin on target tissues. Deficient insulin autoimmune pathologic process occur-
action results from inadequate insulin se- ring in the pancreatic islets and by genetic CLASSIFICATION OF
cretion and/or diminished tissue re- markers. In the other, much more preva- DIABETES MELLITUS AND
sponses to insulin at one or more points in lent category, type 2 diabetes, the cause is OTHER CATEGORIES OF
the complex pathways of hormone action. a combination of resistance to insulin ac- GLUCOSE REGULATION — A s -
Impairment of insulin secretion and de- tion and an inadequate compensatory in- signing a type of diabetes to an individual
fects in insulin action frequently coexist sulin secretory response. In the latter often depends on the circumstances
in the same patient, and it is often unclear category, a degree of hyperglycemia suffi- present at the time of diagnosis, and many
which abnormality, if either alone, is the cient to cause pathologic and functional diabetic individuals do not easily fit into a
primary cause of the hyperglycemia. changes in various target tissues, but single class. For example, a person with
Symptoms of marked hyperglycemia without clinical symptoms, may be gestational diabetes mellitus (GDM) may
include polyuria, polydipsia, weight loss, present for a long period of time before continue to be hyperglycemic after deliv-
sometimes with polyphagia, and blurred diabetes is detected. During this asymp- ery and may be determined to have, in
vision. Impairment of growth and suscep- tomatic period, it is possible to demon- fact, type 2 diabetes. Alternatively, a per-
tibility to certain infections may also ac- strate an abnormality in carbohydrate son who acquires diabetes because of
company chronic hyperglycemia. Acute, metabolism by measurement of plasma large doses of exogenous steroids may be-
life-threatening consequences of uncon- glucose in the fasting state or after a chal- come normoglycemic once the glucocor-
trolled diabetes are hyperglycemia with lenge with an oral glucose load. ticoids are discontinued, but then may
ketoacidosis or the nonketotic hyperos- The degree of hyperglycemia (if any) develop diabetes many years later after re-
molar syndrome. may change over time, depending on the current episodes of pancreatitis. Another
Long-term complications of diabetes extent of the underlying disease process example would be a person treated with
include retinopathy with potential loss of (Fig. 1). A disease process may be present thiazides who develops diabetes years
later. Because thiazides in themselves sel-
● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● dom cause severe hyperglycemia, such in-
The information that follows is based largely on the reports of the Expert Committee on the Diagnosis and dividuals probably have type 2 diabetes
Classification of Diabetes (Diabetes Care 20:1183–1197, 1997, and Diabetes Care 26:3160 –3167, 2003). that is exacerbated by the drug. Thus, for
Abbreviations: FPG, fasting plasma glucose; GAD, glutamic acid decarboxylase; GCT, glucose challenge the clinician and patient, it is less important
test; GDM, gestational diabetes mellitus; HNF, hepatocyte nuclear factor; IFG, impaired fasting glucose; IGT,
impaired glucose tolerance; MODY, maturity-onset diabetes of the young; WHO, World Health Organiza- to label the particular type of diabetes than it
tion. is to understand the pathogenesis of the hy-
© 2004 by the American Diabetes Association. perglycemia and to treat it effectively.

