Diabetes mellitus is a cluster of metabolic diseases distinguished by persistent hyperglycemia. This condition arises from deficiencies in insulin secretion, insulin action, or both. The enduring high blood sugar levels characteristic of diabetes are linked to long-term damage, dysfunction, and eventual failure of various organs, notably the eyes, kidneys, nerves, heart, and blood vessels. Understanding the diagnosis and classification of diabetes is crucial for effective diabetes care.
The development of diabetes involves multiple pathogenic processes. These range from the autoimmune destruction of pancreatic β-cells, leading to insulin deficiency, to abnormalities causing resistance to insulin’s actions. The core issue in diabetes-related metabolic disturbances of carbohydrates, fats, and proteins is the impaired action of insulin on target tissues. This impaired action results from either insufficient insulin secretion or reduced tissue responsiveness to insulin at different points in the complex hormone action pathways. Frequently, both secretion impairment and action defects coexist in a patient, making it difficult to pinpoint the primary cause of hyperglycemia.
Key symptoms of pronounced hyperglycemia include excessive urination (polyuria), increased thirst (polydipsia), unexplained weight loss, sometimes accompanied by increased hunger (polyphagia), and blurred vision. Chronic hyperglycemia can also lead to impaired growth and increased vulnerability to certain infections. Acute, life-threatening complications of uncontrolled diabetes are hyperglycemia with ketoacidosis or the nonketotic hyperosmolar syndrome.
Long-term complications of diabetes encompass 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, and cardiovascular problems, as well as sexual dysfunction. Individuals with diabetes face a higher risk of atherosclerotic cardiovascular, peripheral arterial, and cerebrovascular diseases. Hypertension and abnormal lipoprotein metabolism are commonly observed in diabetic individuals.
Most diabetes cases fall into two main categories: type 1 and type 2 diabetes. Type 1 diabetes is characterized by an absolute deficiency in insulin secretion. Individuals at higher risk can often be identified through serological evidence of autoimmune processes in the pancreatic islets and genetic markers. Type 2 diabetes, the more prevalent form, involves a combination of insulin resistance and an inadequate compensatory insulin secretion. In type 2 diabetes, hyperglycemia may be present for a significant period before diagnosis, often without noticeable clinical symptoms. During this asymptomatic phase, carbohydrate metabolism abnormalities can be detected by measuring plasma glucose levels in a fasting state or after an oral glucose load.
The severity of hyperglycemia in diabetes can fluctuate over time, influenced by the progression of the underlying disease and treatment effectiveness, as illustrated in Figure 1. A disease process might be present but not advanced enough to cause hyperglycemia. The same process can lead to impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) without meeting full diabetes diagnostic criteria. Some individuals with diabetes can manage their glycemic levels through lifestyle modifications like weight reduction and exercise, or with oral glucose-lowering medications, negating the need for insulin. Others may require exogenous insulin to achieve adequate glycemic control despite some residual insulin secretion. However, those with extensive β-cell destruction and no residual insulin secretion depend on insulin for survival. The degree of metabolic abnormality can improve, worsen, or remain stable. Thus, hyperglycemia levels reflect the severity of the metabolic process and its management rather than the fundamental nature of the disease itself.
Figure 1.
Disorders of glycemia: etiologic types and stages. *Even after presenting in ketoacidosis, these patients can briefly return to normoglycemia without requiring continuous therapy (i.e., “honeymoon” remission); **in rare instances, patients in these categories (e.g., Vacor toxicity, type 1 diabetes presenting in pregnancy) may require insulin for survival.
Classification of Diabetes Mellitus and Other Categories of Glucose Regulation
Assigning a specific type of diabetes can be context-dependent at diagnosis, and many cases do not neatly fit into a single category. For instance, gestational diabetes mellitus (GDM) may evolve into persistent hyperglycemia post-delivery, leading to a diagnosis of type 2 diabetes. Conversely, diabetes induced by high doses of exogenous steroids might resolve upon discontinuation, only to reappear years later after pancreatitis episodes. Similarly, thiazide-induced diabetes may develop years after treatment initiation, likely indicating underlying type 2 diabetes exacerbated by the drug. Therefore, for both clinicians and patients, understanding the pathogenesis of hyperglycemia and effective treatment strategies is more critical 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 is further divided into immune-mediated and idiopathic forms.
