Diabetes mellitus is a group of metabolic disorders characterized by hyperglycemia, resulting from defects in insulin secretion, insulin action, or both. This chronic hyperglycemia leads to long-term damage, dysfunction, and failure of various organs, particularly the eyes, kidneys, nerves, heart, and blood vessels. Understanding the diagnosis and classification of diabetes is crucial for effective diabetes care.
Several pathogenic processes contribute to the development of diabetes. These range from autoimmune destruction of pancreatic β-cells, leading to insulin deficiency, to conditions causing resistance to insulin action. The fundamental issue in diabetes is deficient insulin action on target tissues, stemming from inadequate insulin secretion and/or reduced tissue responsiveness to insulin. Often, both impaired insulin secretion and defects in insulin action coexist, making it challenging to pinpoint the primary cause of hyperglycemia.
Symptoms of pronounced hyperglycemia include increased urination (polyuria), excessive thirst (polydipsia), unexplained weight loss, sometimes increased appetite (polyphagia), and blurred vision. Chronic hyperglycemia can also impair growth and increase susceptibility to infections. Acute, life-threatening complications of uncontrolled diabetes are hyperglycemia with ketoacidosis or the nonketotic hyperosmolar syndrome.
Long-term complications are significant and include retinopathy with potential vision loss, nephropathy leading to kidney failure, peripheral neuropathy with risks of foot ulcers, amputations, and Charcot joints, and autonomic neuropathy causing gastrointestinal, genitourinary, cardiovascular issues, and sexual dysfunction. Individuals with diabetes also have a higher risk of atherosclerotic cardiovascular, peripheral arterial, and cerebrovascular diseases. Hypertension and lipoprotein metabolism abnormalities are frequently observed in diabetic patients.
Most diabetes cases fall into two main categories: type 1 and type 2. Type 1 diabetes is characterized by an absolute deficiency of insulin secretion, often due to autoimmune destruction of pancreatic islet β-cells. Type 2 diabetes, the more prevalent form, involves a combination of insulin resistance and an insufficient compensatory insulin secretion. In type 2 diabetes, hyperglycemia may develop gradually over time without noticeable clinical symptoms initially, but can still cause pathological changes. During this asymptomatic period, abnormal carbohydrate metabolism can be detected through plasma glucose measurements in the fasting state or after an oral glucose load.
The degree of hyperglycemia can vary over time depending on the progression of the underlying disease and its management, as illustrated in disorders of glycemia: etiologic types and stages.
Classification of Diabetes Mellitus and Other Categories of Glucose Regulation
Assigning a specific type of diabetes can be complex and depends on the clinical context at diagnosis. Many individuals do not fit neatly into a single classification. For instance, gestational diabetes mellitus (GDM) may transition into type 2 diabetes after pregnancy. Similarly, drug-induced diabetes, such as from steroids, might resolve upon discontinuation but diabetes can reappear later due to other causes like pancreatitis. Therefore, understanding the pathogenesis of hyperglycemia is more crucial for effective treatment than simply labeling the diabetes type.
Type 1 Diabetes: β-Cell Destruction and Insulin Deficiency
Type 1 diabetes is characterized by the destruction of pancreatic β-cells, typically leading to absolute insulin deficiency. It accounts for 5–10% of diabetes cases and was previously known as insulin-dependent diabetes or juvenile-onset diabetes.
Immune-Mediated Diabetes
This subtype is caused by autoimmune destruction of β-cells. Markers of this autoimmune process include islet cell autoantibodies, insulin autoantibodies, GAD (GAD65) autoantibodies, and autoantibodies to tyrosine phosphatases IA-2 and IA-2β. One or more of these autoantibodies are present in 85–90% of individuals at initial diagnosis of fasting hyperglycemia. Genetic factors, particularly HLA associations with DQA, DQB, and DRB genes, play a significant role. These HLA-DR/DQ alleles can either increase or decrease susceptibility to the disease.
The rate of β-cell destruction varies, being rapid in children and slower in adults. Some patients, particularly children and adolescents, may present with diabetic ketoacidosis as the first symptom. Others may initially have mild fasting hyperglycemia that can quickly worsen to severe hyperglycemia and/or ketoacidosis during illness or stress. Adults may retain enough residual β-cell function to prevent ketoacidosis for years but eventually become insulin-dependent and at risk for ketoacidosis. At this advanced stage, insulin secretion is minimal or absent, reflected in low or undetectable plasma C-peptide levels. Immune-mediated diabetes is most common in childhood and adolescence but can occur at any age.
