BACKGROUND: Secondary, "reactive," thrombocytosis has been attributed to bacterial infection and treatment with multiple pharmaceuticals and may be associated with an increase in the incidence of gastrointestinal tract bleeding and thrombotic events (eg, stroke). OBJECTIVE: To characterize the dynamics of thrombocytosis in patients with candidemia receiving antifungal therapy. METHODS: We initiated a retrospective observational description of patients with candidemia who were treated with antifungal agents. A total of 108 patients diagnosed with candidemia between August 1995 and September 2003 at our teaching hospital were enrolled. Three groups (candidemia with antifungal therapy, candidemia without antifungal therapy, antifungal therapy without candidemia) of patients >18 years of age were evaluated for the presence of thrombocytosis. Platelet administration, pharmacologic or pathologic contributors to thrombocytosis, and other pertinent details related to an elevation of platelet counts were scrutinized. RESULTS: Reactive thrombocytosis was observed in approximately 10% of treated patients with candidemia. Within the subgroup developing reactive thrombocytosis, life-threatening thrombotic complications were uncommon. Mean baseline platelet counts were 393 x 10(3)/mm3, with a mean peak (695 x 10(3)/mm3) occurring an average of 13 days after initiation of therapy. All patients had resolution within 7 days after therapy. The maximum peak (1056 x 10(3)/mm3) was observed in a patient after 14 days of antifungal therapy. The onset of thrombocytosis in this patient was 4 days and lasted 4 days after therapy. CONCLUSIONS: Reactive thrombocytosis occurs during treatment of candidemia. The causative agent (drug vs disease), the risk associated with this reaction, and evaluation of treatment need to be elucidated by a larger epidemiologic study or controlled, prospective clinical trial.
BACKGROUND: Secondary, "reactive," thrombocytosis has been attributed to bacterial infection and treatment with multiple pharmaceuticals and may be associated with an increase in the incidence of gastrointestinal tract bleeding and thrombotic events (eg, stroke). OBJECTIVE: To characterize the dynamics of thrombocytosis in patients with candidemia receiving antifungal therapy. METHODS: We initiated a retrospective observational description of patients with candidemia who were treated with antifungal agents. A total of 108 patients diagnosed with candidemia between August 1995 and September 2003 at our teaching hospital were enrolled. Three groups (candidemia with antifungal therapy, candidemia without antifungal therapy, antifungal therapy without candidemia) of patients >18 years of age were evaluated for the presence of thrombocytosis. Platelet administration, pharmacologic or pathologic contributors to thrombocytosis, and other pertinent details related to an elevation of platelet counts were scrutinized. RESULTS: Reactive thrombocytosis was observed in approximately 10% of treated patients with candidemia. Within the subgroup developing reactive thrombocytosis, life-threatening thrombotic complications were uncommon. Mean baseline platelet counts were 393 x 10(3)/mm3, with a mean peak (695 x 10(3)/mm3) occurring an average of 13 days after initiation of therapy. All patients had resolution within 7 days after therapy. The maximum peak (1056 x 10(3)/mm3) was observed in a patient after 14 days of antifungal therapy. The onset of thrombocytosis in this patient was 4 days and lasted 4 days after therapy. CONCLUSIONS: Reactive thrombocytosis occurs during treatment of candidemia. The causative agent (drug vs disease), the risk associated with this reaction, and evaluation of treatment need to be elucidated by a larger epidemiologic study or controlled, prospective clinical trial.