Overview of drug-induced hyperglycaemia

Some drugs can induce hyperglycaemia acutely or are associated with an increased risk of developing diabetes in the longer term. Drugs can induce hyperglycaemia through a variety of mechanisms, including altered insulin production or secretion, increased insulin resistance, direct toxic effects on pancreatic cells, and increased glucose production.

Drug-induced hyperglycaemia is most commonly caused by glucocorticoids, immunosuppressants (see Diabetes and hyperglycaemia in patients post-transplantation), cytotoxic drugs  and antipsychotics.

Antiretroviral drugs used to treat HIV are associated with an increased risk of insulin resistance and diabetes. Patients should be screened for diabetes before and after starting antiretroviral treatment. Treatment of patients who develop diabetes while taking antiretroviral drugs is the same as that of patients with type 2 diabetes (see Type 2 diabetes in adults).

Other drugs, such as statins and thiazide diuretics, have been associated with an increased incidence of diabetes in the longer term. However, the absolute cardiovascular benefit of treatment with these drugs outweighs the increased risk of incident diabetes.

Drug-induced hyperglycaemia can be acute and severe; however, continuing treatment with the causative drug is often required. In this case, hyperglycaemia is treated with antihyperglycaemic drugs.

After a drug causing hyperglycaemia is stopped, the patient should have definitive testing for diabetes. However, even if the patient’s blood glucose concentrations have reduced to normal, they are at greater risk for developing diabetes (see Screening and management of people at risk of developing type 2 diabetes).