DIABETES CARE, VOLUME 27, SUPPLEMENT 1, JANUARY 2004 S5

these adults). defect with insulin resistance) the disease has strong HLA associations. Some forms of type individuals do not need insulin treatment dren and adolescents. with type 1 diabetes fall into this category. that are still poorly defined. other autoimmune disorders such as adult-onset diabetes. There are probably many dif- ketoacidosis as the first manifestation of Some of these patients have permanent ferent causes of this form of diabetes. though the specific etiologies are not S6 DIABETES CARE. may retain of those who do. and children) and slow in others (mainly and pernicious anemia. of diabetes suffer from episodic ketoaci- encompassed by the terms insulin. to glutamic acid decarboxylase (GAD65). to survive. which accounts for only residual ␤-cell function sufficient to pre.e. decades of life. One and usually Autoimmune destruction of ␤-cells predominantly insulin resistance more of these autoantibodies are present has multiple genetic predispositions and with relative insulin deficiency to in 85–90% of individuals when fasting is also related to environmental factors predominantly an insulin secretory hyperglycemia is initially detected. hyperglycemia that can rapidly change to sis. At this latter stage of the dis. but it can oc. may present with 1 diabetes have no known etiologies. encompasses indi- In this form of diabetes.. tients are rarely obese when they present This form of diabetes. Type 2 diabetes (ranging from phatases IA-2 and IA-2␤. being Addison’s disease. Although only a minority of patients deficiency) in the presence of infection or other stress. but have no evidence of autoimmu- usually leading to absolute insulin severe hyperglycemia and/or ketoacidosis nity. or ju. ously referred to as non-insulin- These HLA-DR/DQ alleles can be either nosis. Immune. autoimmunity. usually have relative (rather than abso- rapid in some individuals (mainly infants autoimmune hepatitis. viduals who have insulin resistance and ␤-cell destruction is quite variable. Some patients. previ- and it is influenced by the DRB genes. “honeymoon” remission). myasthenia gravis. even in the 8th and 9th and autoantibodies to the tyrosine phos. cellular-mediated autoimmune destruc. celiac sprue. This venile-onset diabetes. Individuals with this form 5–10% of those with diabetes. particularly chil. and often throughout their lifetime. type I diabetes. Idiopathic diabetes. Al- the disease. This form Still others. Type 1 diabetes (␤-cell destruction. such in. ⴱEven after presenting in ketoacidosis.. may come and go. Asian ancestry. and is not HLA associated. Also. Immune-mediated diabetes. particularly adults.g. previously vent ketoacidosis for many years. ers of the immune destruction of the els of plasma C-peptide. autoantibodies childhood and adolescence. ⴱⴱin rare instances. with this type of diabetes. Others have modest fasting insulinopenia and are prone to ketoacido. type II diabetes. mediated diabetes commonly occurs in placement therapy in affected patients autoantibodies to insulin. the presence of ⬃90 –95% of those with diabetes. vitiligo. as manifested by low or undetectable lev. obesity is not incompatible with the diag. Mark.Position Statement Figure 1—Disorders of glycemia: etiologic types and stages. These patients are also prone to dependent diabetes. lute) insulin deficiency At least initially. cur at any age. on insulin for survival and are at risk for lin deficiency between episodes. there is little or no insulin secretion. JANUARY 2004 . SUPPLEMENT 1. type 1 diabetes presenting in pregnancy) may require insulin for survival. dividuals eventually become dependent dosis and exhibit varying degrees of insu- dependent diabetes. VOLUME 27. Although pa. Vacor toxicity. these patients can briefly return to normogly- cemia without requiring continuous therapy (i. or predisposing or protective. results from a ketoacidosis. which accounts for with linkage to the DQA and DQB genes. lacks immunological evidence for ␤-cell tion of the ␤-cells of the pancreas. patients in these categories (e. form of diabetes is strongly inherited. most are of African or of diabetes. ease. the rate of Graves’ disease. An absolute requirement for insulin re- ␤-cell include islet cell autoantibodies. Hashimoto’s thyroiditis.

