Effects of Coupled Plasma Filtration Adsorption on Immune Function of Patients with Multiple Organ Dysfunction Syndrome

Abstract

To investigate the effects of coupled plasma filtration adsorption (CPFA) on the immune function of patients with multiple organ dysfunction syndrome (MODS). 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-1beta (IL-1beta), 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. 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-1beta (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). 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.