Presentations

Abstract

Introduction: Immune Thrombocytopenia (ITP) is a disorder in which the formation of antiplatelet antibodies leads to platelet destruction. It can be idiopathic or be caused by infections, autoimmune diseases, and medications. We present a case of an individual developing severe thrombocytopenia within days of receiving various antibiotics.

Case Information: A 78-year-old male with past medical history of type 2 diabetes, hypertension, and ESRD on hemodialysis was admitted for colitis and treated with IV vancomycin and aztreonam in the setting of a known penicillin allergy. He was transitioned from vancomycin to oral metronidazole on day 4 and discharged on that medication to complete his course. Three days after discharge, he returned to the ED for lethargy and was found to have a platelet count of 15,000. His labs were notable for baseline chronic anemia without leukocytosis/leukopenia. Imaging showed chronic splenomegaly but was otherwise normal and he did not have any overt signs of bleeding. His platelet count was 175,000 on initial admission, 125,000 on day 3, and 99,000 on discharge. Hemolytic and infectious workups were negative and peripheral smear didn't show any platelet abnormalities. The HIT panel was weakly positive with a HIT score <5%. He was admitted given concern for ITP and received two days of IVIg, four days of dexamethasone and five units of platelets with gradual improvement.

Discussion/Clinical Findings: Drug induced immune thrombocytopenia (DITP) occurs due to formation of IgG autoantibodies against platelet membrane proteins after exposure to an inciting agent, which include hundreds of medications including many antibiotics. These antibody-platelet complexes are sequestered in the spleen and liver causing platelet consumption. DITP tends to cause platelet counts less than 20,000 whereas Heparin induced thrombocytopenia (HIT) rarely does so. Onset also tends to be rapid especially in the setting of prior exposures to inciting medications, which our patient did not have. The HIT panel was weakly positive but the HIT score was very low. Our patient received 3 days of vancomycin, 7 days of aztreonam, and 8 days of metronidazole. This patient's cause of DITP is difficult to elucidate, given that both vancomycin and aztreonam are associated with DITP, as well as metronidazole in very rare cases. His platelets started declining on the second day of vancomycin and aztreonam and decline persisted despite cessation of both drugs, not reaching nadir until cessation of metronidazole. DITP typically resolves a few days after cessation of offending medication, and while aztreonam induced thrombocytopenia is far less rare than metronidazole, it is likely that both antibiotics played a role in development of thrombocytopenia. Vancomycin is less likely given his very short course relative to his course of aztreonam and metronidazole. Treatment of DITP includes discontinuation of the offending agent as well as IVIg and steroids.

Conclusion: This case report highlights an interesting patient who was treated with multiple antibiotics for colitis and later developed drug induced ITP. Of the antibiotics received, it is likely that both aztreonam and metronidazole were implicated in the cause of DITP.