肿瘤坏死因子α
血液透析
医学
发病机制
内科学
超滤(肾)
内分泌学
阿尔法(金融)
化学
外科
生物化学
结构效度
患者满意度
作者
A DREISBACH,T Hendrickson,Donald H. Beezhold,Lee Ann Riesenberg,A.H. Sklar
标识
DOI:10.1177/039139889802100204
摘要
Postdialysis fatigue (PDF) has been ascribed to excessive ultrafiltration and decline in osmolality during hemodialysis. We evaluated the potential role for the sommogenic cytokines, interleukin-1 beta (IL-1β) and tumor necrosis factor alpha (TNFα), in the genesis of PDF. Patients dialyzing with cuprophane membrane were assigned to PDF (N=25) and non-PDF (N=25) groups based on a fatigue index questionnaire. Pre- and postdialysis samples were obtained from 3 consecutive treatments and later assayed for serum levels of IL-1β and TNFα by ELISA. Our results show significant intradialytic elevation of TNFα in both non-PDF groups (non-PDF: pre- 3.36±0.80 pg/ml to post 3.75±0.88 pg/ml, p<0.04; PDF: pre- 5.95±0.80 pg/ml to post- 8.66±1.35 pg/ml, p<0.02). The degree of intradialytic augmentation was significantly greater for TNFα in the PDF group (46 ± 18% vs 11 ± 5%; p<0.03). There were no significant intradialytic changes in serum levels of IL-1β in either the PDF or non-PDF groups. There also were no significant differences in dialysis-related body weights, systolic blood pressures, or osmolalities. These findings suggest that TNFα may be involved in the pathogenesis of PDF. (Int J Artif Organs 1998; 21:83–6)
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