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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 reduction, exercise, and/or oral glucose-
lowering agents. These individuals there-
fore do not require insulin. Other
DEFINITION AND tinal, genitourinary, and cardiovascular individuals who have some residual insu-
DESCRIPTION OF DIABETES symptoms and sexual dysfunction. Patients lin secretion but require exogenous insu-
MELLITUS — Diabetes mellitus is a with diabetes have an increased incidence lin for adequate glycemic control can
group of metabolic diseases characterized of atherosclerotic cardiovascular, periph- survive without it. Individuals with ex-
by hyperglycemia resulting from defects eral arterial, and cerebrovascular disease. tensive ␤-cell destruction and therefore
in insulin secretion, insulin action, or Hypertension and abnormalities of lipopro- no residual insulin secretion require insu-
both. The chronic hyperglycemia of dia- tein metabolism are often found in people lin for survival. The severity of the meta-
betes is associated with long-term dam- with diabetes. bolic abnormality can progress, regress,
age, dysfunction, and failure of various The vast majority of cases of diabetes or stay the same. Thus, the degree of hy-
organs, especially the eyes, kidneys, fall into two broad etiopathogenetic cate- perglycemia reflects the severity of the un-
nerves, heart, and blood vessels. gories (discussed in greater detail below). derlying metabolic process and its
Several pathogenic processes are in- In one category, type 1 diabetes, the cause treatment more than the nature of the
volved in the development of diabetes. is an absolute deficiency of insulin secre- process itself.
These range from autoimmune destruc- tion. Individuals at increased risk of de-
tion of the ␤-cells of the pancreas with veloping this type of diabetes can often be CLASSIFICATION OF
consequent insulin deficiency to abnor- identified by serological evidence of an DIABETES MELLITUS AND
malities that result in resistance to insulin autoimmune pathologic process occur- OTHER CATEGORIES OF
action. The basis of the abnormalities in ring in the pancreatic islets and by genetic GLUCOSE REGULATION —
carbohydrate, fat, and protein metabo- markers. In the other, much more preva- Assigning a type of diabetes to an individ-
lism in diabetes is deficient action of in- lent category, type 2 diabetes, the cause is ual often depends on the circumstances
sulin on target tissues. Deficient insulin a combination of resistance to insulin ac- present at the time of diagnosis, and many
action results from inadequate insulin se- tion and an inadequate compensatory in- diabetic individuals do not easily fit into a
cretion and/or diminished tissue re- sulin secretory response. In the latter single class. For example, a person with
sponses to insulin at one or more points in category, a degree of hyperglycemia suffi- gestational diabetes mellitus (GDM) may
the complex pathways of hormone action. cient to cause pathologic and functional continue to be hyperglycemic after deliv-
Impairment of insulin secretion and de- changes in various target tissues, but ery and may be determined to have, in
fects in insulin action frequently coexist without clinical symptoms, may be fact, type 2 diabetes. Alternatively, a per-
in the same patient, and it is often unclear present for a long period of time before son who acquires diabetes because of
which abnormality, if either alone, is the diabetes is detected. During this asymp- large doses of exogenous steroids may be-
primary cause of the hyperglycemia. tomatic period, it is possible to demon- come normoglycemic once the glucocor-
Symptoms of marked hyperglycemia strate an abnormality in carbohydrate ticoids are discontinued, but then may
include polyuria, polydipsia, weight loss, metabolism by measurement of plasma develop diabetes many years later after re-
sometimes with polyphagia, and blurred glucose in the fasting state or after a chal- current episodes of pancreatitis. Another
vision. Impairment of growth and suscep- lenge with an oral glucose load. example would be a person treated with
tibility to certain infections may also ac- The degree of hyperglycemia (if any) thiazides who develops diabetes years
company chronic hyperglycemia. Acute, may change over time, depending on the later. Because thiazides in themselves sel-
life-threatening consequences of uncon- extent of the underlying disease process dom cause severe hyperglycemia, such in-
trolled diabetes are hyperglycemia with (Fig. 1). A disease process may be present dividuals probably have type 2 diabetes
ketoacidosis or the nonketotic hyperos- but may not have progressed far enough that is exacerbated by the drug. Thus, for
molar syndrome. to cause hyperglycemia. The same disease the clinician and patient, it is less important
Long-term complications of diabetes process can cause impaired fasting glu- to label the particular type of diabetes than it
include retinopathy with potential loss of cose (IFG) and/or impaired glucose toler- is to understand the pathogenesis of the hy-
vision; nephropathy leading to renal failure; ance (IGT) without fulfilling the criteria perglycemia and to treat it effectively.
peripheral neuropathy with risk of foot ul- for the diagnosis of diabetes. In some in-
cers, amputations, and Charcot joints; and dividuals with diabetes, adequate glyce- Type 1 diabetes (␤-cell destruction,
autonomic neuropathy causing gastrointes- mic control can be achieved with weight usually leading to absolute insulin
● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● deficiency)
The information that follows is based largely on the reports of the Expert Committee on the Diagnosis and Immune-mediated diabetes. This form
Classification of Diabetes (Diabetes Care 20:1183–1197, 1997, and Diabetes Care 26:3160 –3167, 2003). of diabetes, which accounts for only
Abbreviations: FPG, fasting plasma glucose; GAD, glutamic acid decarboxylase; GCT, glucose challenge 5–10% of those with diabetes, previously
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- encompassed by the terms insulin-
tion. dependent diabetes, type I diabetes, or ju-
DOI: 10.2337/dc07-S042 venile-onset diabetes, results from a
© 2007 by the American Diabetes Association.
S42 DIABETES CARE, VOLUME 30, SUPPLEMENT 1, JANUARY 2007
Position Statement

