Glucocorticoid-induced hyperglycemia and diabetes: Practical points

Abstract

Glucocorticoids are widely used in medical practice for their anti-inflammatory action, but lead to hyperglycemia in 30% of cases, due to rapid reduction of insulin secretion and action. Endogenous glucose production is less strongly suppressed by insulin, even small doses such as 7.5mg/day. As they are administered in the morning, glucocorticoids induce hyperglycemic excursion in the afternoon, and at this time screening can be performed by capillary glucose measurement. It is also critical to determine, on medical history and HbA1c assay, whether the patient had prior diabetes, sometimes overlooked, in which case diabetes will not resolve after glucocorticoid discontinuation, and poorly controlled diabetes will often require a basal-bolus insulin therapy in the meantime. This heavy therapy is not suitable for de novo diabetes, as it incurs a risk of nocturnal hypoglycemia, whereas intermediate-acting morning insulin injection provides better cover of hyperglycemia in the afternoon. The British Diabetology Societies recently reported that an even simpler prescription of gliclazide in the morning may be sufficient for some patients. The antidiabetic treatment will have to be monitored, and reduced when glucocorticoid dose is scaled off. Other antidiabetic agents are being tested in trials to develop simple alternatives without risk of hypoglycemia.