Saathoff Angela D, Elkins Stephanie L, Chapman Stanley W, McAllister Susan Fleming, Cleary John D
Pediatric Emergency Department, University of Mississippi Medical Center, Jackson, MS 39216-4500, USA.
Ann Pharmacother. 2005 Jul-Aug;39(7-8):1238-43. doi: 10.1345/aph.1E402. Epub 2005 May 24.
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).
To characterize the dynamics of thrombocytosis in patients with candidemia receiving antifungal therapy.
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.
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.
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.
继发性“反应性”血小板增多症被认为与细菌感染及多种药物治疗有关，可能会增加胃肠道出血和血栓形成事件（如中风）的发生率。
描述接受抗真菌治疗的念珠菌血症患者血小板增多症的动态变化。
我们对接受抗真菌药物治疗的念珠菌血症患者进行了一项回顾性观察描述。纳入了1995年8月至2003年9月在我们教学医院诊断为念珠菌血症的108例患者。对三组年龄大于18岁的患者（接受抗真菌治疗的念珠菌血症患者、未接受抗真菌治疗的念珠菌血症患者、未患念珠菌血症但接受抗真菌治疗的患者）进行血小板增多症情况评估。仔细审查了血小板输注情况、血小板增多症的药理学或病理学因素以及与血小板计数升高相关的其他相关细节。
在接受治疗的念珠菌血症患者中，约10%观察到反应性血小板增多症。在发生反应性血小板增多症的亚组中，危及生命的血栓并发症并不常见。平均基线血小板计数为393×10³/mm³，平均峰值（695×10³/mm³）出现在治疗开始后平均13天。所有患者在治疗后7天内血小板计数恢复正常。一名患者在抗真菌治疗14天后观察到最大峰值（1056×10³/mm³）。该患者血小板增多症在治疗后4天开始，持续4天。
念珠菌血症治疗期间会发生反应性血小板增多症。这种反应的致病因素（药物还是疾病）、与之相关的风险以及治疗评估需要通过更大规模的流行病学研究或对照前瞻性临床试验来阐明。