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

cellular-mediated autoimmune destruc- els of plasma C-peptide. Immune- placement therapy in affected patients
tion of the ␤-cells of the pancreas. Mark- mediated diabetes commonly occurs in may come and go.
ers of the immune destruction of the childhood and adolescence, but it can oc-
␤-cell include islet cell autoantibodies, cur at any age, even in the 8th and 9th Type 2 diabetes (ranging from
autoantibodies to insulin, autoantibodies decades of life. predominantly insulin resistance
to glutamic acid decarboxylase (GAD65), Autoimmune destruction of ␤-cells with relative insulin deficiency to
and autoantibodies to the tyrosine phos- has multiple genetic predispositions and predominantly an insulin secretory
phatases IA-2 and IA-2␤. One and usually is also related to environmental factors defect with insulin resistance)
more of these autoantibodies are present that are still poorly defined. Although pa- This form of diabetes, which accounts for
in 85–90% of individuals when fasting tients are rarely obese when they present ⬃90 –95% of those with diabetes, previ-
hyperglycemia is initially detected. Also, with this type of diabetes, the presence of ously referred to as non-insulin-
the disease has strong HLA associations, obesity is not incompatible with the diag- dependent diabetes, type II diabetes, or
with linkage to the DQA and DQB genes, nosis. These patients are also prone to adult-onset diabetes, encompasses indi-
and it is influenced by the DRB genes. other autoimmune disorders such as viduals who have insulin resistance and
These HLA-DR/DQ alleles can be either Graves’ disease, Hashimoto’s thyroiditis, usually have relative (rather than abso-
predisposing or protective. lute) insulin deficiency At least initially,
Addison’s disease, vitiligo, celiac sprue,
In this form of diabetes, the rate of and often throughout their lifetime, these
autoimmune hepatitis, myasthenia gravis,
␤-cell destruction is quite variable, being individuals do not need insulin treatment
and pernicious anemia.
rapid in some individuals (mainly infants to survive. There are probably many dif-
and children) and slow in others (mainly Idiopathic diabetes. Some forms of type ferent causes of this form of diabetes. Al-
adults). Some patients, particularly chil- 1 diabetes have no known etiologies. though the specific etiologies are not
dren and adolescents, may present with Some of these patients have permanent known, autoimmune destruction of
ketoacidosis as the first manifestation of insulinopenia and are prone to ketoacido- ␤-cells does not occur, and patients do
the disease. Others have modest fasting sis, but have no evidence of autoimmu- not have any of the other causes of diabe-
hyperglycemia that can rapidly change to nity. Although only a minority of patients tes listed above or below.
severe hyperglycemia and/or ketoacidosis with type 1 diabetes fall into this category, Most patients with this form of diabe-
in the presence of infection or other stress. of those who do, most are of African or tes are obese, and obesity itself causes
Still others, particularly adults, may retain Asian ancestry. Individuals with this form some degree of insulin resistance. Patients
residual ␤-cell function sufficient to pre- of diabetes suffer from episodic ketoaci- who are not obese by traditional weight
vent ketoacidosis for many years; such in- dosis and exhibit varying degrees of insu- criteria may have an increased percentage
dividuals eventually become dependent lin deficiency between episodes. This of body fat distributed predominantly in
on insulin for survival and are at risk for form of diabetes is strongly inherited, the abdominal region. Ketoacidosis sel-
ketoacidosis. At this latter stage of the dis- lacks immunological evidence for ␤-cell dom occurs spontaneously in this type of
ease, there is little or no insulin secretion, autoimmunity, and is not HLA associated. diabetes; when seen, it usually arises in
as manifested by low or undetectable lev- An absolute requirement for insulin re- association with the stress of another ill-

