Omoregie R, Osakue S I, Ihemeje V, Omokaro E U, Ogeferet H O
School of Medical Laboratory Science, University of Benin Teaching Hospital, PMB 1111, Benin City, Edo State, Nigeria.
West Indian Med J. 2009 Nov;58(5):437-40.
To determine the effect of CD4 count on platelet count, prothrombin time (PT) and activated partial thromboplastin time (APTT) among HIV patients.
Blood samples were collected from 100 subjects consisting of 70 HIV treatment naive patients and 30 HIV seronegative individuals. Platelet count, CD4 count, PT and APTT were performed on the blood samples using standard techniques.
HIV-positive patients had significantly (p < 0.001) lower CD4 and platelet counts than HIV-negative subjects. Also, PT and APTT were significantly (p < 0.001) higher in HIV patients compared with their HIV negative counterparts. Among the HIV-infected patients, platelet count did not differ significantly (p > 0.05) between those with CD4 count < 200 cells//L and those with CD4 count 2 200 cells/microL. However PT and APTT were significantly (p < 0.005 and p < 0.001 respectively) higher in HIV patients with CD4 count < 200 cell/microL. Only PT significantly correlated with CD4 count (r = 0.5406, p < 0.001) and this correlation was observed only among HIV patients with CD4 count < 200 cell/pL (r = 0.6227, p < 0.001).
HIV patients with CD4 count < 200 cell/pL have higher PT and APTT values; PT only correlated with CD4 count and endothelial activation is suggested as the possible mechanism for the coagulation defect.
确定CD4细胞计数对HIV患者血小板计数、凝血酶原时间(PT)和活化部分凝血活酶时间(APTT)的影响。
采集100名受试者的血样,其中包括70例未接受过HIV治疗的患者和30例HIV血清学阴性个体。使用标准技术对血样进行血小板计数、CD4细胞计数、PT和APTT检测。
HIV阳性患者的CD4细胞计数和血小板计数显著低于HIV阴性受试者(p < 0.001)。此外,与HIV阴性患者相比,HIV患者的PT和APTT显著更高(p < 0.001)。在HIV感染患者中,CD4细胞计数<200个细胞/微升的患者与CD4细胞计数≥200个细胞/微升的患者之间血小板计数无显著差异(p > 0.05)。然而,CD4细胞计数<200个细胞/微升的HIV患者的PT和APTT显著更高(分别为p < 0.005和p < 0.001)。只有PT与CD4细胞计数显著相关(r = 0.5406,p < 0.001),且这种相关性仅在CD4细胞计数<200个细胞/微升的HIV患者中观察到(r = 0.6227,p < 0.001)。
CD4细胞计数<200个细胞/微升的HIV患者的PT和APTT值更高;只有PT与CD4细胞计数相关,提示内皮细胞活化可能是凝血缺陷的机制。