Amy L Blommel1, Ronald A Lutes. 1. Monongahela Valley Hospital, Monongahela, PA, USA. ablommel@monvalleyhospital.com
Abstract
OBJECTIVE: To report a case of severe hyperglycemia in a nondiabetic patient receiving gatifloxacin that was properly dosed based on renal function. CASE SUMMARY: A 65-year-old nondiabetic female with progressive renal dysfunction was admitted for severe hyperglycemia. The patient had received 9 days of a 10-day course of renally adjusted therapy with gatifloxacin 200 mg/day for bronchitis. Her blood glucose level on admission was 1121 mg/dL, at which point the gatifloxacin was discontinued. After several days of intensive insulin therapy, the blood glucose levels returned to normal, and the patient was subsequently discharged. DISCUSSION: Gatifloxacin-induced hyperglycemia has been reported in the literature, but based on a MEDLINE search (1966-December 2004), no such cases were found in a nondiabetic patient receiving the proper gatifloxacin dose, adjusted for degree of renal insufficiency. The available case reports seem to suggest the increase in blood glucose concentrations could have been precipitated by high drug concentrations in patients not receiving the renally adjusted dose or in those with preexisting, undiagnosed diabetes. A definite mechanism of action for gatifloxacin-induced hyperglycemia is not known. The Naranjo probability scale revealed a probable adverse reaction of hyperglycemia associated with gatifloxacin therapy. CONCLUSIONS: Healthcare professionals should be more aware of the possible development of hyperglycemia in all patients taking gatifloxacin, including those who are not diabetic and those receiving appropriately reduced doses for renal dysfunction.
OBJECTIVE: To report a case of severe hyperglycemia in a nondiabetic patient receiving gatifloxacin that was properly dosed based on renal function. CASE SUMMARY: A 65-year-old nondiabetic female with progressive renal dysfunction was admitted for severe hyperglycemia. The patient had received 9 days of a 10-day course of renally adjusted therapy with gatifloxacin 200 mg/day for bronchitis. Her blood glucose level on admission was 1121 mg/dL, at which point the gatifloxacin was discontinued. After several days of intensive insulin therapy, the blood glucose levels returned to normal, and the patient was subsequently discharged. DISCUSSION: Gatifloxacin-induced hyperglycemia has been reported in the literature, but based on a MEDLINE search (1966-December 2004), no such cases were found in a nondiabetic patient receiving the proper gatifloxacin dose, adjusted for degree of renal insufficiency. The available case reports seem to suggest the increase in blood glucose concentrations could have been precipitated by high drug concentrations in patients not receiving the renally adjusted dose or in those with preexisting, undiagnosed diabetes. A definite mechanism of action for gatifloxacin-induced hyperglycemia is not known. The Naranjo probability scale revealed a probable adverse reaction of hyperglycemia associated with gatifloxacin therapy. CONCLUSIONS: Healthcare professionals should be more aware of the possible development of hyperglycemia in all patients taking gatifloxacin, including those who are not diabetic and those receiving appropriately reduced doses for renal dysfunction.