DIABETES CARE, VOLUME 30, SUPPLEMENT 1, JANUARY 2007 S43


Diagnosis and Classification

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

S44 DIABETES CARE, VOLUME 30, SUPPLEMENT 1, JANUARY 2007


Position Statement

nized drug-, hormone-, or toxin-induced


Table 1—Etiologic classification of diabetes mellitus forms of diabetes.
I. Type 1 diabetes (␤-cell destruction, usually leading to absolute insulin deficiency) Infections. Certain viruses have been as-
A. Immune mediated sociated with ␤-cell destruction. Diabetes
B. Idiopathic occurs in patients with congenital rubella,
II. Type 2 diabetes (may range from predominantly insulin resistance with relative insulin deficiency to a
predominantly secretory defect with insulin resistance) although most of these patients have HLA
III. Other specific types and immune markers characteristic of
A. Genetic defects of ␤-cell function type 1 diabetes. In addition, coxsackievi-
1. Chromosome 12, HNF-1␣ (MODY3) rus B, cytomegalovirus, adenovirus, and
2. Chromosome 7, glucokinase (MODY2)
3. Chromosome 20, HNF-4␣ (MODY1) mumps have been implicated in inducing
4. Chromosome 13, insulin promoter factor-1 (IPF-1; MODY4) certain cases of the disease.
5. Chromosome 17, HNF-1␤ (MODY5) Uncommon forms of immune-medi-
6. Chromosome 2, NeuroD1 (MODY6) ated diabetes. In this category, there are
7. Mitochondrial DNA
8. Others two known conditions, and others are
B. Genetic defects in insulin action likely to occur. The stiff-man syndrome is
1. Type A insulin resistance an autoimmune disorder of the central
2. Leprechaunism nervous system characterized by stiffness
3. Rabson-Mendenhall syndrome
4. Lipoatrophic diabetes of the axial muscles with painful spasms.
5. Others Patients usually have high titers of the
C. Diseases of the exocrine pancreas GAD autoantibodies, and approximately
1. Pancreatitis one-third will develop diabetes.
2. Trauma/pancreatectomy
3. Neoplasia Anti–insulin receptor antibodies can
4. Cystic fibrosis cause diabetes by binding to the insulin
5. Hemochromatosis receptor, thereby blocking the binding of
6. Fibrocalculous pancreatopathy insulin to its receptor in target tissues.
7. Others
D. Endocrinopathies However, in some cases, these antibodies
1. Acromegaly can act as an insulin agonist after binding
2. Cushing’s syndrome to the receptor and can thereby cause hy-
3. Glucagonoma poglycemia. Anti–insulin receptor anti-
4. Pheochromocytoma
5. Hyperthyroidism bodies are occasionally found in patients
6. Somatostatinoma with systemic lupus erythematosus and
7. Aldosteronoma other autoimmune diseases. As in other
8. Others states of extreme insulin resistance, pa-
E. Drug- or chemical-induced
1. Vacor tients with anti–insulin receptor antibod-
2. Pentamidine ies often have acanthosis nigricans. In the
3. Nicotinic acid past, this syndrome was termed type B
4. Glucocorticoids insulin resistance.
5. Thyroid hormone
6. Diazoxide Other genetic syndromes sometimes
7. ␤-adrenergic agonists associated with diabetes. Many genetic
8. Thiazides syndromes are accompanied by an in-
9. Dilantin creased incidence of diabetes mellitus.
10. ␣-Interferon
11. Others These include the chromosomal abnor-
F. Infections malities of Down’s syndrome,
1. Congenital rubella Klinefelter’s syndrome, and Turner’s syn-
2. Cytomegalovirus
3. Others
drome. Wolfram’s syndrome is an autoso-
G. Uncommon forms of immune-mediated diabetes mal recessive disorder characterized by
1. “Stiff-man” syndrome insulin-deficient diabetes and the absence
2. Anti–insulin receptor antibodies of ␤-cells at autopsy. Additional manifes-
3. Others
H. Other genetic syndromes sometimes associated with diabetes
tations include diabetes insipidus, hypo-
1. Down’s syndrome gonadism, optic atrophy, and neural
2. Klinefelter’s syndrome deafness. Other syndromes are listed in
3. Turner’s syndrome Table 1.
4. Wolfram’s syndrome
5. Friedreich’s ataxia
6. Huntington’s chorea Gestational diabetes mellitus (GDM)
7. Laurence-Moon-Biedl syndrome GDM is defined as any degree of glucose
8. Myotonic dystrophy intolerance with onset or first recognition
9. Porphyria
10. Prader-Willi syndrome
during pregnancy. The definition applies
11. Others regardless of whether insulin or only diet
IV. Gestational diabetes mellitus (GDM) modification is used for treatment or
Patients with any form of diabetes may require insulin treatment at some stage of their disease. Such use of whether the condition persists after preg-
insulin does not, of itself, classify the patient. nancy. It does not exclude the possibility
that unrecognized glucose intolerance may