Genetic predisposition and environmental factors, still not fully understood, contribute to autoimmune β-cell destruction. While patients are usually not obese at diagnosis, obesity does not rule out this diagnosis. These individuals are also more susceptible to other autoimmune disorders like Graves’ disease, Hashimoto’s thyroiditis, Addison’s disease, and celiac disease.
Idiopathic Diabetes
Some cases of type 1 diabetes lack known causes (idiopathic). These patients have permanent insulinopenia and are prone to ketoacidosis but lack evidence of autoimmunity. This form is rare, predominantly affecting individuals of African or Asian descent. Episodic ketoacidosis and varying degrees of insulin deficiency characterize this diabetes type. It shows strong hereditary patterns but lacks immunological markers for β-cell autoimmunity and HLA associations. Insulin therapy requirements may fluctuate in these patients.
Type 2 Diabetes: Insulin Resistance and Relative Insulin Deficiency
Type 2 diabetes represents the vast majority of diabetes cases (∼90–95%). It is characterized by insulin resistance combined with relative insulin deficiency. Patients with type 2 diabetes may not require insulin for survival, especially initially, and often throughout life. Multiple factors likely contribute to this form of diabetes, but autoimmune β-cell destruction and other specific causes of diabetes are absent.
Obesity is a major risk factor for type 2 diabetes, causing insulin resistance. Even non-obese individuals might have increased abdominal fat, contributing to insulin resistance. Spontaneous ketoacidosis is rare in type 2 diabetes, typically occurring under stress from illness like infections. Type 2 diabetes often remains undiagnosed for years due to the gradual development of hyperglycemia and initially mild symptoms. Despite this, patients are at increased risk of macrovascular and microvascular complications. While insulin levels may appear normal or elevated, they are insufficient to compensate for insulin resistance, indicating defective β-cell function. Insulin resistance can improve with weight loss or medication, but rarely returns to normal. The risk of type 2 diabetes increases with age, obesity, physical inactivity, prior GDM, hypertension, dyslipidemia, and varies among racial/ethnic groups. Genetic predisposition is strong, more so than in autoimmune type 1 diabetes, but the genetic basis is complex and not fully defined.
Other Specific Types of Diabetes
Beyond type 1 and type 2, several other specific types of diabetes exist, often due to identifiable causes.
Genetic Defects of β-Cell Function
Several monogenic defects in β-cell function cause diabetes, often with onset before age 25. These are known as maturity-onset diabetes of the young (MODY), characterized by impaired insulin secretion with minimal insulin action defects, and inherited in an autosomal dominant manner. Six genetic loci on different chromosomes are implicated. The most common form involves mutations in hepatocyte nuclear factor (HNF)-1α on chromosome 12. Another form is due to mutations in the glucokinase gene on chromosome 7p, resulting in defective glucokinase. Glucokinase acts as the “glucose sensor” in β-cells, converting glucose to glucose-6-phosphate to stimulate insulin secretion. Defects in glucokinase require higher glucose levels to trigger normal insulin secretion. Less common MODY forms involve mutations in other transcription factors like HNF-4α, HNF-1β, insulin promoter factor (IPF)-1, and NeuroD1.
Mitochondrial DNA mutations, particularly at position 3,243 in the tRNA leucine gene, are also linked to diabetes and deafness. This mutation is also seen in MELAS syndrome but with different phenotypic expressions.
Genetic abnormalities affecting proinsulin conversion to insulin and mutant insulin molecules with impaired receptor binding are rare genetic causes of mild glucose intolerance, inherited in an autosomal dominant pattern.
Genetic Defects in Insulin Action
Rarely, diabetes results from genetically determined defects in insulin action. Mutations in the insulin receptor can cause a spectrum of metabolic abnormalities, from hyperinsulinemia and mild hyperglycemia to severe diabetes. Acanthosis nigricans may be present. Women may exhibit virilization and polycystic ovaries, previously termed type A insulin resistance. Leprechaunism and Rabson-Mendenhall syndrome are severe pediatric syndromes with insulin receptor gene mutations, extreme insulin resistance, and characteristic features, often with poor prognosis.
