Stamm Pamela L, Jenkins J Kimble, Vigrass Howard G
Department of Pharmacy Practice, Harrison School of Pharmacy, Auburn University, 125 Walker Boulevard, Auburn, AL 36849-0001, USA.
Ann Pharmacother. 2005 Mar;39(3):555-8. doi: 10.1345/aph.1D311. Epub 2005 Feb 8.
To report a case of possible beta-antagonist-induced thrombocytopenia.
A 44-year-old African American woman with systemic lupus erythematosus developed thrombocytopenia. Splenic sequestration was suspected, but the rise in platelets after splenectomy was temporary. Bacterial and viral etiologies were ruled out, since thrombocytopenia continued 6 months after splenectomy. Her medications acetaminophen, amitriptyline, amlodipine, beta-antagonists, and diphenhydramine were suspected. Nadolol and labetalol were started immediately prior to splenectomy. Six months after splenectomy, the woman was hospitalized for pneumonia; the platelet count was 50 x 10(3)/mm(3). Nadolol was discontinued on day 2. Within 24 hours, the platelet count rose to 128 x 10(3)/mm(3) and exceeded 200 x 10(3)/mm(3) by day 7. Labetalol was discontinued on day 8, but no additional significant rise occurred. The patient developed thrombocytopenia one year later when placed on nadolol and famotidine during admission for a gastrointestinal bleed. The platelet count decreased during the admission. Both drugs were discontinued after the last platelet count (100 x 10(3)/mm(3)). The platelet count had normalized by the follow-up visit 16 days later and remained normal until the patient's death almost a year later.
Thrombocytopenia is not a common adverse effect of beta-antagonist therapy. As of February 1, 2005, only 4 case reports of suspected beta-antagonist-associated thrombocytopenia have been published in English, and the medications cited are unavailable within the US. After splenectomy, the thrombocytopenia might have resolved if the beta-antagonists had not been present. Since thrombocytopenia resolved within 24 hours of discontinuation of nadolol, it is likely that the continued thrombocytopenia was beta-antagonist induced. The likelihood that the beta-antagonist caused the adverse event is possible according to the Naranjo probability scale.
The temporal association between the discontinuation of nadolol and the rise in platelets suggests that the thrombocytopenia resulted from nadolol.
报告一例可能由β受体拮抗剂诱发血小板减少症的病例。
一名44岁患有系统性红斑狼疮的非裔美国女性出现血小板减少症。怀疑是脾扣押，但脾切除术后血小板升高是暂时的。细菌和病毒病因被排除，因为脾切除术后6个月血小板减少仍持续存在。怀疑其服用的对乙酰氨基酚、阿米替林、氨氯地平、β受体拮抗剂和苯海拉明等药物有问题。纳多洛尔和拉贝洛尔在脾切除术前立即开始使用。脾切除术后6个月，该女性因肺炎住院；血小板计数为50×10³/mm³。第2天停用纳多洛尔。24小时内，血小板计数升至128×10³/mm³，第7天超过200×10³/mm³。第8天停用拉贝洛尔，但未出现进一步显著升高。该患者1年后因胃肠道出血入院期间服用纳多洛尔和法莫替丁时再次出现血小板减少症。住院期间血小板计数下降。最后一次血小板计数（100×10³/mm³）后两种药物均停用。1个月后随访时血小板计数已恢复正常，直至近1年后患者死亡一直保持正常。
血小板减少症并非β受体拮抗剂治疗的常见不良反应。截至2005年2月1日，仅有四份英文报告疑似β受体拮抗剂相关血小板减少症，且所提及药物在美国无法获取。脾切除术后，如果没有β受体拮抗剂，血小板减少症可能已得到缓解。由于停用纳多洛尔后24小时内血小板减少症得到缓解，持续的血小板减少症很可能是由β受体拮抗剂诱发的。根据Naranjo概率量表，β受体拮抗剂导致该不良事件是有可能的。
停用纳多洛尔与血小板升高之间的时间关联表明血小板减少症是由纳多洛尔引起的。
