Role of serum complement, immunoglobulins, and cell-mediated immune system in the pathogenesis of spontaneous bacterial peritonitis (SBP).

Spontaneous bacterial peritonitis (SBP) is a common complication of advanced liver disease, which has a reported prevalence of between 4 and 27%. Frequent bacteremias due to inadequate host defense mechanisms, particularly the reticuloendothelial system (RES), with seeding of an ascitic fluid that lacks a normal opsonic activity, is believed to be the principal cause of SBP. Little data exist as to the role of serum levels of complement and immunoglobulins as well as the cell-mediated immune system in the pathogenesis of SBP. The aim of this study was to determine the serum levels of the third and fourth components of complement (C3, C4), total hemolytic complement activity (CH100), and properdin factor B (PFB) and immunoglobulins G, A, and M and various T-cell parameters in individuals admitted to hospital with ascites and advanced liver disease and to determine whether one or more of these factors could be used to predict the development of SBP in patients with advanced liver disease. Fourteen consecutive patients (nine male and five female; age 47.5±3.1 years, mean±Sem) with end-stage liver disease and ascites, who were evaluated for possible liver transplant at the University of Pittsburgh and who developed SBP, comprised the study group. The diagnosis of SBP was determined by positive ascitic fluid culture (three patients) and/or ascitic fluid neutrophil count of>250 cells/mm3 (all patients). The control group consisted of 14 patients, matched for type of liver disease, age, and sex, who did not develop SBP. Each patient studied underwent a prospective elective abdominal paracentesis, and the recovered fluid was assayed for total protein, total white blood cell count, total neutrophil count, and culture. The immunological status of each individual was accomplished by determining the serum levels of C3, C4, PFB, CH100, and immunoglobulins G, A, and M. Finally the percentage of lymphocytes and their distribution in the various T-cell subsets was determined also. No difference in the immunological status between these two groups was evident. However, the ascitic fluid protein level, although not significantly different between the two groups studied, was less than 2 g/dl more often in the group developing SBP than in the control group that did not subsequently develop SBP. The estimated risk for developing SBP in individuals with ascitic fluid protein level of <2 g/dl was increased eightfold (95% CI: 50.05, 1.28) compared to those with ascitic fluid total protein levels above this cutoff level. Based on these data, it is concluded that serum immunoglobulin and complement levels and the cell-mediated immune system activity are similar in patients with advanced liver disease who develop and do not develop SBP. Thus, these parameters cannot be used as predictors for the development of SBP. In contrast, the ascitic fluid protein level was found to be a simple readily measurable parameter capable of identifying patients at high risk for the development of SBP.