Immune-Mediated Diabetes
This form, accounting for 5–10% of diabetes cases, was formerly known as insulin-dependent diabetes, type 1 diabetes, or juvenile-onset diabetes. It results from autoimmune destruction of pancreatic 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 detection of fasting hyperglycemia. The disease also shows strong HLA associations, particularly with DQA and DQB genes, and is influenced by DRB genes. These HLA-DR/DQ alleles can be either predisposing or protective.
The rate of β-cell destruction varies significantly, being rapid in infants and children and slower in adults. Some patients, especially children and adolescents, may present with ketoacidosis as the first sign. Others may have mild fasting hyperglycemia that can quickly escalate to severe hyperglycemia and/or ketoacidosis under stress or infection. Adults may retain enough residual β-cell function to prevent ketoacidosis for years but eventually become insulin-dependent and at risk for ketoacidosis. In later stages, 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.
The autoimmune destruction is influenced by multiple genetic predispositions and environmental factors that are still not fully understood. Although patients are typically not obese at diagnosis, obesity does not rule out this diagnosis. These patients are also susceptible to other autoimmune disorders like Graves’ disease, Hashimoto’s thyroiditis, Addison’s disease, vitiligo, celiac sprue, autoimmune hepatitis, myasthenia gravis, and pernicious anemia.
Idiopathic Diabetes
Some type 1 diabetes cases lack known causes (idiopathic). These patients experience permanent insulinopenia and are prone to ketoacidosis but show no evidence of autoimmunity. This category is a minority of type 1 diabetes cases, predominantly affecting individuals of African or Asian descent. Idiopathic diabetes is characterized by episodic ketoacidosis with varying degrees of insulin deficiency between episodes. It is strongly inherited, lacks immunological markers for β-cell autoimmunity, and is not HLA-associated. The need for insulin replacement therapy in these patients can be intermittent.
Type 2 Diabetes: Insulin Resistance and Relative Insulin Deficiency
Type 2 diabetes, accounting for 90–95% of diabetes cases, was previously termed non–insulin-dependent diabetes or adult-onset diabetes. It involves insulin resistance combined with a relative insulin deficiency. These individuals typically do not require insulin for survival, at least initially. The exact causes are diverse and not fully understood, but autoimmune β-cell destruction is not involved, and other specific diabetes causes are absent.
Obesity is a major contributing factor, causing insulin resistance. Even non-obese patients may have increased abdominal fat, which is linked to insulin resistance. Ketoacidosis is rare in type 2 diabetes, usually occurring under severe stress like infection. Type 2 diabetes often remains undiagnosed for years due to gradual hyperglycemia development, which may not initially cause noticeable symptoms. Despite this, patients are at increased risk of macrovascular and microvascular complications. While insulin levels might appear normal or elevated, they are insufficient to compensate for insulin resistance. Insulin resistance can improve with weight loss and medication but rarely returns to normal. Risk factors include age, obesity, physical inactivity, prior GDM, hypertension, dyslipidemia, and certain racial/ethnic backgrounds. Genetic predisposition is strong, more so than in autoimmune type 1 diabetes, but the genetics are complex and not fully defined.
Other Specific Types of Diabetes
Beyond type 1 and type 2, several other specific types of diabetes exist, each with distinct etiologies.
Genetic Defects of β-cell Function
Several diabetes forms stem from monogenetic defects in β-cell function, often manifesting as hyperglycemia 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 are inherited in an autosomal dominant pattern. Mutations at six genetic loci have been identified. The most common involves mutations in the hepatic transcription factor HNF-1α on chromosome 12. Another form is due to mutations in the glucokinase gene on chromosome 7p, leading to a defective glucokinase molecule. Glucokinase acts as the “glucose sensor” in β-cells. Defects require higher glucose levels to trigger normal insulin secretion. Less common forms involve mutations in other transcription factors like HNF-4α, HNF-1β, IPF-1, and NeuroD1.