Insulin-resistant lipoatrophic diabetes, however, does not show insulin receptor defects, suggesting postreceptor signal transduction pathway lesions are responsible.
Diseases of the Exocrine Pancreas
Pancreatic damage from various conditions can lead to diabetes. These include pancreatitis, trauma, infection, pancreatectomy, and pancreatic cancer. Except for cancer, extensive pancreatic damage is usually needed to cause diabetes. However, even small pancreatic adenocarcinomas have been linked to diabetes, suggesting mechanisms beyond simple β-cell mass reduction. Cystic fibrosis and hemochromatosis, if severe enough, can also impair β-cell function and insulin secretion. Fibrocalculous pancreatopathy, characterized by abdominal pain, pancreatic calcifications, fibrosis, and ductal stones, can also lead to diabetes.
Endocrinopathies
Excess hormones that antagonize insulin action, such as growth hormone, cortisol, glucagon, and epinephrine, can cause diabetes. Conditions like acromegaly, Cushing’s syndrome, glucagonoma, and pheochromocytoma can induce diabetes, typically in individuals with pre-existing insulin secretion defects. Hyperglycemia often resolves upon correcting the hormonal excess.
Somatostatinoma and aldosteronoma-induced hypokalemia can also cause diabetes, partly by inhibiting insulin secretion. Hyperglycemia usually resolves after tumor removal.
Drug- or Chemical-Induced Diabetes
Various drugs can impair insulin secretion or action. While not always causing diabetes alone, they can trigger diabetes in susceptible individuals with insulin resistance. Toxins like Vacor and intravenous pentamidine can permanently destroy β-cells. Drugs like nicotinic acid and glucocorticoids impair insulin action. Alpha-interferon has been associated with diabetes and islet cell antibodies in some patients. Table 1 summarizes drug-, hormone-, and toxin-induced diabetes forms.
Table 1. Etiologic classification of diabetes mellitus
| 1. Type 1 diabetes (β-cell destruction, usually leading to absolute insulin deficiency) 1. Immune mediated 2. Idiopathic | 2. Type 2 diabetes (may range from predominantly insulin resistance with relative insulin deficiency to a predominantly secretory defect with insulin resistance) | 3. Other specific types 1. Genetic defects of β-cell function 1. Chromosome 12, HNF-1α (MODY3) 2. Chromosome 7, glucokinase (MODY2) 3. Chromosome 20, HNF-4α (MODY1) 4. Chromosome 13, insulin promoter factor-1 (IPF-1; MODY4) 5. Chromosome 17, HNF-1β (MODY5) 6. Chromosome 2, NeuroD1 (MODY6) 7. Mitochondrial DNA 8. Others 2. Genetic defects in insulin action 1. Type A insulin resistance 2. Leprechaunism 3. Rabson-Mendenhall syndrome 4. Lipoatrophic diabetes 5. Others 3. Diseases of the exocrine pancreas 1. Pancreatitis 2. Trauma/pancreatectomy 3. Neoplasia 4. Cystic fibrosis 5. Hemochromatosis 6. Fibrocalculous pancreatopathy 7. Others 4. Endocrinopathies 1. Acromegaly 2. Cushing’s syndrome 3. Glucagonoma 4. Pheochromocytoma 5. Hyperthyroidism 6. Somatostatinoma 7. Aldosteronoma 8. Others 5. Drug or chemical induced 1. Vacor 2. Pentamidine 3. Nicotinic acid 4. Glucocorticoids 5. Thyroid hormone 6. Diazoxide 7. β-adrenergic agonists 8. Thiazides 9. Dilantin 10. γ-Interferon 11. Others 6. Infections 1. Congenital rubella 2. Cytomegalovirus 3. Others 7. Uncommon forms of immune-mediated diabetes 1. “Stiff-man” syndrome 2. Anti-insulin receptor antibodies 3. Others 8. Other genetic syndromes sometimes associated with diabetes 1. Down syndrome 2. Klinefelter syndrome 3. Turner syndrome 4. Wolfram syndrome 5. Friedreich ataxia 6. Huntington chorea 7. Laurence-Moon-Biedl syndrome 8. Myotonic dystrophy 9. Porphyria 10. Prader-Willi syndrome 11. Others | 4. Gestational diabetes mellitus |
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Insulin treatment at any stage does not define diabetes type.
