title: Is smoking a prognostic factor in patients with chronic hepatitis C?
abstract: The progression of chronic liver diseases is characterized by a common histopathological pathway comprising fibrosis formation and distortion of hepatic architecture which are the hallmark of evolution to cirrhosis. Several factors are responsible for the severity and progression of chronic hepatitis C. Here, we describe the most important data regarding the association between regular smoking and histological hepatic lesions. Some reports have shown that the proportion of patients with moderate or significant histological activity gradually increases with the daily consumption of tobacco. Moreover, fibrosis is associated with regular smoking in some studies. However, controversies result from other studies. Nicotine is mainly metabolised by the liver, and its administration in experimental animals showed development of steatosis and focal or confluent hepatic necrosis, probably linked to the oxidative stress associated with lipid peroxidation. In chronic hepatitis C patients, preliminary studies have suggested that hypoxia caused by smoking may induce expression of the cytokines vascular endothelial growth factor (VEGF) and VEGF-D and their corresponding soluble tyrosine kinase receptors fms-like tyrosine kinase receptor and kinase insert domain receptor. Since this issue is controversial and smoking is in any case unsafe, stopping is recommended for patients with liver diseases.
authors.affiliation: Department of Gastroenterology and Digestive Endoscopy, Pellegrini Hospital, Naples, Italy.
authors.forename: L
authors.initials: L
authors.lastname: De Luca
authors.forename: C
authors.initials: C
authors.lastname: De Angelis
authors.forename: S
authors.initials: S
authors.lastname: Fagoonee
authors.forename: S
authors.initials: S
authors.lastname: Di Bella
authors.forename: M
authors.initials: M
authors.lastname: Rizzetto
authors.forename: R
authors.initials: R
authors.lastname: Pellicano
mesh_terms: D000818:Animals; D016207:Cytokines / Q000378:metabolism; D018450:Disease Progression; D019317:Evidence-Based Medicine; D019698:Hepatitis C, Chronic / Q000150:complications / Q000175:diagnosis / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D000860:Hypoxia / Q000139:chemically induced; D015227:Lipid Peroxidation / Q000187:drug effects; D008103:Liver Cirrhosis / Q000209:etiology / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects; D011379:Prognosis; D020794:Receptor Protein-Tyrosine Kinases / Q000187:drug effects; D012307:Risk Factors; D012720:Severity of Illness Index; D012907:Smoking / Q000009:adverse effects*; D042461:Vascular Endothelial Growth Factor A / Q000187:drug effects; D042643:Vascular Endothelial Growth Factor D / Q000187:drug effects
chemical_list: D016207:Cytokines; D042461:Vascular Endothelial Growth Factor A; D042643:Vascular Endothelial Growth Factor D; D020794:Receptor Protein-Tyrosine Kinases