Purpose. The development of gatifloxacin-induced dysglycemia in 13 patients is described; the details of the 3 most severe cases are presented.
Summary. Three elderly patients developed dysglycemia after initiation of gatifloxacin therapy. Both patients who developed hypoglycemia were receiving concomitant insulin or oral antidiabetic agents. Repeated doses of dextrose were required for management. The Naranjo et al. probability rating scale revealed that gatifloxacin was the probable cause in the majority of the 13 cases, primarily because of the temporal relationship with gatifloxacin and, in some instances, resolution of dysglycemia after drug discontinuation. Although the mechanism of gatifloxacin-induced hyperglycemia is not known, in vitro studies have found that certain quinolone antimicrobials can lower serum glucose levels by blocking adenosine 5'-triphosphate-dependent potassium channels in the pancreatic ß-cell, stimulating insulin release. It is difficult to unequivocally implicate gatifloxacin as the only cause of dysglycemia in the cases presented, as there are many explanations for poor glycemic control in hospitalized patients, such as stress, infection, decreased renal function, and concomitant drug therapies. However, the patients’ medication regimens appeared to be stable before gatifloxacin administration.
Conclusion. Thirteen patients developed dysglycemia after receiving gatifloxacin. Gatifloxacin was found to be the probable cause in the majority of cases.
Index terms: Antidiabetic agents; Caloric agents; Dextrose; Diabetes mellitus; Gatifloxacin; Geriatrics; Hyperglycemia; Hypoglycemia; Insulin; Kidney failure; Mechanism of action; Quinolones; Toxicity
