We have read the elegant case report in Diabetes Care by Umapathysivam et al. (1) with great interest. They have treated two patients for euglycemic ketoacidosis, each of whom was taking a sodium glucose cotransporter 2 inhibitor (SGLT2i) but did not have diabetes. The authors intended to treat congestive heart failure with the inhibitors, but rather unexpectedly, the patients developed euglycemic ketoacidosis. Their observation is important, because it reinforces that the administration of a drug should be balanced against the possible risk or side effect of the drug. We are afraid that glucocorticoids taken by the patients were doing at least some harm in terms of the occurrence of ketoacidosis. Glucocorticoids have been known to suppress insulin secretion by the β-cell (2,3), possibly through its action mediated by glucocorticoid-inducible inhibitory proteins (4,5). Such an insulin inhibitory effect of glucocorticoid may well be a contributory factor for ketoacidosis in these patients. In these cases, one patient had been taking 25 mg prednisolone and the other took a “low dose” of the same agent. Despite the clear-cut direct effect of glucocorticoids on insulin secretion, the possibility that this is one of the causative factors for ketoacidosis is not discussed at all by Umapathysivam et al. (1). It is strongly recommended that clinicians comprehensively review the known pathophysiology when encountered a seemingly rare clinical phenomenon. Doing so will help clinicians, and ultimately patients, avoid untoward drug effects.
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Duality of Interest. No potential conflicts of interest relevant to this article were reported.
