Moxifloxacin-Induced Thrombocytopenia Mediated by Moxifloxacin-Dependent IgM and IgG Antiplatelet Antibodies: A Case Report

Abstract

Moxifloxacin is a rare but important cause of drug-induced immune thrombocytopenia (DIT). We describe a patient who presented with an acute onset of severe thrombocytopenia complicated by petechial rash, epistaxis, and melena. Recent new drug exposures included moxifloxacin and two proton pump inhibitors. On presentation to the hospital, all recently initiated medications were discontinued and the patient's thrombocytopenia was treated with platelet transfusions, intravenous immunoglobulin, and high-dose corticosteroids. Her thrombocytopenia improved over the next seven days and she was discharged on hospital day 8. Serologic testing revealed strongly positive moxifloxacin-dependent IgM and IgG antiplatelet antibodies, confirming a diagnosis of moxifloxacin-induced immune thrombocytopenia. DIT has been reported with other fluoroquinolone antibiotics, especially ciprofloxacin. This case documents a rare but potentially fatal complication of exposure to moxifloxacin and is the first to demonstrate objective evidence of acute sensitization with IgM antibody positivity. It highlights the need to consider this potential reaction when choosing antibiotic therapy, particularly in patients who are at high risk for bleeding, have hematologic disorders, or are receiving myelosuppressive therapies, and perhaps in those with a history of multiple drug allergies.

The Emerging Role of the Innate Immune Response in Idiosyncratic Drug Reactions

“…Depending on the offending drug, several mechanisms responsible for the decrease have been proposed, including myelosuppression or the expedited clearance of platelets caused by anti-platelet or antihaptenated platelet antibodies or platelet-specific autoantibodies (Narayanan et al, 2019). One recent example is a case of moxifloxacin-induced thrombocytopenia, in which IgM and IgG antiplatelet antibodies were detected in serologic testing and were found to be enhanced in the presence of moxifloxacin, but not with pantoprazole or esomeprazole (Moore et al, 2020).…”