Last reviewed: 7 Jan 2023
Last updated: 15 Feb 2022

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 characterised by insulin resistance and relative insulin deficiency. Most patients are asymptomatic and are diagnosed through screening (abnormal fasting plasma glucose, haemoglobin A1c, and/or oral glucose tolerance test).[1] Strong risk factors include older age, overweight/obesity, physical inactivity, prior gestational diabetes, pre-diabetes, non-white ancestry, family history of diabetes, or polycystic ovary syndrome.[1] 

Characterised by absolute insulin deficiency. Most cases result from autoimmune pancreatic beta-cell destruction in genetically susceptible individuals.[1] Usually presents with acute symptoms or ketoacidosis in childhood or adolescence.  

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.[2] Commonly accompanied by acanthosis nigricans (90% to 95% of patients).[3] 

GDM is diagnosed in the second or third trimester of pregnancy (usually between 24 to 28 weeks of gestation) on the basis of abnormal glucose tolerance testing.[1] Women at high risk of type 2 diabetes are tested at their first antenatal visit to detect pre-existing (overt) diabetes.[1]Risk factors for GDM include advanced maternal age (>40 years), obesity, personal history of gestational diabetes or macrosomia of previous child, polycystic ovary syndrome, non-white ancestry, and family history of diabetes mellitus.[1][4] 

DKA and hyperosmolar hyperglycaemic states are acute metabolic emergencies. DKA is characterised by absolute insulin deficiency and is the most common acute hyperglycaemic complication of type 1 diabetes.[5] Successful treatment includes correction of volume depletion, hyperglycaemia and ketosis/acidosis, electrolyte imbalances, and comorbid precipitating events (e.g., infection), along with frequent monitoring.

Severe hyperglycaemia, hyperosmolality, and volume depletion, in the absence of severe ketoacidosis.[5] 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.

Coronary artery disease and stroke are the most common manifestations, and account for most deaths in people with diabetes. Modification of cardiovascular risk factors (e.g., hypertension, dyslipidaemia) are important long-term treatment issues. [1][6]

Defined by albuminuria (increased urinary albumin excretion is defined as ≥3.4 mg/mmol [30 mg/g]) and progressive estimated reduction in 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.[7] Peripheral neuropathy may present as loss of sensation, painless ulcers on pressure points, or pain, although many patients are asymptomatic.  

Encompasses the conditions of diabetic foot ulcer (i.e., a full-thickness epithelial defect below/distal to the ankle) and diabetic foot infections (i.e., any soft-tissue or bone infection occurring in the diabetic foot). Prevention and/or healing of diabetic foot ulcers helps to prevent infections and minimizes the risk of limb loss.[8][9]

Consequence of chronic progressive diabetic microvascular leakage and occlusion.[10] Sight-threatening signs include macular oedema, ischaemia, or traction; vitreous haemorrhage; or retinal detachment. 

Refers to identification and treatment of hyperglycaemia in hospital, in patients with either pre-existing diabetes or new-onset hyperglycaemia. The development of hyperglycaemia during acute medical or surgical illness may not be a physiological or benign condition but rather a marker of poor clinical outcomes and increased mortality.

Cluster of common abnormalities, including insulin resistance, impaired glucose tolerance, abdominal obesity, reduced high-density lipoprotein-cholesterol levels, elevated triglycerides, and hypertension. However, this syndrome is not universally accepted as more clinically useful than assessment of individual cardiovascular risk factors.[11][12]

Characterised by polydipsia, polyuria, increased thirst, and hypotonic urine. Central DI is due to defective synthesis or release of arginine vasopressin (AVP).[13] Nephrogenic DI is due to renal insensitivity to AVP.[14]



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