Drug-induced hyperglycemia in obstetrics: key offending drugs, mechanisms, and practical management.
Drug-induced hyperglycemia is an important metabolic complication that may arise when medications disrupt insulin secretion, insulin sensitivity, or glucose homeostasis. In obstetric practice, several commonly used drugs, including glucocorticoids, progesterone, antihypertensive agents, tocolytic drugs, and immunosuppressants, may impair glycemic control to varying degrees, and prolonged exposure may even lead to drug-induced diabetes mellitus. These effects are particularly important in pregnant women with pregestational diabetes, gestational diabetes, obesity, or other risk factors for dysglycemia.
We systematically reviewed the literature from major databases over the past decade on the association between commonly used obstetric medications and hyperglycemia, with a focus on glucocorticoids, beta-adrenergic agonists, tacrolimus, nifedipine, and indomethacin. Evidence from clinical studies, case reports, and mechanistic investigations was summarized.
Among the drugs reviewed, glucocorticoids, beta-adrenergic agonists, and tacrolimus showed relatively prominent diabetogenic effects, mainly through increased insulin resistance, β-cell dysfunction, and reduced insulin secretion. In contrast, nifedipine and indomethacin appeared to have less clinically significant effects on blood glucose. The use of high-risk agents during pregnancy was associated with a higher incidence of hyperglycemia and increased complexity of glycemic management.
Early identification of high-risk drugs and high-risk patients, together with individualized glucose monitoring and timely intervention, may reduce related complications and improve medication safety during pregnancy. Further prospective studies are warranted to define safe thresholds across different gestational stages and maternal conditions.
We systematically reviewed the literature from major databases over the past decade on the association between commonly used obstetric medications and hyperglycemia, with a focus on glucocorticoids, beta-adrenergic agonists, tacrolimus, nifedipine, and indomethacin. Evidence from clinical studies, case reports, and mechanistic investigations was summarized.
Among the drugs reviewed, glucocorticoids, beta-adrenergic agonists, and tacrolimus showed relatively prominent diabetogenic effects, mainly through increased insulin resistance, β-cell dysfunction, and reduced insulin secretion. In contrast, nifedipine and indomethacin appeared to have less clinically significant effects on blood glucose. The use of high-risk agents during pregnancy was associated with a higher incidence of hyperglycemia and increased complexity of glycemic management.
Early identification of high-risk drugs and high-risk patients, together with individualized glucose monitoring and timely intervention, may reduce related complications and improve medication safety during pregnancy. Further prospective studies are warranted to define safe thresholds across different gestational stages and maternal conditions.