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重度吸烟与肝脏

Heavy smoking and liver.

作者信息

El-Zayadi Abdel-Rahman

机构信息

Hepatology and Gastroenterology, Ain Shams University and Director of Cairo Liver Center. 5, El-Gergawy St. Dokki, Giza, Egypt.

出版信息

World J Gastroenterol. 2006 Oct 14;12(38):6098-101. doi: 10.3748/wjg.v12.i38.6098.

Abstract

Smoking causes a variety of adverse effects on organs that have no direct contact with the smoke itself such as the liver. It induces three major adverse effects on the liver: direct or indirect toxic effects, immunological effects and oncogenic effects. Smoking yields chemical substances with cytotoxic potential which increase necro-inflammation and fibrosis. In addition, smoking increases the production of pro-inflammatory cytokines (IL-1, IL-6 and TNF- alpha) that would be involved in liver cell injury. It contributes to the development of secondary polycythemia and in turn to increased red cell mass and turnover which might be a contributing factor to secondary iron overload disease promoting oxidative stress of hepatocytes. Increased red cell mass and turnover are associated with increased purine catabolism which promotes excessive production of uric acid. Smoking affects both cell-mediated and humoral immune responses by blocking lymphocyte proliferation and inducing apoptosis of lymphocytes. Smoking also increases serum and hepatic iron which induce oxidative stress and lipid peroxidation that lead to activation of stellate cells and development of fibrosis. Smoking yields chemicals with oncogenic potential that increase the risk of hepatocellular carcinoma (HCC) in patients with viral hepatitis and are independent of viral infection as well. Tobacco smoking has been associated with suppression of p53 (tumour suppressor gene). In addition, smoking causes suppression of T-cell responses and is associated with decreased surveillance for tumour cells. Moreover, it has been reported that heavy smoking affects the sustained virological response to interferon (IFN) therapy in hepatitis C patients which can be improved by repeated phlebotomy. Smoker's syndrome is a clinico-pathological condition where patients complain of episodes of facial flushing, warmth of the palms and soles of feet, throbbing headache, fullness in the head, dizziness, lethargy, prickling sensation, pruritus and arthralgia.

摘要

吸烟会对诸如肝脏等与烟雾本身没有直接接触的器官产生多种不良影响。它对肝脏会引发三种主要的不良影响:直接或间接的毒性作用、免疫作用和致癌作用。吸烟会产生具有细胞毒性潜力的化学物质,从而增加坏死性炎症和纤维化。此外,吸烟会增加促炎细胞因子(白细胞介素 -1、白细胞介素 -6 和肿瘤坏死因子 -α)的产生,这些细胞因子会参与肝细胞损伤。吸烟会导致继发性红细胞增多症的发生,进而使红细胞数量和周转率增加,这可能是促进肝细胞氧化应激的继发性铁过载疾病的一个促成因素。红细胞数量和周转率的增加与嘌呤分解代谢增加有关,而嘌呤分解代谢增加会促进尿酸的过度产生。吸烟通过阻止淋巴细胞增殖和诱导淋巴细胞凋亡来影响细胞介导的免疫反应和体液免疫反应。吸烟还会增加血清铁和肝铁,从而诱导氧化应激和脂质过氧化,导致星状细胞活化和纤维化的发展。吸烟会产生具有致癌潜力的化学物质,这会增加病毒性肝炎患者患肝细胞癌(HCC)的风险,并且与病毒感染无关。吸烟与 p53(肿瘤抑制基因)的抑制有关。此外,吸烟会导致 T 细胞反应受到抑制,并与对肿瘤细胞的监测减少有关。而且,据报道,重度吸烟会影响丙型肝炎患者对干扰素(IFN)治疗的持续病毒学应答,而通过反复放血可以改善这种情况。吸烟者综合征是一种临床病理状况,患者会抱怨出现面部潮红、手掌和脚底发热、搏动性头痛、头部胀满、头晕、嗜睡、刺痛感、瘙痒和关节痛等症状。

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