DIABETES CARE, VOLUME 30, SUPPLEMENT 1, JANUARY 2007 S45


Diagnosis and Classification

Table 2—Criteria for the diagnosis of diabetes mellitus (A1C) for the diagnosis of diabetes is not
1. Symptoms of diabetes plus casual plasma glucose concentration ⱖ200 mg/dl (11.1 mmol/ recommended at this time.
l). Casual is defined as any time of day without regard to time since last meal. The classic
symptoms of diabetes include polyuria, polydipsia, and unexplained weight loss. Diagnosis of GDM
The criteria for abnormal glucose toler-
OR ance in pregnancy are those of Carpenter
2. FPG ⱖ126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h. and Coustan (3). Recommendations from
OR the American Diabetes Association’s
Fourth International Workshop-
3. 2-h postload glucose ⱖ200 mg/dl (11.1 mmol/l) during an OGTT. The test should be
Conference on Gestational Diabetes Mel-
performed as described by WHO, using a glucose load containing the equivalent of 75 g
litus held in March 1997 support the use
anhydrous glucose dissolved in water.
of the Carpenter/Coustan diagnostic cri-
In the absence of unequivocal hyperglycemia, these criteria should be confirmed by repeat testing on a
different day. The third measure (OGTT) is not recommended for routine clinical use.
teria as well as the alternative use of a di-
agnostic 75-g 2-h OGTT. These criteria
are summarized below.
Testing for gestational diabetes. Previ-
have antedated or begun concomitantly abetes (the diagnosis must be con- ous recommendations included screening
with the pregnancy. GDM complicates firmed, as described below). for GDM performed in all pregnancies.
⬃4% of all pregnancies in the U.S., result- However, there are certain factors that
ing in ⬃135,000 cases annually. The prev- Patients with IFG and/or IGT are now place women at lower risk for the devel-
alence may range from 1 to 14% of referred to as having “pre-diabetes” indi- opment of glucose intolerance during
pregnancies, depending on the population cating the relatively high risk for develop- pregnancy, and it is likely not cost-
studied. GDM represents nearly 90% of all ment of diabetes in these patients. In the effective to screen such patients. Pregnant
pregnancies complicated by diabetes. absence of pregnancy, IFG and IGT are women who fulfill all of these criteria
Deterioration of glucose tolerance oc- not clinical entities in their own right but need not be screened for GDM.
curs normally during pregnancy, particu- rather risk factors for future diabetes as This low-risk group comprises
larly in the 3rd trimester. well as cardiovascular disease. They can women who
be observed as intermediate stages in any
Impaired glucose tolerance (IGT) of the disease processes listed in Table 1. ● are ⬍25 years of age
and impaired fasting glucose (IFG) IFG and IGT are associated with the met- ● are a normal body weight
The Expert Committee (1,2) recognized abolic syndrome, which includes obesity ● have no family history (i.e., first-degree
an intermediate group of subjects whose (especially abdominal or visceral obesity), relative) of diabetes
