口腔卡波西肉瘤在hiv感染中的发病机制:血液和唾液中内源性糖皮质激素过量的相关性

C.O. Enwonwu
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引用次数: 4

摘要

内源性糖皮质激素过量,同时伴有高糖血症和唾液游离活性激素水平升高,是hiv感染/艾滋病患者的共同特征。口腔组织通过唾液几乎不间断地暴露于糖皮质激素的高负荷可能导致这些患者口腔卡波西肉瘤(KS)的高频率。艾滋病- ks细胞含有异常高水平的糖皮质激素受体蛋白,最近的研究表明,糖皮质激素在培养中显著刺激这些细胞的生长,特别是在生长因子存在的情况下,如癌他汀- m。糖皮质激素过量可能在艾滋病中KS的发病机制中起重要作用,这与新报道的KS相关疱疹病毒(KSHV)的病原学作用并不冲突,因为类固醇激素可能上调病毒基因的表达。后者与观察结果一致,即特定致癌病毒的感染并不一定导致人类癌症,确实需要其他细胞因素或事件的存在。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pathogenesis of oral Kaposi's sarcoma in HIV-infection: Relevance of endogenous glucocorticoid excess in blood and saliva

Endogenous glucocorticoid excess with concomitant hypercortisolaemia and increased saliva level of the free active hormone, is a common feature of HIV-infected/AIDS patients. Exposure of the oral tissues to virtually uninterrupted high burden of glucocorticoids through saliva may contribute to the high frequency of oral Kaposi's sacoma (KS) in these patients. AIDS-KS cells contain unusually high levels of glucocorticoid receptor protein and recent studies indicate that growth of these cells in culture is significantly stimulated by glucocorticoids, particularly in the presence of growth factors, such as oncostatin-M. The suggestion that glucocorticoid excess may be important in the pathogenesis of KS in AIDS is not in conflict with the suspected aetiological role of newly reported KS-associated herpesviruses (KSHV), since steroid hormones may upregulate the expression of the viral gene. The latter is consistent with the observation that infection by specific oncogenic viruses does not necessarily result in cancers in the human, and does require the presence of other cellular factors or events.

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