Viral Hepatitis
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Oct 15, 2004; 10(20): 2963-2966
Published online Oct 15, 2004. doi: 10.3748/wjg.v10.i20.2963
Impact of cigarette smoking on response to interferon therapy in chronic hepatitis C Egyptian patients
A. El-Zayadi, Osaima Selim, H. Hamdy, A. El-Tawil, Hanaa M. Badran, M. Attia, A. Saeed
A. El-Zayadi, H. Hamdy, Departments of Tropical Medicine, Ain Shams University, Cairo, Egypt
Osaima Selim, Department of Clinical Pathology, Ain Shams University, Cairo, Egypt
A. El-Tawil, Department of Pathology, Ain Shams University, Cairo, Egypt
Hanaa M. Badran, Department of Hepatology, National Liver Institute, Menoufeya, Egypt
M. Attia, Department of Hepatology and Gastroenterology, Theodor Bilharz Research Institute, Cairo, Egypt
A. Saeed, Cairo Liver Center, Giza, Egypt
Author contributions: All authors contributed equally to the work.
Correspondence to: Professor A. El-Zayadi, Cairo Liver Center, 5 El-Gergawy St., Dokki, Giza, Egypt.
Telephone: +202-7603002 Fax: +202-7481900
Received: February 3, 2004
Revised: February 14, 2004
Accepted: March 13, 2004
Published online: October 15, 2004

AIM: Smoking may affect adversely the response rate to interferon-α . Our objective was to verify this issue among chronic hepatitis C patients.

METHODS: Over the year 1998, 138 chronic hepatitis C male Egyptian patients presenting to Cairo Liver Center, were divided on the basis of smoking habit into: group I which comprised 38 smoker patients ( > 30 cigarettes/d) and group II which included 84 non-smoker patients. Irregular and mild smokers (16 patients) were excluded. Non eligible patients for interferon-α therapy were excluded from the study and comprised 3/38 (normal ALT) in group I and 22/84 in group II (normal ALT, advanced cirrhosis and thrombocytopenia). Group I was randomly allocated into 2 sub-groups: group Ia comprised 18 patients who were subjected to therapeutic phlebotomy while sub-group Ib consisted of 17 patients who had no phlebotomy. In sub-group Ia, 3 patients with normal ALT after repeated phlebotomies were excluded from the study. Interferon-α 2b 3 MU/TIW was given for 6 mo to 15 patients in group Ia, 17 patients in group Ib and 62 patients in group II. Biochemical, virological end-of- treatment and sustained responses were evaluated.

RESULTS: At the end of interferon-α treatment, ALT was normalized in 3/15 patients (20%) in group Ia and 2/17 patients (11.8%) in group Ib compared to17/62 patients (27.4%) in group II (P = 0.1). Whereas 2/15 patients (13.3%) in group Ia. and 2/17 patients (11.8%) in group Ib lost viraemia compared to 13/62 patients (26%) in group II (P = 0.3). Six months later, ALT was persistently normal in 2/15 patients (13.3%) in group 1a and 1/17 patients (5.9%) in group Ib compared to 9/62 patients (14.5%) in group II (P = 0.47). Viraemia was eliminated in 1/15 patients (6.7%) in group Ia and 1/17 patients (5.9%) in group Ib compared to 7/62 patients (11.3%) in group II, but the results did not mount to statistical significance (P = 0.4).

CONCLUSION: Smokers suffering from chronic hepatitis C tend to have a lower response rate to interferon-α compared to non-smokers. Therapeutic phlebotomy improves the response rate to interferon-α therapy among this group.

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