Cholongitas Evangelos, Papatheodoridis George V, Manesis Emanuel K, Burroughs Andrew K, Archimandritis Athanasios J
Second Department of Internal Medicine, Hippokration General Hospital of Athens, University of Athens School of Medicine, Greece.
J Gastroenterol Hepatol. 2006 Mar;21(3):581-7. doi: 10.1111/j.1440-1746.2005.03982.x.
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.
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.
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).
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.
有人提出，普萘洛尔可能通过增加肠道蠕动和降低门静脉压力，对自发性细菌性腹膜炎的发展具有保护作用。本研究的目的是评估普萘洛尔的使用与肝硬化腹水患者自发性细菌性腹膜炎发生之间的关联。
我们回顾性评估了连续2年收治的134例肝硬化腹水患者。自发性细菌性腹膜炎的诊断基于腹水中性粒细胞计数>250/mm³和/或培养阳性且无继发性腹膜炎证据。
134例患者中有39例（29%）被诊断为自发性细菌性腹膜炎，其中12例（31%）在医院死亡，而无自发性细菌性腹膜炎的患者中仅有4%（95例中的4例）死亡（P<0.001）。入院时，与无自发性细菌性腹膜炎的患者相比，有自发性细菌性腹膜炎的患者脑病（28%对11%，P=0.02）或发热（18%对4%，P=0.01）明显更多，而张力性腹水则较少见（33%对57%，P=0.02）。接受普萘洛尔治疗的33例患者中有6例（18%）被诊断为自发性细菌性腹膜炎，未接受普萘洛尔治疗的101例患者中有33例（33%）被诊断为自发性细菌性腹膜炎（比值比=0.46，95%置信区间：0.17-1.22，P=0.17）。
我们的数据表明，自发性细菌性腹膜炎显著增加肝硬化患者的死亡率。未发现普萘洛尔治疗与自发性细菌性腹膜炎风险显著降低相关，但不能完全排除II型统计错误。普萘洛尔对自发性细菌性腹膜炎发生率的潜在保护作用可能值得在设计合理的前瞻性研究中进行评估。
