Ballem P J, Belzberg A, Devine D V, Lyster D, Spruston B, Chambers H, Doubroff P, Mikulash K
Department of Medicine, St. Paul's Hospital, Vancouver, British Columbia, Canada.
N Engl J Med. 1992 Dec 17;327(25):1779-84. doi: 10.1056/NEJM199212173272503.
Isolated thrombocytopenia accompanied by increased amounts of platelet-associated antibody is a common manifestation of human immunodeficiency virus (HIV) infection, and the thrombocytopenia often improves with zidovudine. It is not clear whether the mechanism of HIV-related thrombocytopenia primarily involves autoimmune destruction of platelets or reduced platelet production by megakaryocytes.
We studied the survival of 111In-labeled autologous platelets and performed platelet imaging in 24 men with isolated HIV-related thrombocytopenia (16 who received no treatment and 8 who received zidovudine). We also studied 20 HIV-infected men with normal platelet counts (10 who received no treatment and 10 who received zidovudine) and studied 12 healthy seronegative men as controls.
Mean (+/- SD) platelet survival was significantly decreased in both the untreated and the zidovudine-treated patients with HIV-related thrombocytopenia (to 92 +/- 33 and 129 +/- 44 hours, respectively; both P < 0.001), as compared with the normal controls (198 +/- 15 hours). Mean platelet survival was also significantly decreased in the HIV-infected patients with normal platelet counts (untreated, 162 +/- 23 hours, P < 0.01; zidovudine-treated, 166 +/- 35 hours, P < 0.05). Imaging studies, however, revealed no evidence of increased clearance of autologous platelets in the liver or spleen in any of these groups. Mean platelet production was significantly depressed in the untreated patients with thrombocytopenia (23,000 +/- 11,000 platelets per cubic millimeter per day, P < 0.001) as compared with the healthy controls (45,000 +/- 6,000 per cubic millimeter per day). Mean platelet production was significantly increased, however, in the men treated with zidovudine, both in those with thrombocytopenia (60,000 +/- 31,000 platelets per cubic millimeter per day, P < 0.01 vs. controls) and in those without thrombocytopenia (68,000 +/- 22,000 per cubic millimeter per day, P < 0.01).
Although there was a moderate reduction in platelet survival in HIV-infected persons, these patients, regardless of platelet counts, also had decreased production of platelets, possibly due to viral infection of the megakaryocytes. Zidovudine appears to improve platelet production.
孤立性血小板减少症伴有血小板相关抗体量增加是人类免疫缺陷病毒（HIV）感染的常见表现，且血小板减少症通常用齐多夫定治疗后会改善。目前尚不清楚HIV相关血小板减少症的机制主要是涉及血小板的自身免疫性破坏还是巨核细胞产生血小板减少。
我们研究了111In标记的自体血小板的存活情况，并对24例孤立性HIV相关血小板减少症男性患者（16例未接受治疗，8例接受齐多夫定治疗）进行了血小板成像。我们还研究了20例HIV感染且血小板计数正常的男性患者（10例未接受治疗，10例接受齐多夫定治疗），并以12例健康血清学阴性男性作为对照。
与正常对照组（198±15小时）相比，未治疗和接受齐多夫定治疗的HIV相关血小板减少症患者的平均（±标准差）血小板存活时间均显著缩短（分别降至92±33小时和129±44小时；P均<0.001）。血小板计数正常的HIV感染患者的平均血小板存活时间也显著缩短（未治疗组为162±23小时，P<0.01；接受齐多夫定治疗组为166±35小时，P<0.05）。然而，成像研究显示，这些组中的任何一组均未发现肝脏或脾脏中自体血小板清除增加的证据。与健康对照组（每立方毫米每天45,000±6,000个血小板）相比，未治疗的血小板减少症患者的平均血小板生成显著降低（每立方毫米每天23,000±11,000个血小板，P<0.001）。然而，接受齐多夫定治疗的男性，无论是血小板减少症患者（每立方毫米每天60,000±31,000个血小板，与对照组相比P<0.01）还是无血小板减少症患者（每立方毫米每天68,000±22,000个血小板，P<0.01），其平均血小板生成均显著增加。
尽管HIV感染者的血小板存活时间有适度缩短，但这些患者无论血小板计数如何，血小板生成也均减少，这可能是由于巨核细胞受到病毒感染所致。齐多夫定似乎可改善血小板生成。
