Gottschall J L, Neahring B, McFarland J G, Wu G G, Weitekamp L A, Aster R H
Blood Center of Southeastern Wisconsin, Inc., Milwaukee 53201-2178.
Am J Hematol. 1994 Dec;47(4):283-9. doi: 10.1002/ajh.2830470407.
Quinine-induced immune thrombocytopenia with hemolytic uremic syndrome (HUS) is a recently defined clinical entity. In this paper we have attempted to characterize the natural history and laboratory abnormalities typical of quinine-induced immune thrombocytopenia associated with hemolytic uremic syndrome in nine patients experiencing ten episodes of the disease. In addition, review of other reported cases of probable quinine-induced HUS is presented. The disease was characterized by the onset of chills, diapheresis, nausea and vomiting, abdominal pain, decreased urine output, and petechiae following quinine exposure. All patients experience significant anemia, severe thrombocytopenia, increased lactate dehydrogenase, elevated serum creatinine, and oliguria. Quinine-dependent platelet-reactive antibodies were identified in eight of nine using flow cytometry. Unexpectedly, drug-dependent antibodies reactive with red cells and granulocytes were identified in four and eight patients, respectively. All patients were treated with plasma exchange (range 1-12 procedures), and seven required hemodialysis. All survive without residual abnormality. Our experience with nine patients with quinine-induced HUS and the nine additional cases reported by others and reviewed in this paper establishes this condition as a distinct clinical entity. Adult patients presenting with HUS should routinely be asked about exposure to quinine in the form of medication or beverages. The mechanism by which quinine-dependent antibodies produce renal failure is uncertain, but preliminary studies (described elsewhere) suggest that drug-induced antibodies reactive with endothelial cells and possibly margination of granulocytes in renal glomeruli may be responsible for this complication. The prognosis in quinine-induced HUS is better than in other forms of adult HUS.
奎宁诱导的免疫性血小板减少症合并溶血性尿毒症综合征(HUS)是一种最近才被定义的临床实体。在本文中,我们试图描述9例患者经历10次该疾病发作时,奎宁诱导的免疫性血小板减少症合并溶血性尿毒症综合征的自然病程及典型的实验室异常表现。此外,还对其他报道的可能由奎宁诱导的HUS病例进行了综述。该疾病的特点是在接触奎宁后出现寒战、发汗、恶心、呕吐、腹痛、尿量减少和瘀点。所有患者均出现明显贫血、严重血小板减少、乳酸脱氢酶升高、血清肌酐升高和少尿。9例患者中有8例通过流式细胞术检测到奎宁依赖性血小板反应性抗体。出乎意料的是,分别在4例和8例患者中检测到与红细胞和粒细胞反应的药物依赖性抗体。所有患者均接受了血浆置换(1 - 12次)治疗,7例患者需要进行血液透析。所有患者均存活且无残留异常。我们对9例奎宁诱导的HUS患者的经验以及本文中回顾的其他作者报道的另外9例病例,证实了这种情况是一种独特的临床实体。对于出现HUS的成年患者,应常规询问其是否接触过药物或饮料形式的奎宁。奎宁依赖性抗体导致肾衰竭的机制尚不清楚,但初步研究(在其他地方描述)表明,与内皮细胞反应的药物诱导抗体以及可能在肾小球中粒细胞的边缘化可能是导致这种并发症的原因。奎宁诱导的HUS的预后优于其他形式的成人HUS。