Infections
Certain viruses, such as congenital rubella, coxsackievirus B, cytomegalovirus, adenovirus, and mumps, have been linked to β-cell destruction and diabetes. Congenital rubella-associated diabetes often shares HLA and immune markers with type 1 diabetes.
Uncommon Forms of Immune-Mediated Diabetes
Stiff-man syndrome, an autoimmune CNS disorder, is associated with high GAD autoantibody titers, and about one-third of patients develop diabetes.
Anti-insulin receptor antibodies can cause diabetes by blocking insulin binding. Paradoxically, they can also act as insulin agonists, causing hypoglycemia. These antibodies are found in some patients with systemic lupus erythematosus and other autoimmune diseases, and are associated with acanthosis nigricans, previously termed type B insulin resistance.
Other Genetic Syndromes
Several genetic syndromes increase diabetes risk, including Down syndrome, Klinefelter syndrome, and Turner syndrome. Wolfram syndrome, an autosomal recessive disorder, includes insulin-deficient diabetes, diabetes insipidus, hypogonadism, optic atrophy, and neural deafness, with β-cell absence at autopsy. Table 1 lists other associated syndromes.
Gestational Diabetes Mellitus (GDM)
GDM is defined as glucose intolerance first recognized during pregnancy. It usually resolves after delivery, but the definition applies regardless of persistence post-pregnancy and includes cases where glucose intolerance may have pre-existed or started with pregnancy. This definition facilitates consistent detection and classification, but its limitations have long been acknowledged. The rising prevalence of obesity and type 2 diabetes in women of childbearing age has increased the number of pregnant women with undiagnosed type 2 diabetes.
In 2008–2009, the International Association of Diabetes and Pregnancy Study Groups (IADPSG), with representatives from organizations like the American Diabetes Association (ADA), recommended that women with diabetes diagnosed at their initial prenatal visit using standard criteria be classified as having overt diabetes, not GDM. GDM complicates approximately 7% of pregnancies, with over 200,000 cases annually.
Table 3. Criteria for the diagnosis of diabetes
| 1. A1C ≥6.5%. The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay.* |
|---|
| OR |
| 2. FPG ≥126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h.* |
| OR |
| 3. 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 a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.* |
| OR |
| 4. In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥200 mg/dl (11.1 mmol/l). |
*In the absence of unequivocal hyperglycemia, criteria 1–3 should be confirmed by repeat testing.
Categories of Increased Risk for Diabetes
In 1997 and 2003, expert committees recognized an intermediate group with glucose levels higher than normal but not meeting diabetes criteria. This group includes individuals with impaired fasting glucose (IFG) [FPG 100–125 mg/dl (5.6–6.9 mmol/l)] or impaired glucose tolerance (IGT) [2-h OGTT values 140–199 mg/dl (7.8–11.0 mmol/l)].
IFG and/or IGT are termed pre-diabetes, indicating a high risk of future diabetes and cardiovascular disease, not clinical entities themselves. They represent intermediate stages in various diabetes etiologies (Table 1). IFG and IGT are associated with obesity (especially abdominal), dyslipidemia, and hypertension. Lifestyle interventions (increased physical activity, 5–10% weight loss) and certain medications can prevent or delay diabetes in IGT individuals, though impacts on mortality or cardiovascular disease are not yet demonstrated. The ADA in 2003 lowered the IFG threshold from 110 mg/dl to 100 mg/dl, aligning IFG prevalence with IGT, but the WHO and others did not adopt this change.
A1C is increasingly used to identify individuals at risk for diabetes. While the International Expert Committee in 2009 acknowledged the continuous risk of diabetes across glycemic measures, it did not formally define an intermediate A1C category. However, it noted increased risk at A1C levels above the lab “normal” range but below the diagnostic cut point for diabetes (6.0–6.4%). Incidence rates at A1C 5.5–6.0% are significantly higher than in the general US population. NHANES data suggest A1C 5.5–6.0% best identifies IFG/IGT. Diabetes Prevention Program (DPP) data showed preventive interventions effective even below 5.9% A1C. Thus, A1C 5.5–6% is a reasonable range to initiate preventive measures.
