Aim: The aim of this study was to observe the effects of coupled plasma filtration adsorption (CPFA) on septic patients with multiple organ dysfunction syndrome (MODS). Methods: A total of 14 patients were randomly divided into two groups, and, respectively, received 10 h of CPFA or high-volume hemofiltration (HVHF). The mean arterial pressure (MAP), electrolytes and acid-base balance, the sequential organ failure assessment (SOFA) score, and the acute physiology and chronic health evaluation II (APACHE II) score were analyzed. Serum levels of high-mobility group box-1 (HMGB-1) protein, tumor necrosis factor-α (TNF-α), and intercellular adhesion molecule-1 (ICAM-1) were also measured by enzymelinked immunosorbent assay. Results: After CPFA and HVHF, temporary reduction in blood urea nitrogen and serum creatinine, electrolytes and acid-base metabolism balance were well maintained. Both the SOFA and the APACHE II scores were markedly reduced after CPFA (p < 0.01), while only the SOFA score was significantly decreased after HVHF (p < 0.05). After 10-h treatment with CPFA, the MAP and oxygen index (PaO 2 /FiO 2 ) were significantly higher than those at 0 h. Furthermore, the serum levels of HMGB-1, ICAM-1, and TNF-α decreased after 10 h of CPFA (p < 0.05), while the serum levels of HMGB-1 declined at 5 h of HVHF, but rebounded at 10 h, and the serum levels of TNF-α and ICAM-1 were no significant change after treatment with HVHF. Conclusions: The study indicated that CPFA could be superior to HVHF in improving the clinical manifestations and eliminating inflammatory mediators, which had implications in the optimal treatment of septic patients with MODS.
TNF-α and IL12B 3'UTR gene polymorphisms may be associated with HBV susceptibility and IL-10 gene polymorphisms may be related to the HBV persistence infection in Chinese Han HD patients.
Background and aims: The aim of this study was to investigate the possible influence of tumor necrosis factor-α (TNF-α) gene promoter polymorphisms on the hepatitis C virus (HCV) infection in Chinese hemodialysis (HD) patients. Methods: A total of 884 HD patients from 14 HD centers in south China were investigated. The TNF-α gene promoter polymorphisms at positions 238 and 308 of the patients were detected by the polymerase chain reaction (PCR)-restriction fragment length polymorphism method. Results: Among the 884 patients, 176 (19.9%) were anti-HCV (+), and 142 (80.7%) of the anti-HCV (+) patients became chronically infected. The anti-HCV (+) patients showed longer duration of HD, higher rate of blood transfusion, kidney transplantation, and dialyzer reuse, compared with the anti-HCV (−) patients. However, the distributions of TNF-α −238 and −308 alleles and genotypes had no significant differences between the anti-HCV (+) and the anti-HCV (−) patients (p > 0.05). And the frequencies of the above alleles and genotypes were also approximately equally distributed in the persistent infection and in the viral clearance HD patients (p > 0.05). Conclusions: This study did not suggest that the TNF-α −238 and −308 polymorphisms had influence on the infection of HCV in Chinese HD patients.
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