Severe acute respiratory syndrome (SARS) has recently recognized as a new human infectious disease. Anovel coronavirus was identified as the causative agent of SARS. This report summarizes the hematological findings inSARS patients and proposes a hypothesis for the pathophysiology of SARS coronavirus related abnormal hematopoiesis.Hematological changes in patients with SARS were common and included lymphopenia (68% -90% of adults; 100% ofchildren, n = 10), thrombocytopenia (20 % - 45 % of adults, 50 % of children), and leukopenia (20 % - 34 % of adults,70 % of children). The possible mechanisms of this coronavirus on blood system may include (1) directly infect blood cellsand bone marrow stromal cells via CD13 or CD66a; and/or (2) induce auto-antibodies and immune complexes to damagethese cells. In addition, lung damage in SARS patients may also play a role on inducing thrombocytopenia by (1)increasing the consumption of platelets/megakaryocytes; and/or (2) reducing the production of platelets in the lungs.Since the most common hematological changes in SARS patients were lymphopenia and immunodeficiency. We postulatethat hematopoietic growth factors such as G-CSF, by mobilizing endogenous blood stem cells and endogenous cytokines,could become a hematological treatment for SARS patients, which may enhance the immune system against these virus.%2002年11月在广东发现首例严重急性呼吸综合征(俗称"非典型性肺炎")病例.2003年2月世界卫生组织(WHO)在越南河内正式确认此疾病为新的人类传染病,并命名为严重急性呼吸综合征(severe acute respiratorysyndrome,SARS).2003年3月在香港发现其病原体为新的冠状病毒(coronavirus),称之为SARS冠状病毒(SARS-CoV).SARS患者常常出现异常的血液学改变,包括淋巴细胞减少(在成人为68%-90%;在儿童为100%,n=10),血小板减少(成人20%-45%,儿童50%),和白细胞减少(成人20%-34%,儿童70%).同时在部份患者D-二聚体水平可见升高.初步的研究表明SARS冠状病毒可侵犯造血细胞,但作用机制尚不清楚.我们推测其病理生理过程可能包括:(1)通过CD13或CD66a受体,SARS病毒直接侵入造血细胞或感染骨髓基质细胞等,加重细胞凋亡,引致造血抑制;(2)通过生成自身抗体或免疫复合物等免疫介导造成细胞损害.肺部损害也可部分解释血小板减少.肺部可能是成熟巨核细胞释出血小板的器官之一.SARS病人有广泛肺泡损害,包括充血、水肿、透明膜形成和肺纤维化,使肺部有效毛细血管床减少,从而血小板生成减少.同时,炎症损伤使肺部血小板聚集、血栓形成,也引致血小板消耗及破坏增加.由于SARS病人常有淋巴细胞减少及免疫功能受损,我们认为造血生长因子如G-CSF,通过动员自身造血干细胞和内源性生长因子,可以增强免疫功能对抗病毒.造血生长因子和造血干细胞在SARS的治疗上,可能有一定的价值.
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