and lack of physical ac. HNF-1␤. noma. when the hormone excess is resolved. epinephrine) antagonize insulin ac- with a strong genetic predisposition. cortisol. This gen- clearly defined. scription factors. However. If extensive enough. growth hormone. preexisting defects in insulin secretion. the inability to convert proinsulin to in. Nevertheless. autoimmune destruction of sulin action. adre- cose levels in these diabetic patients with diabetes mellitus and deafness The nocarcinomas that involve only a small would be expected to result in even most common mutation occurs at posi. the exocrine ducts have been found at women with prior GDM and in individu. resolves after successful removal of the tu- years). insulin se. the Rabson-Mendenhall syndrome are not have any of the other causes of diabe. In Many drugs can impair insulin secretion. or even normal glucose metabolism. (mitochondrial myopathy. often not severe enough for the patient to cose are necessary to elicit normal levels Diseases of the exocrine pancreas. cystic insufficient to compensate for insulin re. of which. and obesity itself causes with mutations on chromosome 12 in a function and extreme insulin resistance. mosomes have been identified to date. and pancreatic carci- Whereas patients with this form of diabe. ing to an A-to-G transition. notypic expressions of this genetic lesion. Some individu. portion of the pancreas have been associ- higher insulin values had their ␤-cell tion 3243 in the tRNA leucine gene. diabetes is not part of tion. however. while criteria may have an increased percentage second form is associated with mutations the latter is associated with abnormalities of body fat distributed predominantly in in the glucokinase gene on chromosome of teeth and nails and pineal gland the abdominal region. Acquired processes increased risk of developing macrovascu. trauma. type 1 diabetes. pancreatectomy. gluca- ethnic subgroups. including HNF-4␣. fibrosis and hemochromatosis will also sistance. two pediatric syndromes that have muta- tes listed above or below. It occurs more frequently in sulin have been identified in a few fami. Fibrocalculous pancreatopathy may logical treatment of hyperglycemia but is this syndrome. increased plasma levels of glu. ated with diabetes. the genetics of families and is associated with an autoso. Leprechaunism and ␤-cells does not occur.. betes frequently goes undiagnosed for serves as the “glucose sensor” for the it is assumed that the lesion(s) must reside many years because the hyperglycemia ␤-cell. obesity. lar and microvascular complications. Other specific types of diabetes There are unusual causes of diabetes that and hyperglycemia typically resolves Genetic defects of the ␤-cell. the metabolism tion of the insulin receptor cannot be association with the stress of another ill. Patients hepatic transcription factor referred to as The former has characteristic facial fea- who are not obese by traditional weight hepatocyte nuclear factor (HNF)-1␣. Similarly.g. tions in the insulin receptor gene with Most patients with this form of diabe. Because of defects in the glucoki. lies. and patients do autosomal dominant pattern. of insulin secretion. insulin promoter factor (IPF)-1. The result. Abnormali. The most common form is associated subsequent alterations in insulin receptor tes are obese. encephalopa. Drug. They are inherited in an insulin resistance. An identical nism other than simple reduction in cretion is defective in these patients and lesion occurs in the MELAS syndrome ␤-cell mass. onset diabetes of the young (MODY) and acanthosis nigricans. Several hormones and its frequency varies in different racial/ ant glucose intolerance is mild. this syndrome was termed type A These drugs may not cause diabetes by DIABETES CARE. in turn. DNA have been found to be associated be extensive for diabetes to occur. erally occurs in individuals with Genetic defects in insulin action. Several result from genetically determined abnor. (e. drome). glucokinase resistant lipoatrophic diabetes.g. in the postreceptor signal transduction develops gradually and at earlier stages is nase gene. als with these mutations may have mor. Therefore. Ketoacidosis sel. cretion with minimal or no defects in in. some degree of insulin resistance. 