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Volume 48, Issue 5, Pages 721-727 (May 2008)


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Effect of sustained virological response to treatment on the incidence of abnormal glucose values in chronic hepatitis C

Manuel Romero-Gómez1Corresponding Author Informationemail address, Conrado M. Fernández-Rodríguez2, Raúl J. Andrade3, Moisés Diago4, Sonia Alonso2, Ramón Planas5, Ricard Solá6, José A. Pons7, Javier Salmerón8, Rafael Barcena9, Ramón Perez10, Isabel Carmona11, Santiago Durán12

Received 25 September 2007; received in revised form 25 October 2007; accepted 1 November 2007. published online 15 January 2008.

Background/Aims

To investigate the effect of sustained virological response (SVR) on impaired fasting glucose (IFG) and/or type 2 diabetes (T2DM); to assess the influence of glucose abnormalities on the SVR rate.

Methods

1059 patients with chronic HCV; normal glucose (< 100mg/dl) in 734, IFG (between 100 and 125mg/dl) in 218, and T2DM (⩾126mg/dl) in 107 cases, were treated with interferon plus ribavirin over 24 or 48 weeks, depending on viral genotype.

Results

The SVR rate was lower in patients with IFG and/or T2DM than in patients with normal glucose concentrations [143/325 (44%) vs. 432/734 (58.8%); P=0.002]. In the follow-up, abnormal glucose concentrations were observed in 74 of 304 (24.3%) non-responders and in 49 of 430 (11.4%) sustained responders (log-rank: 13.8; P=0.00002). Reverse stepwise logistic regression analysis identified the independent variables predictive of IFG or T2DM development as: sustained response (OR: 0.44; 95%CI=0.20–0.97; P=0.004) and fibrosis stage (OR: 1.46; 95%CI=1.06–2.01;P=0.02). Family history of DM, steatosis, gender, HCV viral load, genotype, triglycerides, cholesterol and BMI did not enter the multivariate analysis equation.

Conclusions

SVR reduces the risk of IFG and/or T2DM development in patients with chronic hepatitis C while altered glucose metabolism impairs sustained response to viral treatment.

Associate Editor: M.P. Manns

1 Unit for the Clinical Management of Digestive Diseases and CIBEREHD, Hospital Universitario de Valme, Seville, Spain

2 Gastroenterology Unit, Fundación Hospital Alcorcón, Madrid, Spain

3 Hepatology Unit, Hospital Universitario Virgen de la Victoria, Malaga, Spain

4 Hepatology Unit, Hospital General de Valencia, Valencia, Spain

5 Hepatology Unit, Hospital Germans Trias i Pujol, Barcelona, Spain

6 Hepatology Section, Hospital del Mar, Barcelona, Spain

7 Hepatology Section, Hospital Arrixaca, Murcia, Spain

8 Digestive Unit, Hospital San Cecilio, Granada, Spain

9 Hepatology Unit, Hospital Ramón y Cajal, Madrid, Spain

10 Digestive Unit, Hospital Central de Asturias, Oviedo, Spain

11 Digestive Departament, Hospital Virgen Macarena, Seville, Spain

12 Endocrinology Unit, Hospital Universitario de Valme, Seville, Spain

Corresponding Author InformationCorresponding author. Tel.: +34 955 01 57 69; fax: +34 955 01 58 85.

 The authors who have taken part in the research of this paper declared that they do not have a relationship with the manufacturers of the drug involved either in the past or present and they did not receive funding from the manufacturers to carry out their research. They did not receive funding from any source to carry out this study.

PII: S0168-8278(08)00010-X

doi:10.1016/j.jhep.2007.11.022


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