Last reviewed: 28 Apr 2023
Last updated: 28 Mar 2023

This page compiles our content related to diabetes. For further information on diagnosis and treatment, follow the links below to our full BMJ Best Practice topics on the relevant conditions and symptoms.



Common disorder characterized by insulin resistance and relative insulin deficiency. Most patients are asymptomatic and are diagnosed through screening (abnormal fasting plasma glucose, hemoglobin A1c, and/or oral glucose tolerance test).[1]​ Strong risk factors include older age, overweight/obesity, physical inactivity, prior gestational diabetes mellitus, prediabetes, nonwhite ancestry, family history of diabetes, or polycystic ovary syndrome.​[1]

Characterized by absolute insulin deficiency. Usually develops as a result of autoimmune pancreatic beta-cell destruction in genetically susceptible individuals.[2]​ Type 1 diabetes can be diagnosed at any age, but the highest incidence is in children aged 10-14 years.[2] Patients most often present with a few days or weeks of polyuria, polydipsia, weight loss, and weakness. Some patients may present with diabetic ketoacidosis.

Obesity, leading to insulin resistance, is the primary cause of type 2 diabetes in children. The incidence of type 2 diabetes in youths (age 10 to 19 years) is increasing.[3] Commonly accompanied by acanthosis nigricans (90% to 95% of patients).[4]

GDM develops during pregnancy and is diagnosed on the basis of elevated plasma glucose levels, although the precise diagnostic criteria remain controversial. Risk factors for GDM include advanced maternal age (>40 years), obesity, personal history of gestational diabetes or macrosomia of previous child, polycystic ovary syndrome, nonwhite ancestry, and family history of type 2 diabetes mellitus.[1]​​[5][6]​ The risk for recurrence of GDM in subsequent pregnancies or progression to type 2 diabetes is high.

DKA and hyperosmolar hyperglycemic states are acute metabolic emergencies. DKA is characterised by absolute insulin deficiency and is the most common acute hyperglyemic complication of type 1 diabetes.[7] Successful treatment includes correction of volume depletion, hyperglycemia, electrolyte imbalances, and comorbid precipitating events (e.g., infection), with frequent monitoring.

Severe hyperglycemia, hyperosmolality, and volume depletion, in the absence of severe ketoacidosis.[7] Occurs most commonly in older patients with type 2 diabetes, with high mortality. Treatment includes correction of fluid deficit and electrolyte abnormalities, and intravenous insulin.

Cardiovascular disease is the leading cause of death in people with diabetes. People with diabetes have up to a fourfold increased risk of stroke and are twice as likely to die after myocardial infarction than people without diabetes.[8][9]​ Modification of cardiovascular risk factors (e.g., hypertension, dyslipidemia) are important long-term treatment issues.​[1][10]

Defined by albuminuria (increased urinary albumin excretion is defined as 30 mg/g) and progressive reduction in estimated glomerular filtration rate (eGFR) in the setting of a long duration of diabetes (>10 years' duration of type 1 diabetes; may be present at diagnosis in type 2 diabetes), and is typically associated with retinopathy.[1]​ Symptoms may be absent until the disease is advanced. 

The most common chronic complication in diabetes affecting different parts of the nervous system and presenting with diverse clinical manifestations.[11] Peripheral neuropathy may present as pain, loss of sensation, or painless ulcers on pressure points, although many patients are asymptomatic. 

Encompasses the conditions of diabetic foot ulcer (i.e., a break in the skin that includes as a minimum the epidermis and part of the dermis and occurs below/distal to the malleoli in a person with diabetes) and diabetic foot infections (i.e., any soft-tissue or bone infection occurring in the diabetic foot, including osteomyelitis). Prevention and/or healing of ulcers helps to prevent infections and thereby minimizes the risk of limb loss.[12] 

The chronic progressive retinal manifestation of hyperglycemic vascular damage and neurodegenerative change. It increases in prevalence with duration of diabetes.[1]​ Sight-threatening signs include macular edema, retinal or optic disc new vessels, and vitreous hemorrhage.

Refers to identification and treatment of hyperglycemia in the setting of acute illness in hospitalized patients with either preexisting diabetes or new-onset hyperglycemia. The development of hyperglycemia during acute medical or surgical illness is not be a physiologic or benign condition but rather a marker of poor clinical outcomes and increased mortality.[13]

Cluster of common abnormalities, including insulin resistance, impaired glucose tolerance, abdominal obesity, reduced high-density lipoprotein-cholesterol levels, elevated triglycerides, and hypertension.[14][15]​​​ The main utility of diagnosing metabolic syndrome is the identification of people at high risk of cardiovascular disease beyond low-density lipoprotein-cholesterol levels. However, whether a diagnosis of metabolic syndrome provides more useful information than its individual components regarding cardiovascular risk is greatly controversial.

Characterized by polydipsia, polyuria, and formation of inappropriately hypotonic (dilute) urine. Central DI is due to defective synthesis or release of arginine vasopressin (AVP).[16] Nephrogenic DI is due to renal insensitivity to AVP.[17]



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