Role of immunosuppression in the development of quinolone-resistant Escherichia coli spontaneous bacterial peritonitis and in the mortality of E. coli spontaneous bacterial peritonitis.

BACKGROUND: Norfloxacin decreases the incidence of spontaneous bacterial peritonitis in cirrhotics, but promotes the appearance of quinolone-resistant Escherichia coli. AIM: : To define the characteristics of quinolone-resistant E. coli spontaneous bacterial peritonitis. METHODS: E. coli-positive ascitic fluid cultures were identified during a 6-year period. Data on quinolone-sensitive and quinolone-resistant E. coli spontaneous bacterial peritonitis were compared. RESULTS: One hundred and two E. coli-positive ascitic fluid cultures were detected. Cirrhotics accounted for 67 cases. Spontaneous bacterial peritonitis was found in 47 of the 67 (70%) cases [35 (74%) caused by quinolone-sensitive and 12 (26%) caused by quinolone-resistant E. coli]. Norfloxacin prophylaxis was higher in the quinolone-resistant group (92% vs. 6%, P < 0.001). Compared with patients with quinolone-sensitive E. coli spontaneous bacterial peritonitis, those with quinolone-resistant E. coli spontaneous bacterial peritonitis showed a higher prevalence of associated immunosuppressive factors (immunosuppressive drugs, human immunodeficiency virus infection or cancer) (92% vs. 20%, P < 0.001). Steroid therapy was independently associated with quinolone-resistant E. coli spontaneous bacterial peritonitis (odds ratio, 49; 95% confidence interval, 3.4-699; P = 0.004). The Child-Pugh score (P = 0.03), immunosuppression (P = 0.02) and renal failure (P = 0.01) were independent predictors of E. coli spontaneous bacterial peritonitis-related mortality. CONCLUSIONS: Associated immunosuppression is an important co-factor for the development of quinolone-resistant E. coli spontaneous bacterial peritonitis and for E. coli spontaneous bacterial peritonitis-related mortality.

Nitric oxide may contribute to nocturnal hemodynamic changes in cirrhotic patients.

OBJECTIVE: Patients with liver cirrhosis have a nocturnal worsening of hemodynamic parameters that has been associated with an increased risk of variceal bleeding at nighttime. The aim of this study was to investigate whether nitric oxide and cytokines are implicated in these hemodynamic changes. METHODS: Ten cirrhotic patients and eight controls were studied. Mean blood pressure, heart rate, plasma norepinephrine, tumor necrosis factor alpha and interleukin-6 levels, and serum nitrite + nitrate levels were determined at 0800, 1600, and 2400 h. All determinations were performed in supine rest and at least 4 h after meals. In a second study, nitrite + nitrate levels were assessed in 10 cirrhotic patients before and after eating a standard meal. RESULTS: Mean arterial pressure levels that were always lower in the patient group showed a nocturnal decrease in both groups of subjects. Heart rate values that were always higher in cirrhotic patients showed a nocturnal fall in controls, whereas cirrhotics maintained elevated values at nighttime. Norepinephrine levels were higher in cirrhotics and maintained similar values during the study, whereas controls had a significant nocturnal decrease. Nitrite + nitrate levels that were higher in cirrhotic patients showed a significant mean increase of 40% from morning (0800 h) to night (2400 h) in the patient group, whereas in controls no change was observed (p < 0.05). Tumor necrosis factor alpha and interleukin-6 levels did not change either in patients or controls during the entire period. Cirrhotic patients with or without ascites maintained a pattern of hemodynamic and biochemical changes similar to the pattern observed in the entire group of patients. Finally, no changes in serum nitrite + nitrate levels were observed in patients before and after eating the standard meal. CONCLUSION: An increased nocturnal nitric oxide production might contribute to the hemodynamic changes observed in cirrhotic patients during nighttime.