Defining a lower limit for intermediate A1C is somewhat arbitrary, as diabetes risk is a continuum. The A1C cut point should balance identifying those who will develop diabetes against over-identification and resource allocation.
Compared to FPG 100 mg/dl, A1C 5.7% is less sensitive but more specific and has higher positive predictive value for diabetes risk. A large study showed 5.7% A1C having 66% sensitivity and 88% specificity for 6-year diabetes incidence. NHANES data indicate A1C 5.7% has modest sensitivity but high specificity for IFG/IGT. Other analyses suggest A1C 5.7% risk is similar to high-risk DPP participants. Therefore, A1C 5.7–6.4% can identify individuals at high risk, termed pre-diabetes.
Individuals with A1C 5.7–6.4% should be informed of increased diabetes and cardiovascular disease risk and advised on lifestyle strategies like weight loss and exercise. Risk increases disproportionately with A1C. Interventions and follow-up should be more intensive for those above 6.0% A1C, considered very high risk. However, risk is continuous, and individuals below 5.7% A1C may still be at risk depending on other factors.
Table 2 summarizes increased risk categories. Evaluation should include global risk factor assessment for diabetes and cardiovascular disease, considering comorbidities, life expectancy, lifestyle change capacity, and overall health goals.
Table 2. Categories of increased risk for diabetes*
| FPG 100 mg/dl (5.6 mmol/l) to 125 mg/dl (6.9 mmol/l) [IFG] |
|---|
| 2-h PG in the 75-g OGTT 140 mg/dl (7.8 mmol/l) to 199 mg/dl (11.0 mmol/l) [IGT] |
| A1C 5.7–6.4% |
*For all three tests, risk is continuous, extending below the lower limit of the range and becoming disproportionately greater at higher ends of the range.
Diagnostic Criteria for Diabetes Mellitus
Diabetes diagnosis has long relied on glucose criteria, FPG or 75-g OGTT. In 1997, diagnostic criteria were revised based on the association between FPG levels and retinopathy. Studies showed glycemic levels below which retinopathy prevalence was low and above which it increased linearly. Retinopathy onset deciles were consistent across glucose measures and populations, informing the new FPG diagnostic cut point of ≥126 mg/dl (7.0 mmol/l) and confirming the 2-h PG value of ≥200 mg/dl (11.1 mmol/l).
A1C, reflecting average glucose over 2–3 months, is crucial in diabetes management, correlating with microvascular and macrovascular complications and used to assess glycemic control. Past committees did not recommend A1C for diagnosis due to assay standardization issues. However, A1C assays are now highly standardized. An International Expert Committee in 2009 recommended A1C for diabetes diagnosis at a threshold of ≥6.5%, affirmed by the ADA. This 6.5% A1C cut point, like FPG and 2-h PG thresholds, is associated with an inflection point for retinopathy prevalence. Diagnostic A1C tests should be NGSP certified and standardized to the Diabetes Control and Complications Trial reference assay. Point-of-care A1C assays are currently not accurate enough for diagnosis.
Using A1C offers advantages over FPG, including convenience (no fasting), greater preanalytical stability, and less variability during stress or illness. However, A1C is more costly, less available in developing regions, and has incomplete correlation with average glucose in some individuals. A1C can be misleading in certain anemias and hemoglobinopathies, which may have ethnic/geographic distributions. For hemoglobinopathies without abnormal red cell turnover, use A1C assays without hemoglobin interference (list at www.ngsp.org/prog/index3.html). For conditions with abnormal red cell turnover, glucose criteria must be used exclusively.
Established glucose criteria (FPG, 2-h PG) remain valid. Random plasma glucose ≥200 mg/dl (11.1 mmol/l) in patients with severe hyperglycemia symptoms or hyperglycemic crisis also diagnoses diabetes. While A1C might be measured in such cases, it may not be elevated in rapidly evolving diabetes like type 1 in children.
There is not full concordance between FPG, 2-h PG, and A1C tests. NHANES data indicate A1C ≥6.5% identifies fewer undiagnosed diabetes cases than FPG ≥126 mg/dl. However, A1C’s greater practicality might increase overall diagnoses due to wider application.
