Yang Mo, Ng Margaret H L, Li Chi Kong
Department of Paediatrics, The Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong.
Hematology. 2005 Apr;10(2):101-5. doi: 10.1080/10245330400026170.
Severe Acute Respiratory Syndrome (SARS) has been recognized as a new human infectious disease caused by a novel coronavirus (SARS-CoV). Hematological changes in patients with SARS were common, including notably lymphopenia and thrombocytopenia. While the former is the result of decreases in CD4+ or CD8+ T-lymphocytes related to the onset of disease or use of glucocorticoids, the latter may involve a number of potential mechanisms. Although the development of autoimmune antibodies or immune complexes triggered by viral infection may play a significant role in inducing thrombocytopenia, SARS-CoV may also directly infect hematopoietic stem/progenitor cells, megakaryocytes and platelets inducing their growth inhibition and apoptosis. Moreover, the increased consumption of platelets and/or the decreased production of platelets in the damaged lungs are a potential alternative mechanism that can contribute to thrombocytopenia in severe critical pulmonary conditions, which has been rarely revealed and will be discussed.
严重急性呼吸综合征(SARS)已被确认为一种由新型冠状病毒(SARS-CoV)引起的新型人类传染病。SARS患者的血液学变化很常见,尤其包括淋巴细胞减少和血小板减少。前者是与疾病发作或使用糖皮质激素相关的CD4+或CD8+ T淋巴细胞减少的结果,而后者可能涉及多种潜在机制。虽然病毒感染引发的自身免疫抗体或免疫复合物的产生可能在诱导血小板减少中起重要作用,但SARS-CoV也可能直接感染造血干/祖细胞、巨核细胞和血小板,导致其生长抑制和凋亡。此外,受损肺中血小板消耗增加和/或血小板生成减少是导致严重危重症肺部疾病患者血小板减少的一种潜在替代机制,这一点很少被揭示,将在此进行讨论。