7p and results in a defective glucokinase hyperplasia.or chemical-induced diabetes. glucagonoma. Hyperglycemia generally at an early age (generally before age 25 cemia to severe diabetes. tion by the ␤-cell. by inhibiting in- characterized by onset of hyperglycemia hyperinsulinemia and modest hypergly. re- this form of diabetes are complex and not mal inheritance and only mildly impaired spectively) can cause diabetes. pheochromocytoma. They are referred to as maturity. suggesting different phe. autosomal dominant pattern. when seen. such patients are at forms result from mutations in other tran. lead.. ilized and have enlarged. lactic acidosis. Diagnosis and Classification known. are characterized by impaired insulin se. damage ␤-cells and impair insulin secre- with weight reduction and/or pharmaco. infection. sulin secretion. malities of insulin action. be accompanied by abdominal pain radi- seldom restored to normal The risk of de. Women may be vir. JANUARY 2004 S7 . forms of diabetes are associated with mo. The less common process that diffusely injures the pancreas abetes. the past. gon. demonstrated in patients with insulin- ness such as infection. Insulin resistance may improve thy. cystic ovaries.and aldoster- nogenetic defects in ␤-cell function. Excess amounts of these hormones more so than is the autoimmune form of binding has also been identified in a few (e. VOLUME 27. Endocrinopathies. Cushing’s syndrome. Any notice any of the classic symptoms of di. Pancreatic fibrosis and calcium stones in tivity. The metabolic Somatostatinoma. Thus. SUPPLEMENT 1. abnormalities associated with mutations onoma-induced hypokalemia can cause These forms of diabetes are frequently of the insulin receptor may range from diabetes. and NeuroD1. Thus. cules with resultant impaired receptor tion. the higher blood glu. and such traits are inherited in an autopsy. can cause diabetes. at least in part. ating to the back and pancreatic calcifica- veloping this form of diabetes increases Genetic abnormalities that result in tions identified on X-ray examination. With the exception of that caused tes may have insulin levels that appear Point mutations in mitochondrial by cancer. it usually arises in to glucose-6-phosphate. pathways. als with hypertension or dyslipidemia. A tures and is usually fatal in infancy. ties at six genetic loci on different chro. stimulates insulin secre. with age. This form of dia. acromegaly. include pancreatitis. Glucokinase converts glucose Alterations in the structure and func- diabetes. It is often associated the production of mutant insulin mole. and stroke-like syn. dom occurs spontaneously in this type of molecule. damage to the pancreas must normal or elevated. This implies a mecha- function been normal.

Chromosome 7. Laurence-Moon-Biedl syndrome ies often have acanthosis nigricans. Turner’s syndrome other autoimmune diseases. JANUARY 2004 . NeuroD1 (MODY6) can impair insulin action. The 5. “Stiff-man” syndrome can act as an insulin agonist after binding 2. Others clude nicotinic acid and glucocorticoids. Others occurs in patients with congenital rubella. HNF-1␤ (MODY5) are also many drugs and hormones that 6. G. Anti–insulin receptor antibodies to the receptor and can thereby cause hy- 3. In such cases. Type 1 diabetes (␤-cell destruction. Cystic fibrosis Infections. Lipoatrophic diabetes instances. Other genetic syndromes sometimes associated with diabetes poglycemia. In this category. ␤-adrenergic agonists Patients usually have high titers of the 8. ␣-Interferon one-third will develop diabetes. Cytomegalovirus 3. Congenital rubella receptor. and approximately 9. Acromegaly and immune markers characteristic of 2. Type 2 diabetes (may range from predominantly insulin resistance with relative insulin deficiency to a predominantly secretory defect with insulin resistance) importance of ␤-cell dysfunction and in- III. Aldosteronoma Uncommon forms of immune-medi- 8. Many genetic Patients with any form of diabetes may require insulin treatment at some stage of their disease. Friedreich’s ataxia states of extreme insulin resistance. coxsackievi- 3. Diazoxide of the axial muscles with painful spasms. of itself. Mitochondrial DNA 8. in certain 4. severe insulin deficiency. SUPPLEMENT 1. Gestational diabetes mellitus (GDM) associated with diabetes. Others list shown in Table 1 is not all-inclusive. 