Pellicelli A M, Palmieri F, Cicalini S, Petrosillo N
Istituto Nazionale per le Malattie Infettive, Lazzaro Spallanzani, IRCCS, Rome, Italy.
Ann N Y Acad Sci. 2001 Nov;946:82-94. doi: 10.1111/j.1749-6632.2001.tb03904.x.
Human immunodeficiency virus (HIV)-related pulmonary hypertension (HRPR) is a cardiovascular complication of HIV infection that has been recognized in the last years with increasing frequency. The etiology of HRPH is unknown. All the attempts to isolate HIV on pulmonary vessels in HRPH patients failed, and an indirect role for HIV in this disease has been hypothesized. Current theories on the pathogenesis focus on abnormalities of endothelial and smooth muscle cells of pulmonary vasculature. Endothelial and smooth muscle cell injury could be due to a high production or to a reduced clearance of cytokines in these patients. In fact, in several studies high levels of ET-1, IL-1alpha, IL-6 and PDGF in primary pulmonary hypertension (PPH) and in HRPH have been found. HIV gp 120 could induce the production of these cytokines by a stimulation of monocytes/macrophages. A high alpha1-adrenoreceptors stimulation of pulmonary vessels could be also implicated in the pathogenesis of HRPH. Chronic hypoxia is observed with increased frequency in HIV patients, and this could induce a chronic stimulation of alpha1-receptors of pulmonary vasculature with typical pathological changes. However, only a small percentage of HIV- patients develop HRPH. This observation suggests the existence of an idiosyncratic susceptibility to the development of vascular disease. This susceptibility could have a genetic basis, and might be determined by particular major histocompatibility complex alleles.
人类免疫缺陷病毒（HIV）相关肺动脉高压（HRPR）是HIV感染的一种心血管并发症，在过去几年中其被认识到的频率越来越高。HRPH的病因尚不清楚。在HRPH患者的肺血管上分离HIV的所有尝试均失败，因此推测HIV在这种疾病中起间接作用。目前关于发病机制的理论集中在肺血管内皮细胞和平滑肌细胞的异常。内皮细胞和平滑肌细胞损伤可能是由于这些患者细胞因子产生过多或清除减少所致。事实上，在多项研究中发现，原发性肺动脉高压（PPH）和HRPH患者体内ET-1、IL-1α、IL-6和血小板衍生生长因子（PDGF）水平较高。HIV gp 120可通过刺激单核细胞/巨噬细胞诱导这些细胞因子的产生。肺血管的高α1-肾上腺素能受体刺激也可能与HRPH的发病机制有关。在HIV患者中慢性缺氧的发生率增加，这可能会导致肺血管α1-受体的慢性刺激并伴有典型的病理变化。然而，只有一小部分HIV患者会发生HRPH。这一观察结果表明存在对血管疾病发展的特异易感性。这种易感性可能有遗传基础，并且可能由特定的主要组织相容性复合体等位基因决定。
