Small intestinal bacterial overgrowth versus antimicrobial capacity in patients with spontaneous bacterial peritonitis

Background: Spontaneous bacterial peritonitis (SBP) is a serious infection in cirrhotic patients with ascites. Both defects in the host defense mechan isms and the enhancement of the offensive factor (small intestinal bacteria l overgrowth (SIBO)) may contribute to the development of SEP. Therefore, t he aim of this study was to evaluate the role of SIBO versus various antimi crobial capacities in the pathogenesis of SEP in cirrhotic patients. Method s: Forty-five cirrhotic patients were enrolled in this study. Bacterial ove rgrowth was evaluated by breath hydrogen test (BH2T). The hepatic reticuloe ndothelial system phagocytic index (HRESPI) was measured by intravenously i njected colloid suspensions. Results: The Child-Pugh scores in the SEP grou p were higher than in the non-SEP group (10.5 +/- 2.0 versus 8.0 +/- 1.8, P < 0.01). The ascitic protein concentration was significantly lower in the SEP group than in the non-SEP group (897 +/- 475 mg/l versus 1325 +/- 453 m gn, P < 0.01). Furthermore, the serum C-3 concentration was lower in the SE P group than in the non-SEP group (43.1 +/- 13.6 ng/dl versus 73.2 +/- 26.4 ng/dl, P < 0.01). The serum C-4 concentration was also lower in the SEP gr oup than in the non-SEP group (12.4 +/- 4.0 ng/dl versus 16.9 +/- 6.6 ng/dl , P < 0.05). The incidence of SIBO was higher in the SEP group than in the non-SBP group (68.2% versus 17.4%, P < 0.01). HRESPI values were significan tly higher in the two groups of cirrhotic patients than in the normal refer ence. However, there were no statistical differences in HRESPI between the two groups (8.4 +/- 2.8 min in the SEP group versus 7.9 +/- 2.8 min in the non-SEP group). Conclusions: The results of this study showed that the hepa tic reticuloendothelial function is impaired in cirrhotic patients, but the degree of impairment does not differ between patients with and without pre vious history of SEP. Lower ascitic total protein, lower serum C-3 and C-4 concentrations, and presence of SIBO are all risk factors for SEP. Based on the results of our study, defects in the host defense mechanisms and the e nhancement of the offensive factor (SIBO) may act in concert for the develo pment of SEP.