Editorial
Copyright ©2006 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Oct 14, 2006; 12(38): 6098-6101
Published online Oct 14, 2006. doi: 10.3748/wjg.v12.i38.6098
Heavy smoking and liver
Abdel-Rahman El-Zayadi
Abdel-Rahman El-Zayadi, Department of Tropical Medicine, Ain Shams University and Director of Cairo Liver Center, Cairo, Egypt
Correspondence to: Professor Abdel-Rahman El-Zayadi, MD, Hepatology and Gastroenterology, Ain Shams University and Director of Cairo Liver Center. 5, El-Gergawy St. Dokki, Giza, Egypt. clcz@tedata.net.eg
Telephone: +202-7-603002 Fax: +202-7-481900
Received: January 25, 2006
Revised: January 28, 2006
Accepted: February 28, 2006
Published online: October 14, 2006
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 necroinflammation and fibrosis. In addition, smoking increases the production of pro-inflammatory cytokines (IL-1, IL-6 and TNF-α) 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 supression 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’ssyndrome 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.

Keywords: Iron overload; Interferon response; Hepatitis C virus; Smoking; Fibrosis; Hepatocellular carcinoma; Polycythemia