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Diabetes Mellitus, Diagnosis and Classification
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| Population | Occurrence of diabetes mellitus |
|---|---|
| DM (all ages) | In 2021, 529 million people had DM worldwide, with 96% of cases reported as T2DM (type 2 DM)13 Globally, the age-standardized prevalence of DM increased from 3.2% in 1990 to 6.1% in 202113 In the US (United States) in 2021, an estimated 38.4 million people (11.6% of the population) had DM and, of these people, 22.8% of adults were undiagnosed14 |
| DM (adults only) | In the US in 2021, an estimated 38.1 million adults aged ≥ 18 years (14.7% of all adults) had DM. The prevalence of DM significantly increased among adults aged ≥ 18 years from 10.3% during 2001 through 2004 to 13.2% during 2017 through 202014 In the US in 2021, an estimated 1.2 million new cases of DM were diagnosed among adults aged ≥ 18 years14 Among adults aged ≥ 18 years in the US, the age-adjusted incidence of diagnosed DM was similar in the years 2000 (6.2 per 1000 adults) and 2021 (5.8 per 1000 adults), and there has been a significant decreasing trend in incidence after 2008 (8.4 per 1000 adults) through 202114 In the US in 2021, 1.7 million adults aged ≥ 20 years reported having T1DM (type 1 DM), which is 5.7% of all US adults with diagnosed DM14 |
| Prediabetes (adults only) | In the US in 2021, an estimated 97.6 million people aged ≥ 18 years had prediabetes (38.0% of the adult US population). There have been no significant changes in age-adjusted prevalence of prediabetes from 2005 through 2008 to 2017 through 202014 |
| T1DM (youth only) | In the US in 2021, an estimated 352,000 youth < 20 years of age had diagnosed DM, 304,000 of whom had T1DM14 For youth < 20 years of age, the incidence of T1DM increased from 2002 through 2018. The incidence of T1DM was 22.2 per 100,000 youth (average of 2017/2018 incidence) compared with 19.5 per 100,000 youth (average 2002/20023 incidence), with an adjusted annual percentage change (95% confidence interval) of 2.02 (1.54, 2.49)15 |
| T2DM (youth only) | For youth < 20 years of age, the incidence of T2DM has increased over the period of 2002 through 2018. The incidence of T2DM was 17.9 per 100,000 youth (average 2017/2018 incidence) compared with 9.0 per 100,000 youth (average 2002/20023 incidence), with an adjusted annual percentage change (95% confidence interval) of 5.31 (4.46, 6.17)15 |
| 1. People who are overweight (BMI ≥ 25 kg/m2 or ≥ 23 kg/m2 for Asian individuals) and have one or more of the following risk factors: •First-degree relative with DM •High-risk race and ethnicity (eg, African, Latino, Native American, Asian, Pacific Islander) •History of cardiovascular disease •Hypertension •HDL cholesterol < 35 mg/dL and/or a triglyceride level > 250 mg/dL •Polycystic ovarian syndrome •Physical inactivity •Other conditions associated with insulin resistance (eg, acanthosis nigricans) |
| 2. People with exposure to high-risk medications (eg, glucocorticoids, statins, thiazide diuretics, second-generation antipsychotic medications) •In people who are prescribed second-generation antipsychotic medications (eg, olanzapine), consider screening for DM at baseline and 12 to 16 weeks after medication initiation, or sooner if clinically indicated, and annually |
| 3. People with a history of pancreatitis, cystic fibrosis, HIV, etc |
| 4. People with prediabetes should be tested yearly |
| 5. People who had gestational DM should have lifelong testing, at least every 3 years |
| 6. For all other asymptomatic adults, testing should begin at age 35 as the risk of T2DM increases with age |
| 7. If test results are normal, testing should be repeated at a minimum of 3-year intervals, with consideration of more frequent testing depending on initial results and risk status |
| 1. Consider screening youth after the onset of puberty or after 10 years of age, whichever occurs earlier, who are overweight (≥ 85th percentile) or obese (≥ 95th percentile) and who have one or more of the following risk factors: •Maternal history of DM or gestational DM during the child's gestation •Family history of T2DM in a first- or second-degree relative •High-risk race and ethnicity (eg, African, Latino, Native American, Asian, Pacific Islander) •Signs of insulin resistance or conditions associated with insulin resistance (eg, acanthosis nigricans, hypertension, dyslipidemia, polycystic ovarian syndrome, or small-for-gestational-age birth weight) |
| 2. If numerous risk factors exist, consider screening prior to age 10 |
| 3. If tests are normal, repeat testing at a minimum of 3-year intervals |
| HbA1c: 5.7% - 6.4% or Fasting plasma glucose: 100 - 125 mg/dL (impaired fasting glucose) or 2-h PG during a 75-g oral glucose tolerance test: 140 - 199 mg/dL (impaired glucose tolerance) |
| HbA1c ≥ 6.5% or Fasting plasma glucose ≥ 126 mg/dL or 2-h PG ≥ 200 mg/dL during a 75-g oral glucose tolerance test or A random* plasma glucose ≥ 200 mg/dL in a person with classic symptoms of hyperglycemia or hyperglycemic crisis |
| I. Type 1 diabetes A. Immune mediated B. Idiopathic |