Further research is needed to understand discrepancies between different tests. Discordance might arise from measurement variability, time changes, or tests measuring different physiological processes. Elevated A1C with “nondiabetic” FPG might indicate greater postprandial glucose or glycation rates. High FPG with A1C below the cut point might suggest augmented hepatic glucose production or reduced glycation rates.
Diagnostic test results should be repeated to rule out lab error, unless clinically evident. Repeating the same test is preferable for confirmation. For discordant results from different tests, repeat the test above the diagnostic threshold; diagnosis is based on the confirmed test. If A1C is diagnostic (two results ≥6.5%) but FPG is not, diabetes is diagnosed.
If a repeated test falls below the diagnostic cut point, close monitoring and repeat testing in 3–6 months may be appropriate due to potential test variability.
The choice of diagnostic test is at the healthcare professional’s discretion, considering test availability and practicality. Crucially, diabetes testing should be performed when indicated. Under-testing and inadequate counseling for diabetes and cardiovascular risk factors remain concerns. Table 3 summarizes current diagnostic criteria.
Diagnosis of GDM
GDM diagnostic criteria at the time of this publication are those of Carpenter and Coustan, with ADA supporting both Carpenter/Coustan criteria and a 75-g 2-h OGTT.
Testing for Gestational Diabetes
Universal GDM screening was previously recommended but may not be cost-effective for low-risk women. Low-risk criteria include age <25, normal weight, no family history of diabetes, no history of abnormal glucose metabolism or poor obstetric outcomes, and not belonging to a high-risk ethnic/racial group.
Risk assessment for GDM should occur at the first prenatal visit. High-risk women (marked obesity, prior GDM, glycosuria, strong family history) should be tested immediately. If initial screening is negative, retest at 24–28 weeks. Average-risk women should be tested at 24–28 weeks.
FPG >126 mg/dl (7.0 mmol/l) or random plasma glucose >200 mg/dl (11.1 mmol/l) meets diabetes diagnostic threshold. Confirmation is needed on a subsequent day unless unequivocal hyperglycemia is present. For women not meeting these criteria, GDM evaluation follows one of two approaches.
One-Step Approach
Diagnostic OGTT without prior screening, potentially cost-effective in high-risk populations.
Two-Step Approach
Initial screening with 50-g glucose challenge test (GCT). Diagnostic OGTT for women exceeding the GCT glucose threshold. A threshold >140 mg/dl (7.8 mmol/l) identifies ~80% of GDM cases, increased to 90% with a cutoff of >130 mg/dl (7.2 mmol/l).
Both approaches use OGTT for GDM diagnosis. Diagnostic criteria for 100-g OGTT (Carpenter and Coustan modification of O’Sullivan and Mahan) and 75-g glucose load are in Table 4.
Table 4. Diagnosis of GDM with a 100-g or 75-g glucose load
| mg/dl | mmol/l | |
|---|---|---|
| 100-g glucose load | ||
| Fasting | 95 | 5.3 |
| 1-h | 180 | 10.0 |
| 2-h | 155 | 8.6 |
| 3-h | 140 | 7.8 |
| 75-g glucose load | ||
| Fasting | 95 | 5.3 |
| 1-h | 180 | 10.0 |
| 2-h | 155 | 8.6 |
Two or more venous plasma concentrations must be met or exceeded for positive diagnosis. Test should be done in the morning after 8–14 h overnight fast, following ≥150 g carbohydrate/day diet for at least 3 days and unlimited physical activity. Subject should remain seated and not smoke during the test.
The Hyperglycemia and Adverse Pregnancy Outcomes (HAPO) study, a large multinational study, showed a continuous increase in adverse pregnancy outcomes with increasing maternal glycemia at 24–28 weeks, even within previously considered normal ranges. The IADPSG recommended 75-g OGTT for all women at 24–28 weeks without prior diabetes, with diagnostic cut points for fasting, 1-h, and 2-h plasma glucose conveying an odds ratio for adverse outcomes of at least 1.75 compared to mean glucose levels in the HAPO study.
At the time of this update, ADA is considering adopting IADPSG diagnostic criteria, which will significantly increase GDM prevalence, but evidence suggests treating even mild GDM reduces morbidity for both mother and baby.
Acknowledgments
The American Diabetes Association acknowledges the contributions of the writing group members for updating sections on diagnosis and risk categories.
