Dănulescu Răzvana Munteanu, Ciobică A, Stanciu C, Trifan Anca
Discipline of Gastroenterology and Hepatology University Alexandru loan Cuza, Iaşi.
Department of Biology, University of Medicine and Pharmacy Grigore T. Popa, Iaşi.
Rev Med Chir Soc Med Nat Iasi. 2013 Jul-Sep;117(3):598-604.
Bacterial infections play an important role in liver cirrhosis complications, being together with variceal bleeding and hepatic encephalopathy an important cause of morbidity and mortality in cirrhotic patients. Spontaneous bacterial peritonitis (SBP) is a major complication of liver cirrhosis, with a significant mortality. Recent studies have demonstrated the involvement of oxygen free radicals in the pathogenesis of liver cirrhosis, but the role of oxidative stress in the development of SBP is not very clear yet.
This study aims to evaluate the role of oxidative stress in the pathogenesis of spontaneous bacterial peritonitis and its changes after therapy.
The study is a prospective case-control, which included 33 patients divided into 3 groups: group I- 10 patients with decompensated cirrhosis and SBP, group II - 17 patients diagnosed with decompensated liver cirrhosis with ascites, and group Ill - 6 patients with compensated liver cirrhosis. The control group consisted of 19 healthy subjects recruited from hospital staff, adapted to patients by age and sex. Malonildyaldehida (MDA), a product of lipid peroxidation, was dosed in the blood and ascitic fluid of patients by assay thiobarbituric acid reactive substances (TBARS).
Serum MDA significantly increased in the group with decompensated cirrhosis and SBP compared with the control group. MDA levels in ascitic fluid showed a statistically significant increase in the SBP group compared with patients without SBP. There was a decrease of MDA after 6 months of antibiotic treatment compared with the initial stage, while MDA values increased in the absence of treatment.
The study demonstrates the increased oxidative stress markers in the blood and ascitic fluid of cirrhotic patients with SBP, which can be considered a predictor of SBP and also a marker of treatment response.
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细菌感染在肝硬化并发症中起重要作用,与静脉曲张破裂出血和肝性脑病一起,是肝硬化患者发病和死亡的重要原因。自发性细菌性腹膜炎(SBP)是肝硬化的主要并发症,死亡率很高。最近的研究表明氧自由基参与了肝硬化的发病机制,但氧化应激在SBP发生发展中的作用尚不完全清楚。
本研究旨在评估氧化应激在自发性细菌性腹膜炎发病机制中的作用及其治疗后的变化。
本研究为前瞻性病例对照研究,纳入33例患者,分为3组:I组-10例失代偿期肝硬化合并SBP患者,II组-17例诊断为失代偿期肝硬化腹水患者,III组-6例代偿期肝硬化患者。对照组由19名从医院工作人员中招募的健康受试者组成,根据年龄和性别与患者匹配。通过检测硫代巴比妥酸反应物质(TBARS)来测定患者血液和腹水中脂质过氧化产物丙二醛(MDA)的含量。
与对照组相比,失代偿期肝硬化合并SBP组血清MDA显著升高。与无SBP患者相比,SBP组腹水MDA水平有统计学意义的升高。与初始阶段相比,抗生素治疗6个月后MDA下降,而未治疗时MDA值升高。
本研究表明,肝硬化合并SBP患者血液和腹水中氧化应激标志物增加,可被视为SBP的预测指标及治疗反应的标志物。
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