11. Chromosome 13. Pentamidine likely to occur.or chemical-induced ated diabetes. adenovirus. cytomegalovirus. The stiff-man syndrome is 3. usually leading to absolute insulin deficiency) betes in individuals with insulin resis- A. HNF-4␣ (MODY1) nently destroy pancreatic ␤-cells. 7. but they may precipitate dia- I. Others insulin to its receptor in target tissues. As in other 4. glucokinase (MODY2) 3. Immune mediated tance. Hemochromatosis sociated with ␤-cell destruction. pa- 6. S8 DIABETES CARE. Glucagonoma 4. In the 8. Glucocorticoids 5. Others H. Infections cause diabetes by binding to the insulin 1. the classification is B. Diabetes 6. Neoplasia forms of diabetes. Pheochromocytoma rus B. Thyroid hormone nervous system characterized by stiffness 6. D. Diseases of the exocrine pancreas but reflects the more commonly recog- 1. Huntington’s chorea tients with anti–insulin receptor antibod- 7. Chromosome 2. Chromosome 20. these antibodies 1. classify the patient. There 5. Others Other genetic syndromes sometimes IV. this syndrome was termed type B 9. C. Certain tox- A. Anti–insulin receptor anti- 1. Prader-Willi syndrome insulin resistance. there are 1. Others E. Myotonic dystrophy past. Such use of syndromes are accompanied by an in- insulin does not. Type A insulin resistance reported to develop diabetes associated 2. Examples in- 7. Nicotinic acid an autoimmune disorder of the central 4. Uncommon forms of immune-mediated diabetes However. MODY4) drug reactions fortunately are rare. Thiazides GAD autoantibodies. Wolfram’s syndrome 5. Such 4. Dilantin 10. Porphyria 10. Leprechaunism 3. HNF-1␣ (MODY3) intravenous pentamidine can perma- 2. B. Pancreatitis 2. Cushing’s syndrome type 1 diabetes. Certain viruses have been as- 5. Klinefelter’s syndrome with systemic lupus erythematosus and 3. Genetic defects of ␤-cell function ins such as Vacor (a rat poison) and 1. VOLUME 27. 4. thereby blocking the binding of 2. Hyperthyroidism mumps have been implicated in inducing 6. and others are 2. creased incidence of diabetes mellitus. in some cases. insulin promoter factor-1 (IPF-1. Somatostatinoma certain cases of the disease. 7. Down’s syndrome bodies are occasionally found in patients 2. Chromosome 12. or toxin-induced 3. Others Anti–insulin receptor antibodies can F. Rabson-Mendenhall syndrome with islet cell antibodies and. Trauma/pancreatectomy nized drug-. and 5. Fibrocalculous pancreatopathy 7. Chromosome 17. In addition. Vacor two known conditions.Position Statement Table 1—Etiologic classification of diabetes mellitus themselves. Drug. hormone-. 11. Endocrinopathies although most of these patients have HLA 1. Genetic defects in insulin action Patients receiving ␣-interferon have been 1. Idiopathic unclear because the sequence or relative II. Other specific types sulin resistance is unknown.

Recommendations from intolerance with onset or first recognition the American Diabetes Association’s during pregnancy. ment of diabetes in these patients. Symptoms of diabetes plus casual plasma glucose concentration ⱖ200 mg/dl (11. although not meeting cri. teria as well as the alternative use of a di- that unrecognized glucose intolerance may ● 2-h postload glucose ⱖ200 mg/dl (11. and certain come 2-h values in the oral glucose tolerance pharmacological agents have been vari. (A1C) for the diagnosis of diabetes is not gonadism. ● have no family history (i. It is worth mentioning that medical nutri. and it is likely not cost- Deterioration of glucose tolerance oc. and hypertension. as described Table 1.S. place women at lower risk for the devel- studied.1 mmol/l). Indi- 2.1 mmol/l) during an OGTT. there are certain factors that pregnancies. and unexplained weight loss. first-degree teria for diabetes. Wolfram’s syndrome is an autoso. SUPPLEMENT 1. not clinical entities in their own right but women who fulfill all of these criteria larly in the 3rd trimester. It does not exclude the possibility glucose tolerance). absence of pregnancy. The third measure (OGTT) is not recommended for routine clinical use. which includes obesity ● are a normal body weight glucose levels. using a glucose load containing the equivalent of 75 g with the oral glucose load used in the anhydrous glucose dissolved in water. Conference on Gestational Diabetes Mel- modification is used for treatment or ● 2-h postload glucose 140 –199 mg/dl litus held in March 1997 support the use whether the condition persists after preg. rather risk factors for future diabetes as need not be screened