glucose levels, although not meeting cri- dyslipidemia of the high-triglyceride ● have no history of abnormal glucose
teria for diabetes, are nevertheless too and/or low-HDL type, and hypertension. metabolism
high to be considered normal. This group It is worth mentioning that medical nutri- ● have no history of poor obstetric out-
is defined as having fasting plasma glu- tion therapy aimed at producing 5–10% come
cose (FPG) levels ⱖ100 mg/dl (5.6 loss of body weight, exercise, and certain ● are not members of an ethnic/racial
mmol/l) but ⬍126 mg/dl (7.0 mmol/l) or pharmacological agents have been vari- group with a high prevalence of diabe-
2-h values in the oral glucose tolerance ably demonstrated to prevent or delay the tes (e.g., Hispanic American, Native
test (OGTT) of ⱖ140 mg/dl (7.8 mmol/l) development of diabetes in people with American, Asian American, African
but ⬍200 mg/dl (11.1 mmol/l). Thus, the IGT; the potential impact of such inter- American, Pacific Islander)
categories of FPG values are as follows: ventions to reduce cardiovascular risk has
not been examined to date. Risk assessment for GDM should be
● FPG ⬍100 mg/dl (5.6 mmol/l) ⫽ nor- Note that many individuals with IGT undertaken at the first prenatal visit.
mal fasting glucose; are euglycemic in their daily lives. Indi- Women with clinical characteristics con-
● FPG 100 –125 mg/dl (5.6 – 6.9 mmol/ sistent with a high risk of GDM (marked
viduals with IFG or IGT may have normal
l) ⫽ IFG (impaired fasting glucose); or near normal glycated hemoglobin lev- obesity, personal history of GDM, glyco-
● FPG ⱖ126 mg/dl (7.0 mmol/l) ⫽ pro- els. Individuals with IGT often manifest suria, or a strong family history of diabe-
visional diagnosis of diabetes (the diag- hyperglycemia only when challenged tes) should undergo glucose testing (see
nosis must be confirmed, as described with the oral glucose load used in the below) as soon as feasible. If they are
below). standardized OGTT. found not to have GDM at that initial
screening, they should be retested be-
The corresponding categories when the tween 24 and 28 weeks of gestation.
OGTT is used are the following: DIAGNOSTIC CRITERIA FOR Women of average risk should have test-
DIABETES MELLITUS — The cri- ing undertaken at 24 –28 weeks of
● 2-h postload glucose ⬍140 mg/dl (7.8 teria for the diagnosis of diabetes are gestation.
mmol/l) ⫽ normal glucose tolerance; shown in Table 2. Three ways to diagnose A fasting plasma glucose level ⬎126
● 2-h postload glucose 140 –199 mg/dl diabetes are possible, and each, in the ab- mg/dl (7.0 mmol/l) or a casual plasma
(7.8 –11.1 mmol/l) ⫽ IGT (impaired sence of unequivocal hyperglycemia, glucose ⬎200 mg/dl (11.1 mmol/l) meets
glucose tolerance); must be confirmed, on a subsequent day, the threshold for the diagnosis of diabe-
● 2-h postload glucose ⱖ200 mg/dl (11.1 by any one of the three methods given in tes. In the absence of unequivocal hyper-
mmol/l) ⫽ provisional diagnosis of di- Table 2. The use of the hemoglobin A1c glycemia, the diagnosis must be

