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Platelet Count of Zero: A Case of Vancomycin-Induced Immune Thrombocytopenia
Shiv B Gakhar1, Adam Hurwitz1, Colton Sellars1
1Internal Medicine, HCA Florida Largo Hospital, Largo, USA.
Immune thrombocytopenia (ITP) is an acquired hematologic disorder marked by immune-mediated destruction of platelets, leading to profound thrombocytopenia and increased bleeding risk. Drug-induced immune thrombocytopenia (DITP), specifically vancomycin-induced immune thrombocytopenia (VIIT), is a rare but serious adverse drug reaction, caused by drug-dependent antibodies that accelerate platelet clearance. We present a case of a 72-year-old male who developed life-threatening thrombocytopenia, with a nadir of <1 K/µL, following re-exposure to vancomycin. The decline began within three days of treatment reinitiation and persisted despite platelet transfusions, corticosteroids, and intravenous immunoglobulin (IVIG). A diagnosis of VIIT was made after excluding other etiologies, including heparin-induced thrombocytopenia (HIT), thrombotic microangiopathy, and sepsis-associated thrombocytopenia. Platelet counts remained refractory until plasmapheresis and drug discontinuation, with recovery to 71 K/µL within one week. This case highlights the importance of early recognition of VIIT and suggests a potential role for plasmapheresis in refractory cases. Prompt drug discontinuation is critical for recovery.
Immune thrombocytopenia (ITP) is an acquired hematologic disorder marked by immune-mediated destruction of platelets, leading to profound thrombocytopenia and increased bleeding risk. Drug-induced immune thrombocytopenia (DITP), specifically vancomycin-induced immune thrombocytopenia (VIIT), is a rare but serious adverse drug reaction, caused by drug-dependent antibodies that accelerate platelet clearance. We present a case of a 72-year-old male who developed life-threatening thrombocytopenia, with a nadir of <1 K/µL, following re-exposure to vancomycin. The decline began within three days of treatment reinitiation and persisted despite platelet transfusions, corticosteroids, and intravenous immunoglobulin (IVIG). A diagnosis of VIIT was made after excluding other etiologies, including heparin-induced thrombocytopenia (HIT), thrombotic microangiopathy, and sepsis-associated thrombocytopenia. Platelet counts remained refractory until plasmapheresis and drug discontinuation, with recovery to 71 K/µL within one week. This case highlights the importance of early recognition of VIIT and suggests a potential role for plasmapheresis in refractory cases. Prompt drug discontinuation is critical for recovery.
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