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Relationship of smoking and fibrosis in patients with chronic hepatitis C.

Publication ,  Journal Article
Dev, A; Patel, K; Conrad, A; Blatt, LM; McHutchison, JG
Published in: Clin Gastroenterol Hepatol
June 2006

BACKGROUND & AIMS: Preliminary studies have suggested that in patients with chronic hepatitis C (CHC), cigarette smoking increases the risk for developing liver fibrosis. 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 (s-Flt) and kinase insert domain receptor (s-KDR). These cytokine levels are increased in animals with cirrhosis and in human beings with CHC. We studied whether the concentrations of VEGF, VEGF-D, s-Flt, and s-KDR were increased in CHC smokers with and without hepatic fibrosis. METHODS: A total of 170 CHC patients were identified retrospectively from a single center's database. In 59 patients, serum levels of VEGF, VEGF-D, s-Flt, and s-KDR were measured using an enzyme-linked immunosorbent assay. RESULTS: All 170 patients were hepatitis C virus RNA positive, 117 (69%) were men, 43 (25%) were smokers, and their mean (+/-SD) age was 47 (+/-6) years. Overall, 21% of smokers had Metavir fibrosis scores of 3 and 4 compared with 14% of nonsmokers (P < .01). In an age-weighted multivariate model using step-wise logistic regression, smoking, infection with hepatitis C virus genotype 1, male sex, and increased VEGF-D concentration all were significant independent predictors of more severe liver fibrosis (P < .05 for all observations). CONCLUSIONS: These data suggest that CHC patients who smoke may have more hepatic fibrosis. The data also suggest that increased VEGF and VEGF-D concentrations are associated with smoking and may be involved in the molecular mechanisms of fibrogenesis.

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Published In

Clin Gastroenterol Hepatol

DOI

ISSN

1542-3565

Publication Date

June 2006

Volume

4

Issue

6

Start / End Page

797 / 801

Location

United States

Related Subject Headings

  • Vascular Endothelial Growth Factor Receptor-2
  • Vascular Endothelial Growth Factor Receptor-1
  • Vascular Endothelial Growth Factor D
  • Vascular Endothelial Growth Factor B
  • Vascular Endothelial Growth Factor A
  • Smoking
  • Sex Factors
  • Receptor Protein-Tyrosine Kinases
  • Male
  • Liver Cirrhosis
 

Citation

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ICMJE
MLA
NLM
Dev, A., Patel, K., Conrad, A., Blatt, L. M., & McHutchison, J. G. (2006). Relationship of smoking and fibrosis in patients with chronic hepatitis C. Clin Gastroenterol Hepatol, 4(6), 797–801. https://doi.org/10.1016/j.cgh.2006.03.019
Dev, Anouk, Keyur Patel, Andrew Conrad, Lawrence M. Blatt, and John G. McHutchison. “Relationship of smoking and fibrosis in patients with chronic hepatitis C.Clin Gastroenterol Hepatol 4, no. 6 (June 2006): 797–801. https://doi.org/10.1016/j.cgh.2006.03.019.
Dev A, Patel K, Conrad A, Blatt LM, McHutchison JG. Relationship of smoking and fibrosis in patients with chronic hepatitis C. Clin Gastroenterol Hepatol. 2006 Jun;4(6):797–801.
Dev, Anouk, et al. “Relationship of smoking and fibrosis in patients with chronic hepatitis C.Clin Gastroenterol Hepatol, vol. 4, no. 6, June 2006, pp. 797–801. Pubmed, doi:10.1016/j.cgh.2006.03.019.
Dev A, Patel K, Conrad A, Blatt LM, McHutchison JG. Relationship of smoking and fibrosis in patients with chronic hepatitis C. Clin Gastroenterol Hepatol. 2006 Jun;4(6):797–801.
Journal cover image

Published In

Clin Gastroenterol Hepatol

DOI

ISSN

1542-3565

Publication Date

June 2006

Volume

4

Issue

6

Start / End Page

797 / 801

Location

United States

Related Subject Headings

  • Vascular Endothelial Growth Factor Receptor-2
  • Vascular Endothelial Growth Factor Receptor-1
  • Vascular Endothelial Growth Factor D
  • Vascular Endothelial Growth Factor B
  • Vascular Endothelial Growth Factor A
  • Smoking
  • Sex Factors
  • Receptor Protein-Tyrosine Kinases
  • Male
  • Liver Cirrhosis