S46 DIABETES CARE, VOLUME 30, SUPPLEMENT 1, JANUARY 2007


Position Statement

Table 3—Diagnosis of GDM with a 100-g or evaluation for GDM in women with aver- Mahan (4) modified by Carpenter and
75-g glucose load age or high-risk characteristics should fol- Coustan (3) and are shown in the top of
low one of two approaches. Table 3. Alternatively, the diagnosis can
mg/dl mmol/l One-step approach. Perform a diagnos- be made using a 75-g glucose load and the
tic OGTT without prior plasma or serum glucose threshold values listed for fasting,
100-g glucose load glucose screening. The one-step approach 1 h, and 2 h (Table 2, bottom); however,
Fasting 95 5.3 may be cost-effective in high-risk patients this test is not as well validated as the
1-h 180 10.0 or populations (e.g., some Native- 100-g OGTT.
2-h 155 8.6 American groups).
3-h 140 7.8 Two-step approach. Perform an initial
75-g glucose load screening by measuring the plasma or se- References
Fasting 95 5.3 1. The Expert Committee on the Diagnosis
rum glucose concentration 1 h after a and Classification of Diabetes Mellitus:
1-h 180 10.0 50-g oral glucose load (glucose challenge Report of the Expert Committee on the
2-h 155 8.6 test [GCT]) and perform a diagnostic Diagnosis and Classification of Diabetes
Two or more of the venous plasma concentrations OGTT on that subset of women exceeding Mellitus. Diabetes Care 20:1183–1197,
must be met or exceeded for a positive diagnosis. the glucose threshold value on the GCT. 1997
The test should be done in the morning after an
overnight fast of between 8 and 14 h and after at least
When the two-step approach is used, a 2. The Expert Committee on the Diagnosis
3 days of unrestricted diet (ⱖ150 g carbohydrate per glucose threshold value ⬎140 mg/dl (7.8 and Classification of Diabetes Mellitus:
day) and unlimited physical activity. The subject mmol/l) identifies ⬃80% of women with Follow-up report on the diagnosis of dia-
should remain seated and should not smoke GDM, and the yield is further increased to betes mellitus. Diabetes Care 26:3160 –
3167, 2003
throughout the test. 90% by using a cutoff of ⬎130 mg/dl (7.2
3. Carpenter MW, Coustan DR: Criteria for
mmol/l). screening tests for gestational diabetes.
confirmed on a subsequent day. Confir- With either approach, the diagnosis Am J Obstet Gynecol 144:768 –773, 1982
mation of the diagnosis precludes the of GDM is based on an OGTT. Diagnostic 4. O’Sullivan JB, Mahan CM: Criteria for the
need for any glucose challenge. In the ab- criteria for the 100-g OGTT are derived oral glucose tolerance test in pregnancy.
sence of this degree of hyperglycemia, from the original work of O’Sullivan and Diabetes 13:278, 1964

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