3006 Levofloxacin: Beyond Tendon Ruptures

Abstract

INTRODUCTION: Fluoroquinolones have long been an antibiotic of choice for their broad spectrum coverage. The medical community is well aware of its common side effects such as tendon rupture and Qt prolongation. However, there have been documented life threatening hypoglycemic episodes associated with Fluoroquinolones when used concurrently with oral hypoglycemic agents. Severe hypoglycemia may not be evident in this population after a single dose, but multiple factors when present concurrently places these patients at risk of life threatening hypoglycemic events. CASE DESCRIPTION/METHODS: Patient is a 52 year old female with a past medical history of T2DM on glimepiride and metformin, CKD-IIIa, OSA, HTN, HFpEF, presented with AMS for 1 day. On arrival BG was 22 and patient was only responsive to painful stimuli which temporarily resolved with 2 amps of D50. Two days prior patient was treated with levofloxacin for a URI. Patient endorsed decreased oral intake, decreased urine output for 2 days, and taking scheduled 20 mg of Lasix BID for heart failure. Review of systems was otherwise negative and patient was compliant with medications. Shortly after admission, patient started having severe hypoglycemia despite repeated doses of D50 and D 10 ggt was initiated. Pertinent lab findings revealed reduced renal function. After the initial 16-40 hours required for clearance of glimepiride, patient still required D10 drip to maintain euglycemia. At this point we other causes of sustained hypoglycemia such as insulinoma, exogenous insulin use, and levofloxacin induced hypoglycemia were entertained. A hypoglycemic agent screen, insulin levels, c-peptide were consistent with endogenous increase of insulin. Fifty five hours after last dose of levofloxacin blood glucose levels were stabilized and patient was D10 drip was discontinued and subcutaneous insulin was initiated. Renal function returned to baseline and patient was discharged on metformin and lifestyle modifications. DISCUSSION: The mechanism of fluoroquinolones induced hypoglycemia is thought to due to stimulation of pancreatic beta cells causing hyperinsulinemia and interference with the CYT P450 enzymes leading to supratheraputic levels of antihyperglycemic agents such as glimepiride. These factors in conjunction with reduced renal function create the perfect storm which can precipitate life threatening hypoglycemia. Thus, Fluoroquinolones induced hypoglycemia should be on the differential in diabetic patients recently treated for URI infections.