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论中毒性休克综合征的发病机制。

On the pathogenesis of toxic shock syndrome.

作者信息

Kass E H, Parsonnet J

机构信息

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115.

出版信息

Rev Infect Dis. 1987 Sep-Oct;9 Suppl 5:S482-9. doi: 10.1093/clinids/9.supplement_5.s482.

Abstract

Understanding of the pathogenesis of toxic shock syndrome (TSS) has come from the juxtaposition of epidemiologic, clinical, immunologic, and physiologic studies. A hypothesis has been developed for the pathogenesis of menstrually related TSS. Certain tampon fibers that are highly absorbent for water are also ion exchangers for magnesium ions. The latter ions uniquely affect the production of TSS toxin 1 (TSST-1) by appropriate strains of Staphylococcus aureus, with a marked increase in the amount of toxin when magnesium concentrations are limiting and suppression of toxin production when magnesium is in excess. Many epidemiologic features of TSS could be explained by this hypothesis. The absorbability of highly absorptive fibers is not affected by the addition of small amounts of magnesium sufficient to suppress production of TSST-1; thus absorption is distinguishable from toxin production in vitro. TSST-1 stimulates production of interleukin 1 and of tumor necrosis factor and is highly toxic when absorbed slowly. Like TSST-1, staphylococcal enterotoxins are lethal to rabbits when given by slow injection, and some enterotoxins may be more lethal than TSST-1.

摘要

对中毒性休克综合征(TSS)发病机制的认识来自流行病学、临床、免疫学和生理学研究的结合。关于与月经相关的TSS的发病机制已形成一种假说。某些对水具有高吸收性的棉塞纤维也是镁离子的离子交换剂。后一种离子独特地影响金黄色葡萄球菌的合适菌株产生TSS毒素1(TSST - 1),当镁浓度受限毒素量会显著增加,而镁过量时毒素产生受到抑制。该假说可以解释TSS的许多流行病学特征。高吸收性纤维的吸收性不受足以抑制TSST - 1产生的少量镁添加的影响;因此在体外吸收与毒素产生是可区分的。TSST - 1刺激白细胞介素1和肿瘤坏死因子的产生,缓慢吸收时具有高毒性。与TSST - 1一样,葡萄球菌肠毒素缓慢注射给兔子时是致命的,并且一些肠毒素可能比TSST - 1更具致死性。

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