BACKGROUND AND AIM: It has been suggested that propranolol may have a protective effect on the development of spontaneous bacterial peritonitis by increasing the motility of the bowel and lowering the pressure of the portal vein. The aim of this study is to evaluate the association between the use of propranolol and development of spontaneous bacterial peritonitis in patients with cirrhosis and ascites. METHODS: We retrospectively evaluated 134 patients with cirrhosis and ascites admitted consecutively for a period of 2 years. Diagnosis of spontaneous bacterial peritonitis was based on an ascitic fluid neutrophilic count of >250/mm3 and/or a positive culture without evidence of secondary peritonitis. RESULTS: Spontaneous bacterial peritonitis was diagnosed in 39 of 134 (29%) patients and 12 of 39 (31%) patients died in hospital compared to only 4% (four of 95) of those without spontaneous bacterial peritonitis (P < 0.001). At admission, patients with spontaneous bacterial peritonitis, as compared to those without, had significantly more encephalopathy (28 vs 11%, P = 0.02) or fever (18 vs 4%, P = 0.01) and less frequently tense ascites (33 vs 57%, P = 0.02). Spontaneous bacterial peritonitis was diagnosed in six of 33 (18%) patients who did and in 33 of 101 (33%) who did not receive propranolol therapy (OR = 0.46, 95% CI: 0.17-1.22, P = 0.17). CONCLUSION: Our data indicate that spontaneous bacterial peritonitis significantly increases mortality in patients with cirrhosis. Propranolol therapy was not found to be associated with a significantly lower risk for spontaneous bacterial peritonitis, but a Type II statistical error cannot be definitely excluded. The potential protective effect of propranolol on the incidence of spontaneous bacterial peritonitis might deserve evaluation in properly designed prospective studies.
BACKGROUND AND AIM: It has been suggested that propranolol may have a protective effect on the development of spontaneous bacterial peritonitis by increasing the motility of the bowel and lowering the pressure of the portal vein. The aim of this study is to evaluate the association between the use of propranolol and development of spontaneous bacterial peritonitis in patients with cirrhosis and ascites. METHODS: We retrospectively evaluated 134 patients with cirrhosis and ascites admitted consecutively for a period of 2 years. Diagnosis of spontaneous bacterial peritonitis was based on an ascitic fluid neutrophilic count of >250/mm3 and/or a positive culture without evidence of secondary peritonitis. RESULTS: Spontaneous bacterial peritonitis was diagnosed in 39 of 134 (29%) patients and 12 of 39 (31%) patients died in hospital compared to only 4% (four of 95) of those without spontaneous bacterial peritonitis (P < 0.001). At admission, patients with spontaneous bacterial peritonitis, as compared to those without, had significantly more encephalopathy (28 vs 11%, P = 0.02) or fever (18 vs 4%, P = 0.01) and less frequently tense ascites (33 vs 57%, P = 0.02). Spontaneous bacterial peritonitis was diagnosed in six of 33 (18%) patients who did and in 33 of 101 (33%) who did not receive propranolol therapy (OR = 0.46, 95% CI: 0.17-1.22, P = 0.17). CONCLUSION: Our data indicate that spontaneous bacterial peritonitis significantly increases mortality in patients with cirrhosis. Propranolol therapy was not found to be associated with a significantly lower risk for spontaneous bacterial peritonitis, but a Type II statistical error cannot be definitely excluded. The potential protective effect of propranolol on the incidence of spontaneous bacterial peritonitis might deserve evaluation in properly designed prospective studies.