Mitochondrial DNA point mutations are also linked to diabetes and deafness, with the most common mutation at position 3,243 in the tRNA leucine gene. Genetic abnormalities preventing proinsulin conversion to insulin and mutant insulin molecules with impaired receptor binding also exist, both inherited in an autosomal dominant pattern and causing mild glucose intolerance.
Genetic Defects in Insulin Action
Unusual diabetes causes involve genetically determined abnormalities in insulin action, such as mutations in the insulin receptor. These can range from hyperinsulinemia with mild hyperglycemia to severe diabetes. Some patients may exhibit acanthosis nigricans, and women may experience virilization and polycystic ovaries. Syndromes like Leprechaunism and Rabson-Mendenhall syndrome, both pediatric conditions, involve insulin receptor gene mutations leading to extreme insulin resistance. Leprechaunism is typically fatal in infancy, while Rabson-Mendenhall syndrome includes teeth and nail abnormalities and pineal gland hyperplasia.
Insulin-resistant lipoatrophic diabetes likely involves defects in postreceptor signal transduction pathways, as insulin receptor abnormalities are not evident.
Diseases of the Exocrine Pancreas
Conditions diffusely injuring the pancreas can cause diabetes, including pancreatitis, trauma, infection, pancreatectomy, and pancreatic carcinoma. Except for cancer-related cases, significant pancreatic damage is needed for diabetes to occur, suggesting mechanisms beyond β-cell mass reduction. Cystic fibrosis and hemochromatosis, if extensive, can also impair insulin secretion. Fibrocalculous pancreatopathy may present with abdominal pain, pancreatic calcifications, fibrosis, and calcium stones in exocrine ducts.
Endocrinopathies
Excess hormones like growth hormone, cortisol, glucagon, and epinephrine can antagonize insulin action, potentially causing diabetes in individuals with pre-existing insulin secretion defects. Conditions like acromegaly, Cushing’s syndrome, glucagonoma, and pheochromocytoma can induce diabetes, which typically resolves when hormone excess is corrected.
Somatostatinoma- and aldosteronoma-induced hypokalemia can also cause diabetes by inhibiting insulin secretion, generally resolving after tumor removal.
Drug- or Chemical-Induced Diabetes
Numerous drugs can impair insulin secretion and may precipitate diabetes in susceptible individuals. Toxins like Vacor and intravenous pentamidine can permanently destroy β-cells, though such reactions are rare. Drugs such as nicotinic acid and glucocorticoids can impair insulin action. α-interferon has been linked to diabetes with islet cell antibodies and severe insulin deficiency. Table 1 lists common 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 |
Etiologic classification of diabetes mellitus – Table 1
Insulin treatment at any stage does not itself classify the diabetes type.
Infections
Certain viruses can destroy β-cells. Congenital rubella is associated with diabetes, often showing HLA and immune markers of type 1 diabetes. Coxsackievirus B, cytomegalovirus, adenovirus, and mumps have also been implicated in certain diabetes cases.
Uncommon Forms of Immune-Mediated Diabetes
Conditions like stiff-man syndrome, an autoimmune CNS disorder with muscle stiffness and spasms, are linked to diabetes. Patients often have high GAD autoantibody titers, and about one-third develop diabetes. Anti-insulin receptor antibodies can cause diabetes by blocking insulin binding, or hypoglycemia by acting as insulin agonists. These antibodies are sometimes found in systemic lupus erythematosus and other autoimmune diseases and, like other extreme insulin resistance states, may present with acanthosis nigricans. This was previously termed type B insulin resistance.
Other Genetic Syndromes
Several genetic syndromes increase diabetes risk, including Down syndrome, Klinefelter syndrome, and Turner syndrome. Wolfram’s syndrome, an autosomal recessive disorder, features insulin-deficient diabetes with β-cell absence at autopsy, along with diabetes insipidus, hypogonadism, optic atrophy, and neural deafness. Table 1 lists additional syndromes.