| II. Type 2 diabetes |
| III. Other specific types A. Genetic defects of β-cell function I. Example: monogenic DM (formerly called maturity onset diabetes of the young [MODY]) B. Genetic defects in insulin action C. Diseases of the exocrine pancreas II. Examples: pancreatitis, pancreatectomy, neoplasia, cystic fibrosis, and hemochromatosis D. Endocrinopathies III. Example: Cushing syndrome E. Drug or chemical induced IV. Examples: glucocorticoids and immune checkpoint inhibitor therapy F. Infections G. Uncommon forms of immune-mediated DM V. Example: Stiff person syndrome H. Other genetic syndromes sometimes associated with DM |
| IV. Gestational diabetes mellitus |
| T1DM | T2DM | |
|---|---|---|
| Often asymptomatic | - | ++ |
| Polyuria and polydipsia | ++ | + |
| Polyphagia with weight loss | ++ | - |
| Weakness or fatigue | ++ | + |
| Recurrent blurred vision | + | ++ |
| Vulvovaginitis or pruritus | + | ++ |
| Age | Often < 25 years | Typically > 25 years |
| Diabetic ketoacidosis (DKA) frequency | Higher | Lower (but can develop) |
| Diabetes mellitus type | Historical findings that suggest the etiology |
|---|---|
| T1DM | •Disease onset is possible at any age, but often presents in those < 25 years of age ○Children with T1DM often present with classic symptoms of hyperglycemia; approximately 50% have DKA at the time of diagnosis1 ○Adults can present with classic symptoms of hyperglycemia, but not always; some adults have an indolent disease course (eg, latent autoimmune diabetes in adults)1 •Family history of T1DM •Personal or family history of other autoimmune disease (eg, Celiac disease, Graves disease, etc) |
| T2DM | •Typically presents in those > 25 years of age, but disease onset is possible at any age, particularly given the increased prevalence of obesity in youth and young adults •DKA is less common but can develop; when present, there is typically an identifiable cause such as infection, myocardial infarction, use of a sodium-glucose cotransporter 2 inhibitor, etc1 •Family history of T2DM is common |
| Other specific types | |
| •Monogenic DM | •Development of hyperglycemia at a young age (typically < 25 years old)1 •Family history of DM in successive generations (suggesting an autosomal dominant transmission) |
| ○HNF4A-MODY (MODY1) | ○May have large birth weight and transient neonatal hypoglycemia1 ○Sensitive to sulfonylureas ○Microvascular and macrovascular complication rates are similar to people with T1DM and T2DM |
| ○GCK-MODY (MODY2) | ○Microvascular complications are rare1 |
| ○HNF1A-MODY (MODY3) | ○Sensitive to sulfonylureas1 ○Microvascular and macrovascular complication rates are similar to people with T1DM and T2DM |
| •Pancreatitis | •Even a single episode of acute pancreatitis can result in DM1 •Concurrent pancreatic exocrine insufficiency •Can have higher than expected insulin requirements |
| •Pancreatic neoplasia | •New onset DM in an older adult who is losing weight suggests pancreatic neoplasia as a potential cause32 •May present with weakness, abdominal pain, and jaundice33 •Approximately 1% of people diagnosed with DM at age ≥ 50 years are diagnosed with pancreatic cancer within the first 3 years of meeting diagnostic criteria for DM34 |
| •Cystic fibrosis | •20% of adolescents and 40% to 50% of adults with cystic fibrosis have DM1 •The risk of cystic fibrosis-related DM increases with age, decreased lung function, and female sex |
| •Hemochromatosis | •Often diagnosed biochemically in an asymptomatic person •Chronic fatigue, malaise, arthralgias, and decreased libido can be present35 •Can present later in women because menstruation reduces iron accumulation |
| •Cushing syndrome | •Weight gain, characteristic changes in physical appearance due to hypercortisolism (see Table 9), decreased libido, menstrual cycle irregularities, depression, recurrent infections36 |
| •Immune checkpoint inhibitor therapy | •Typically due to programmed cell death‐1/programmed cell death ligand‐1 inhibitors and rarely after cytotoxic T lymphocyte‐associated antigen-4 inhibitor monotherapy37 •Timing of DM onset after initiation of immune checkpoint inhibitor therapy is variable ○DM can develop days to years following immune checkpoint inhibitor initiation; the median time to DM diagnosis is 7 to 17 weeks37 •Immune checkpoint inhibitor therapy precipitates autoimmune β-cell destruction37 •Often rapid onset of severe hyperglycemia; DKA occurs in up to 75% of cases at the time of initial presentation37 •Insulin dependence develops and is often permanent after DM onset37 |
| •Gestational DM | •DM diagnosed in the second or third trimester of pregnancy that was not present prior to conception and is not another type of DM (such as T1DM) that can develop during pregnancy1 |
| General appearance | ○People presenting with DKA or hyperosmolar hyperglycemic state (HHS) typically appear ill |