for GDM. Casual is defined as any time of day without regard to time since last meal. mal recessive disorder characterized by mal fasting glucose. alence may range from 1 to 14% of Patients with IFG and/or IGT are now However. viduals with IFG or IGT may have normal or or near normal glycated hemoglobin lev- els. Note that many individuals with IGT or are euglycemic in their daily lives. ● are ⬍25 years of age an intermediate group of subjects whose abolic syndrome. GDM complicates abetes (the diagnosis must be con. must be confirmed. Other syndromes are listed in nosis must be confirmed. (especially abdominal or visceral obesity). for GDM performed in all pregnancies. The classic ventions to reduce cardiovascular risk has symptoms of diabetes include polyuria. insulin-deficient diabetes and the absence ● FPG 100 –125 mg/dl (5.0 mmol/l) or loss of body weight. In the pregnancy.e.000 cases annually. The definition applies ● 2-h postload glucose ⬍140 mg/dl (7. Thus. result. exercise. the potential impact of such inter- l). Pregnant curs normally during pregnancy.6 – 6. IFG and IGT are effective to screen such patients. JANUARY 2004 S9 . optic atrophy. polydipsia.0 mmol/l) ⫽ pro. Previ- ⬃4% of all pregnancies in the U.8 Fourth International Workshop- regardless of whether insulin or only diet mmol/l) ⫽ normal glucose tolerance. in the ab- drome. Testing for gestational diabetes. are nevertheless too dyslipidemia of the high-triglyceride relative) of diabetes high to be considered normal. not been examined to date. recommended at this time. (7. particu. The prev. ● are not members of an ethnic/racial test (OGTT) of ⱖ140 mg/dl (7. They can This low-risk group comprises Impaired glucose tolerance (IGT) be observed as intermediate stages in any women who and impaired fasting glucose (IFG) of the disease processes listed in Table 1. ● FPG ⱖ126 mg/dl (7. DIAGNOSTIC CRITERIA FOR DIABETES MELLITUS — The cri- These include the chromosomal abnor. GDM represents nearly 90% of all cating the relatively high risk for develop. The test should be hyperglycemia only when challenged performed as described by WHO. deafness. on a subsequent day.1 agnostic 75-g 2-h OGTT. firmed.8 mmol/l) ably demonstrated to prevent or delay the group with a high prevalence of diabe- DIABETES CARE..6 mmol/l) ⫽ nor.. with the pregnancy. below). Three ways to diagnose Klinefelter’s syndrome. opment of glucose intolerance during pregnancies complicated by diabetes. standardized OGTT. The Expert Committee (1. Additional manifes. ous recommendations included screening ing in ⬃135. Diagnosis of GDM The criteria for abnormal glucose toler- Gestational diabetes mellitus (GDM) The corresponding categories when the ance in pregnancy are those of Carpenter GDM is defined as any degree of glucose OGTT is used are the following: and Coustan (3). but ⬍200 mg/dl (11. ● FPG ⬍100 mg/dl (5. Fasting is defined as no caloric intake for at least 8 h. VOLUME 27.1 mmol/l) ⫽ IGT (impaired of the Carpenter/Coustan diagnostic cri- nancy. and each. metabolism cose (FPG) levels ⱖ100 mg/dl (5. depending on the population referred to as having “pre-diabetes” indi. 2-h postload glucose ⱖ200 mg/dl (11. as described below).2) recognized IFG and IGT are associated with the met. diabetes are possible. sence of unequivocal hyperglycemia. Diagnosis and Classification Table 2—Criteria for the diagnosis of diabetes mellitus development of diabetes in people with 1. and neural visional diagnosis of diabetes (the diag. these criteria should be confirmed by repeat testing on a different day.1 mmol/ IGT.6 tion therapy aimed at producing 5–10% ● have no history of poor obstetric out- mmol/l) but ⬍126 mg/dl (7. The use of the hemoglobin A1c tations include diabetes insipidus. FPG ⱖ126 mg/dl (7. This group and/or low-HDL type.9 mmol/ by any one of the three methods given in of ␤-cells at autopsy. hypo. In the absence of unequivocal hyperglycemia. These criteria have antedated or begun concomitantly mmol/l) ⫽ provisional diagnosis of di. categories of FPG values are as follows: shown in Table 2. ● have no history of abnormal glucose is defined as having fasting plasma glu. l) ⫽ IFG (impaired fasting glucose). and Turner’s syn. the teria for the diagnosis of diabetes are malities of Down’s syndrome.8 –11. Table 2. Individuals with IGT often manifest 3.0 mmol/l). are summarized below. well as cardiovascular disease.