Gestational Diabetes Mellitus (GDM)
GDM is defined as any degree of glucose intolerance first recognized during pregnancy. While most cases resolve after delivery, the definition applies regardless of persistence post-pregnancy and includes cases where glucose intolerance may have pre-dated pregnancy. This definition facilitates uniform detection and classification, though its limitations have long been acknowledged. The rising obesity and diabetes epidemic has increased type 2 diabetes among women of childbearing age, leading to more pregnant women with undiagnosed type 2 diabetes.
The International Association of Diabetes and Pregnancy Study Groups (IADPSG) recommends diagnosing overt diabetes, rather than GDM, in high-risk women found to have diabetes at their initial prenatal visit using standard criteria (Table 3). GDM complicates about 7% of pregnancies, with over 200,000 annual cases.
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). |
Criteria for the diagnosis of diabetes – Table 3
*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 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. They are not clinical entities themselves but risk factors and intermediate stages in various disease processes listed in Table 1. IFG and IGT are linked to obesity (especially abdominal), dyslipidemia, and hypertension. Lifestyle interventions and certain medications can prevent or delay diabetes in IGT individuals, though their impact on mortality or cardiovascular disease is not yet fully demonstrated. In 2003, the ADA lowered the IFG threshold to 100 mg/dl (5.6 mmol/l), but the WHO and other organizations did not adopt this change.
A1C is increasingly used to identify those at higher diabetes risk. While a 2009 International Expert Committee highlighted the continuous risk of diabetes across glycemic measures, they did not formally define an A1C-equivalent intermediate category. They noted increased risk at A1C levels above the lab “normal” range but below the diabetes cut point (6.0–6.4%). Incidence rates at A1C 6.0–6.4% are significantly higher than in the general US population. NHANES data suggests A1C 5.5–6.0% accurately identifies IFG or IGT. DPP data shows preventive interventions are effective both below and above A1C 5.9%. Thus, A1C 5.5–6% is a likely threshold for initiating preventive measures.
Defining a lower A1C limit for intermediate risk is somewhat arbitrary due to the continuous nature of diabetes risk. An appropriate A1C cut point balances false negative costs (missing those who will develop diabetes) against false positive costs (unnecessarily intervening on those who won’t).
Compared to the 100 mg/dl fasting glucose cut point, an A1C of 5.7% is less sensitive but more specific and has a higher positive predictive value for future diabetes. A study found 5.7% A1C has 66% sensitivity and 88% specificity for 6-year diabetes incidence. NHANES data indicates 5.7% A1C has modest sensitivity (39-45%) but high specificity (81-91%) for IFG or IGT. Other analyses suggest 5.7% A1C carries similar diabetes risk 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 risk-reducing strategies like weight loss and exercise. Risk increases disproportionately with rising A1C, making interventions and follow-up especially crucial above 6.0%. However, even below 5.7%, risk may still be present depending on A1C level and other risk factors.
Table 2 summarizes increased diabetes risk categories. Risk evaluation should include a global assessment for both 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% |
Categories of increased risk for diabetes – Table 2
*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 was minimal and above which it increased linearly. Retinopathy onset deciles were consistent across measures and populations, informing a new FPG 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 reflects average glucose over 2-3 months and is vital in diabetes management, correlating with microvascular and macrovascular complications. Previous committees hesitated to use A1C for diagnosis due to assay standardization issues. However, with standardized A1C assays, an International Expert Committee recommended A1C for diagnosis at a threshold of ≥6.5%, affirmed by the ADA. This 6.5% cut point aligns with retinopathy prevalence inflection points, similar to FPG and 2-h PG thresholds. Diagnostic A1C testing should use NGSP-certified methods standardized to the DCCT assay. Point-of-care A1C assays are currently insufficiently accurate for diagnosis.
Using a chronic marker like A1C offers advantages over acute markers like 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 or geographic patterns. For hemoglobinopathies without abnormal red cell turnover, interference-free A1C assays should be used. For conditions with abnormal red cell turnover, glucose criteria must be used exclusively.
Established glucose criteria (FPG and 2-h PG) remain valid. Random plasma glucose ≥200 mg/dl (11.1 mmol/l) in patients with severe hyperglycemia symptoms or hyperglycemic crisis can also diagnose diabetes. A1C is likely measured in such cases and usually exceeds the diagnostic cut point, although in rapidly developing diabetes, A1C may not be elevated despite frank diabetes.
