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HIV感染中的内皮细胞功能障碍。

Endothelial cell dysfunction in HIV infection.

作者信息

Lafeuillade A, Alessi M C, Poizot-Martin I, Boyer-Neumann C, Zandotti C, Quilichini R, Aubert L, Tamalet C, Juhan-Vague I, Gastaut J A

机构信息

CISIH, Hôpital Salvator, Marseille, France.

出版信息

J Acquir Immune Defic Syndr (1988). 1992;5(2):127-31.

PMID:1531074
Abstract

We have investigated plasma levels of endothelial cell products playing a role in hemostasis in 125 HIV-positive patients and 30 controls. Antigenic von Willebrand factor increased significantly with disease progression and was closely correlated with CD4+ cell counts and beta 2-microglobulin levels. Tissue-type plasminogen activator was normal in CDC II/III and CDC IVC2 patients and was slightly increased in AIDS patients, whereas plasminogen activator inhibitor was increased in each group, the stage of the disease not having any effect. Mean total protein S levels were lower in HIV-positive patients and, in 27.2% of the cases, were associated with a decrease in free protein S levels. Such abnormalities could be responsible for a hypercoagulable state in these patients and could be explained by endothelial cell damage during HIV infection. Whether this injury is due to HIV itself remains to be further investigated.

摘要

我们研究了125例HIV阳性患者和30例对照者体内参与止血过程的内皮细胞产物的血浆水平。随着疾病进展,血管性血友病因子抗原水平显著升高,且与CD4+细胞计数及β2-微球蛋白水平密切相关。在疾病控制中心(CDC)II/III期和CDC IV C2期患者中,组织型纤溶酶原激活剂水平正常,而在艾滋病患者中略有升高,而纤溶酶原激活剂抑制剂在每组中均升高,疾病阶段对此无任何影响。HIV阳性患者的总蛋白S平均水平较低,在27.2%的病例中,与游离蛋白S水平降低有关。这些异常可能导致这些患者出现高凝状态,并且可以用HIV感染期间的内皮细胞损伤来解释。这种损伤是否由HIV本身引起仍有待进一步研究。

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