Confir. mmol/l). OGTT on that subset of women exceeding Am J Obstet Gynecol 144:768 –773. JANUARY 2004 . 2-h 155 8. however.g. obesity. sence of this degree of hyperglycemia. 2003 Women with clinical characteristics con. the diagnosis can Fasting 95 5. Diabetes Care 26:3160 – 3167. In the absence of unequivocal hyper.1 mmol/l) meets Mahan (4) modified by Carpenter and 3-h 140 7. or a strong family history of diabe. this test is not as well validated as the must be met or exceeded for a positive diagnosis. 50-g oral glucose load (glucose challenge 3. GDM. and the yield is further increased to tween 24 and 28 weeks of gestation. glyco.g. The subject low one of two approaches.0 confirmed on a subsequent day. The Expert Committee on the Diagnosis One-step approach. Two or more of the venous plasma concentrations need for any glucose challenge. below) as soon as feasible. personal history of GDM. Diagnostic Fasting 95 5. and Classification of Diabetes Mellitus: throughout the test. tic OGTT without prior plasma or serum Report of the Expert Committee on the glucose screening.3 A fasting plasma glucose level ⬎126 criteria for the 100-g OGTT are derived 1-h 180 10.2 mg/dl mmol/l Women of average risk should have test. The Expert Committee on the Diagnosis Two-step approach. Hispanic American. 4. Diabetes Care 20:1183–1197. 90% by using a cutoff of ⬎130 mg/dl (7. the diagnosis 100-g Glucose load gestation. should remain seated and should not smoke 1. 1997 American. African or populations (e. Coustan DR: Criteria for sistent with a high risk of GDM (marked test [GCT]) and perform a diagnostic screening tests for gestational diabetes. a oral glucose tolerance test in pregnancy. 1964 S10 DIABETES CARE. rum glucose concentration 1 h after a betes mellitus. The test should be done in the morning after an overnight fast of between 8 and 14 h and after at least evaluation for GDM in women with aver- 3 days of unrestricted diet (ⱖ150 g carbohydrate per age or high-risk characteristics should fol- References day) and unlimited physical activity.8 the threshold for the diagnosis of diabe. SUPPLEMENT 1. of GDM is based on an OGTT. and 2 h (Table 2. If they are glucose threshold value ⬎140 mg/dl (7. Asian American. bottom). 100-g OGTT. Alternatively. Native may be cost-effective in high-risk patients Mellitus.0 mg/dl (7. Follow-up report on the diagnosis of dia- undertaken at the first prenatal visit.6 mation of the diagnosis precludes the 1 h.6 glucose ⬎200 mg/dl (11. they should be retested be.8 Diabetes 13:278. 2. In the ab.Position Statement Table 3—Diagnosis of GDM with a 100-g or found not to have GDM at that initial mmol/l) identifies ⬃80% of women with 75-g glucose load screening. Carpenter MW. 1982 suria.. Table 3.0 mmol/l) or a casual plasma from the original work of O’Sullivan and 2-h 155 8. the diagnosis must be be made using a 75-g glucose load and the 1-h 180 10. VOLUME 27. Perform a diagnos. American. Pacific Islander) American groups). Mahan CM: Criteria for the tes) should undergo glucose testing (see When the two-step approach is used.. the glucose threshold value on the GCT. O’Sullivan JB. some Native.3 glycemia. glucose threshold values listed for fasting. Coustan (3) and are shown in the top of 75-g Glucose load tes. ing undertaken at 24 –28 weeks of With either approach. Perform an initial and Classification of Diabetes Mellitus: Risk assessment for GDM should be screening by measuring the plasma or se. The one-step approach Diagnosis and Classification of Diabetes tes (e.