Discordance between A1C, FPG, and 2-h PG tests exists due to measurement variability, time changes, or each test measuring different physiological processes. Elevated A1C with “nondiabetic” FPG may indicate higher postprandial glucose or glycation rates. High FPG with A1C below the cut point may suggest augmented hepatic glucose production or reduced glycation rates.
A diagnostic test result should be repeated to rule out errors, unless clinically clear. Repeating the same test is preferable. For discordant results between different tests, repeat the test above the diagnostic cut point for confirmation. If two different tests are both above thresholds, diabetes is confirmed.
If a repeated test falls below the diagnostic cut point, close patient monitoring and repeat testing in 3–6 months may be appropriate, as results are likely near threshold margins.
The choice of diagnostic test is at the health professional’s discretion, considering test availability and practicality. Ensuring diabetes testing when indicated is crucial, as evidence suggests under-testing and inadequate counseling for at-risk individuals. Table 3 summarizes current diagnostic criteria.
Diagnosis of GDM
GDM diagnostic criteria are based on Carpenter and Coustan, with ADA’s Fourth International Workshop-Conference on Gestational Diabetes Mellitus supporting Carpenter/Coustan criteria and the 75-g 2-h OGTT.
Testing for Gestational Diabetes
Universal GDM screening was previously recommended, but low-risk women may not require screening. Low-risk criteria include being under 25 years old, normal weight, no family diabetes history, no history of abnormal glucose metabolism or poor obstetric outcomes, and not belonging to a high-risk ethnic/racial group.
Risk assessment should occur at the first prenatal visit. High-risk women (marked obesity, prior GDM, glycosuria, strong family history) should be tested immediately. If not diagnosed initially, retesting is needed at 24–28 weeks. Average-risk women should be tested at 24–28 weeks.
FPG >126 mg/dl (7.0 mmol/l) or casual plasma glucose >200 mg/dl (11.1 mmol/l) diagnoses diabetes, requiring confirmation on a subsequent day. In the absence of these levels, GDM evaluation follows one of two approaches.
One-Step Approach
Perform a diagnostic OGTT without prior screening, potentially cost-effective in high-risk groups.
Two-Step Approach
Initial screening with a 50-g oral glucose load (GCT), measuring 1-h plasma glucose. Diagnostic OGTT follows for women exceeding a glucose threshold on GCT. A threshold of >140 mg/dl (7.8 mmol/l) identifies ~80% of GDM cases, increasing to 90% at >130 mg/dl (7.2 mmol/l).
GDM diagnosis relies on OGTT results. Table 4 shows diagnostic criteria for 100-g OGTT (Carpenter/Coustan modified from O’Sullivan and Mahan) and 75-g glucose load tests.
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 |
Diagnosis of GDM with a 100-g or 75-g glucose load – Table 4
Two or more venous plasma concentrations must be met or exceeded for diagnosis. Testing should be in the morning after an 8-14 hour overnight fast, following ≥150 g carbohydrate per day for at least 3 days, and normal physical activity. Subjects should remain seated and not smoke during testing.
The Hyperglycemia and Adverse Pregnancy Outcomes (HAPO) study showed continuous risk increase for adverse outcomes with maternal glycemia at 24–28 weeks, even within previously normal ranges. The IADPSG recommends a 75-g OGTT at 24–28 weeks for all women without prior diabetes, with diagnostic cut points for fasting, 1-h, and 2-h plasma glucose linked to an odds ratio of ≥1.75 for adverse outcomes compared to mean glucose levels in the HAPO study.
The ADA is considering adopting IADPSG diagnostic criteria, which will significantly increase GDM prevalence, but evidence suggests treating even mild GDM reduces morbidity for mothers and babies.
Acknowledgments
The American Diabetes Association acknowledges the volunteer writing group members for updating sections on diagnosis and risk categories: Silvio Inzucchi, MD; Richard Bergenstal, MD; Vivian Fonseca, MD; Edward Gregg, PhD; Beth Mayer-Davis, MSPH, PhD, RD; Geralyn Spollett, MSN, CDE, ANP; and Richard Wender, MD.
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