| Vital signs and BMI | ○Hyperglycemia (particularly in the setting of DKA or HHS) can result in dehydration, with tachycardia and hypotension People with DKA can have tachypnea T1DM, monogenic DM: disease onset is possible at any BMI, but often presents in those with a lower BMI (< 25 kg/m2). Given the increased prevalence of obesity in youth and adults, an elevated BMI should not prevent consideration of autoimmune DM T2DM: the vast majority will have an elevated BMI (≥ 25 kg/m2 or ≥ 23 kg/m2 in Asian individuals), often with increased abdominal adiposity |
| Neurologic | ○People with DKA or HHS can have altered mentation that can progress to coma if untreated Some people with HHS can develop focal neurologic signs such as hemiparesis and hemianopia and/or seizures38,39,40 The presence of peripheral neuropathy typically indicates a longer duration of DM |
| Eyes | ○The presence of diabetic retinopathy typically indicates a longer duration of DM |
| Thyroid | ○Autoimmune thyroid disease can present with a goiter and is associated with T1DM41 |
| Cardiovascular | ○Hyperglycemia (particularly in the setting of DKA or HHS) can result in dehydration with low jugular venous pressure |
| Respiratory | ○People with DKA can present with rapid, deep respirations (Kussmaul breathing) and their breath can have a fruity odor (due to exhaled acetone) |
| Gastrointestinal | ○People with DKA may develop abdominal pain People with hemochromatosis can develop hepatomegaly35 |
| Skin | ○Hyperglycemia (particularly in the setting of DKA or HHS) can result in dehydration, with dry mucous membranes and reduced skin turgor ○Cushing syndrome manifestations can include facial rounding, plethora, supraclavicular and dorsocervical fat pads, hirsutism, acne, ecchymoses, and wide striae36,42 ○Hemochromatosis can result in skin hyperpigmentation ("bronze-colored")35 ○Acanthosis nigricans, characterized by hyperpigmented, velvety plaques typically involving the neck and axillae, is often associated with insulin resistance43 ○Vitiligo, characterized by depigmented macules or patches, is associated with both T1DM and T2DM44,45 ○Chronic candidiasis of the skin and mucous membranes is associated with autoimmune polyendocrine syndrome type 1, which can include T1DM44 |
| Musculoskeletal | ○Cushing syndrome can result in proximal muscle weakness36 Hemochromatosis can result in joint inflammation35 |
| Condition | Description | Differentiated by |
|---|---|---|
| Transient or "stress" hyperglycemia | •Hyperglycemia that occurs during acute severe illness (eg, hospitalization for myocardial infarction) in a person without known DM •Often due to medications (eg, systemic glucocorticoids) or a "stress response" mediated by counter-regulatory hormones50 | •Hyperglycemia resolves as the clinical condition improves or the culprit medication is discontinued •These individuals should be assessed for DM as an outpatient following hospital discharge and are at increased risk of subsequently developing overt DM50 |
| Transient posttransplant hyperglycemia | •Hyperglycemia that develops in the early posttransplant period or develops later due to infection or rejection therapy •Often due to medications (eg, systemic glucocorticoids or other immunosuppressive therapies) or a "stress response" mediated by counter-regulatory hormones | •Hyperglycemia is typically transient and resolves within several weeks after transplant •In contrast, posttransplant DM should be diagnosed > 45 days after transplant when there is a stable immunosuppression regimen, stable graft function, and no acute infection51 |
| Gestational DM | •Gestational DM is defined as DM diagnosed in the second or third trimester of pregnancy that was not present prior to conception and is not another type of DM, such as T1DM, that can develop during pregnancy1 | •Diagnostic criteria for gestational DM differ from diagnostic criteria for DM in nonpregnant individuals (see the Special Considerations section) |
| •"One-step" strategy ○Perform a 75-g OGTT, with plasma glucose measured when a person is fasting and at 1 and 2 hours, at 24 to 28 weeks of gestation in a person not previously diagnosed with DM ○The OGTT should be performed in the morning after an overnight fast of ≥ 8 hours ○The diagnosis of gestational DM is made when any of the following plasma glucose values are met or exceeded: ■Fasting: 92 mg/dL ■1 hour: 180 mg/dL ■2 hours: 153 mg/dL |
| •"Two-step" strategy ○Step 1: Perform a 50-g glucose load test (nonfasting), with plasma glucose measurement at 1 hour, at 24 to 28 weeks of gestation in a person not previously diagnosed with DM ■If the plasma glucose level measured 1 hour after the glucose load is 130 mg/dL to 140 mg/dL, proceed to Step 2 ○Step 2: Perform a 100-g OGTT when the person is fasting ■The diagnosis of gestational DM is made when ≥ 2 (per the American College of Obstetricians and Gynecologists; some clinicians use one elevated value52) of the following 4 plasma glucose levels (measured fasting and at 1, 2, and 3 hours during the OGTT) are met or exceeded (Carpenter-Coustan criteria53): •Fasting: 95 mg/dL •1 hour: 180 mg/dL •2 hours: 155 mg/dL •3 hours: 140 mg/dL |
Jacob Kohlenberg, MD
Assistant Professor of Medicine
Department of Medicine
Division of Diabetes, Endocrinology and Metabolism
University of Minnesota
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