Nicodemo A C, Del Negro G, Amato Neto V
Department of Infectious Diseases, University of São Paulo Medical School, Brazil.
Rev Inst Med Trop Sao Paulo. 1990 Jul-Aug;32(4):252-9. doi: 10.1590/s0036-46651990000400004.
The present study has intended to contribute to the elucidation of the pathogenic mechanisms, involved in the thrombocytopenia and in the bleeding diathesis seen in the course of Leptospirosis. The group of cases included in the present prospective study consisted of 30 patients with Leptospirosis, admitted to the Infectious and Parasitic Diseases Ward, Hospital das Clínicas, Faculty of Medicine, University of São Paulo. The following possible mechanisms of thrombocytopenia have been considered and therefore investigated: platelet consumption, due to disseminated intravascular coagulation; immune-mediated platelet destruction, due to platelet-associated antibodies and an inhibited platelet production in the bone marrow. Thrombocytopenia occurred in 86.6% of 30 patients and did not seem to be immune-mediated by platelet-associated antibodies. Furthermore it did not seem to be due to a disseminated intravascular coagulation consumption. Although there was a statistically-significant correlation between bone marrow platelet production and platelet counts we think that the static microscopic examination of a bone marrow aspirate cannot accurately depict the dynamic mechanisms of platelet production when these cells are being consumed in peripheral blood. Vasculitis should be considered as the most important factor for the pathogenesis of the bleeding disturbances in Leptospirosis. However, we believe that thrombocytopenia, uremia and coagulation disorders, individually or as a group, should be included among the contributing factors that lead to and worsen bleeding episodes, which represent the leading cause of death in this disease.
本研究旨在有助于阐明钩端螺旋体病过程中所见血小板减少症和出血素质的发病机制。本前瞻性研究纳入的病例组包括30例钩端螺旋体病患者,他们被收治于圣保罗大学医学院临床医院传染病和寄生虫病科病房。以下血小板减少症的可能机制已被考虑并因此进行了研究:由于弥散性血管内凝血导致的血小板消耗;由于血小板相关抗体导致的免疫介导的血小板破坏;以及骨髓中血小板生成受抑制。30例患者中有86.6%出现血小板减少症,似乎并非由血小板相关抗体介导的免疫反应所致。此外,似乎也不是由于弥散性血管内凝血消耗所致。尽管骨髓血小板生成与血小板计数之间存在统计学上的显著相关性,但我们认为,当外周血中的这些细胞正在被消耗时,骨髓穿刺液的静态显微镜检查无法准确描述血小板生成的动态机制。血管炎应被视为钩端螺旋体病出血紊乱发病机制的最重要因素。然而,我们认为,血小板减少症、尿毒症和凝血障碍,单独或作为一个整体,都应被列为导致和加重出血发作的促成因素,而出血发作是该疾病的主要死亡原因。