Effects of coupled plasma filtration adsorption on immune function of patients with multiple organ dysfunction syndrome

Objective: To investigate the effects of coupled plasma filtration adsorption (CPFA) on the immune function of patients with multiple organ dysfunction syndrome (MODS). Methods: This study was a prospective, pilot, before-and-after self-crossover, clinical trial. Seven patients diagnosed with MODS and severe infection were randomly allocated to both 10 hours of CPFA and 10 hours of high-volume hemofiltration (HVHF) with a 12-hour interval and in random order. Serum concentrations of 7 cytokines including tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), interleukin-1 beta (IL-1 beta), interleukin-10 (IL-10), interleukin-1 receptor antagonist (IL-1Ra), and soluble tumor necrosis factor receptors 1 and 2 (sTNFR1 and sTNFR2) were measured during each treatment. The HLA-DR expression by the blood monocytes and the TNF-alpha production by the patients' blood ( both spontaneous and lipopolysaccharide stimulated) were tested before and after the treatment. TNF-alpha production of normal human monocytes (THP-1 cells) incubated in vitro with the patient plasma was also measured. Results: During CPFA, the fall in serum TNF-alpha and rise in serum IL-1Ra coincided with the rise in ratios of sTNFR2/TNF-alpha and IL-1Ra/IL-1 beta (p<0.05), which were different from those seen within HVHF (p<0.05). HLA-DR expression increased after CPFA (84.32% +/- 4.63% vs. 73.65% +/- 11.52%, p=0.037), but there was no change after HVHF (p>0.05). Spontaneous and lipopolysaccharide-induced TNF-alpha production increased over time with CPFA (p=0.038, p=0.034, respectively), but did not change with HVHF (p>0.05). Patient plasma suppressed the production of TNF-alpha by cultured normal monocytes. This effect decreased over time with CPFA (p=0.041), but there was no effect with HVHF (p>0.05). Conclusions: CPFA was superior to HVHF in increasing the ratios of antiinflammatory to proinflammatory mediators, improving antigen presentation ability, and restoring leukocyte responsiveness. These findings suggest a potential role for CPFA in the treatment of MODS. (IntJ Artif Organs 2009; 32: 31-8)