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      Diabetes mellitus, insulin resistance and hepatitis C virus infection: A contemporary review

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          Abstract

          AIM

          To summarise the literature data on hepatitis C virus (HCV)-infected patients concerning the prevalence of glucose abnormalities and associated risk.

          METHODS

          We conducted a PubMed search and selected all studies found with the key words "HCV" or "hepatitis C virus" and "diabetes" or "insulin resistance". We included only comparative studies written in English or in French, published from January 2000 to April 2015. We collected the literature data on HCV-infected patients concerning the prevalence of glucose abnormalities [diabetes mellitus (DM) and insulin resistance (IR)] and associated risk [ i.e., severe liver fibrosis, response to antivirals, and the occurrence of hepatocellular carcinoma (HCC)].

          RESULTS

          HCV infection is significantly associated with DM/IR compared with healthy volunteers and patients with hepatitis B virus infection. Glucose abnormalities were associated with advanced liver fibrosis, lack of sustained virologic response to interferon alfa-based treatment and with a higher risk of HCC development. As new antiviral therapies may offer a cure for HCV infection, such data should be taken into account, from a therapeutic and preventive point of view, for liver and non-liver consequences of HCV disease. The efficacy of antidiabetic treatment in improving the response to antiviral treatment and in decreasing the risk of HCC has been reported by some studies but not by others. Thus, the effects of glucose abnormalities correction in reducing liver events need further studies.

          CONCLUSION

          Glucose abnormalities are strongly associated with HCV infection and show a negative impact on the main liver related outcomes.

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          Metabolic factors and risk of hepatocellular carcinoma by chronic hepatitis B/C infection: a follow-up study in Taiwan.

          San-Lin You, Hwai-I Yang, Ding Chen … (2008)
          This study investigated whether obesity, diabetes, and other metabolic factors are independently associated with hepatocellular carcinoma (HCC), stratified by hepatitis B virus (HBV) and hepatitis C virus (HCV) serostatus, and explored the possible joint influence of obesity/diabetes and HBV/HCV infections on the risk of HCC. A total of 23,820 residents in Taiwan were recruited and followed up for 14 years. All analyses were stratified by hepatitis B surface antigen (HBsAg) and antibody to HCV (anti-HCV) at enrollment, and 218 subjects positive for both seromarkers were excluded. Incident HCC cases were identified via linkage to the national cancer registry. Multivariate-adjusted relative risk (RR(a)) and 95% confidence interval (95% CI) were estimated using Cox proportional hazards models. Extreme obesity (body mass index >or=30 kg/m(2)) was independently associated with a 4-fold risk of HCC (RR(a), 4.13; 95% CI, 1.38-12.4) among anti-HCV-seropositive subjects and a 2-fold risk (RR(a), 2.36; 95% CI, 0.91-6.17) in persons without HBV and HCV infections, after controlling for other metabolic components, but not in HBsAg-seropositive subjects (RR(a), 1.36; 95% CI, 0.64-2.89). Diabetes was associated with HCC in all 3 groups, with the highest risk in those with HCV infection (RR(a), 3.52; 95% CI, 1.29-9.24) and lowest in HBV carriers (RR(a), 2.27; 95% CI, 1.10-4.66). We found more than 100-fold increased risk in HBV or HCV carriers with both obesity and diabetes, indicating synergistic effects of metabolic factors and hepatitis. The finding that both obesity and diabetes are predictors of HCC risk, possibly differently depending on HBV and HCV infection status, may shed some light in preventing HCC.
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            Hepatitis C infection and risk of diabetes: a systematic review and meta-analysis.

            H Serag, Tyler D. White, Vlad Ratziu (2008)
            Several studies found hepatitis C (HCV) increases risk of Type II diabetes mellitus (DM). However, others found no or only sub-group specific excess risk. We performed meta-analyses to examine whether HCV infection does increase DM risk in comparison to the general population and in other sub-groups with increased liver disease rates including with hepatitis B (HBV). We followed standard guidelines for performance of meta-analyses. Two independent investigators identified eligible studies through structured keyword searches in relevant databases including PubMed. We identified 34 eligible studies. Pooled estimators indicated significant DM risk in HCV-infected cases in comparison to non-infected controls in both retrospective (OR(adjusted)=1.68, 95% CI 1.15-2.20) and prospective studies (HR(adjusted)=1.67, 95% CI 1.28-2.06). Excess risk was also observed in comparison to HBV-infected controls (OR(adjusted)=1.80, 95% CI 1.20-1.40) with suggestive excess observed in HCV+/HIV+ cases in comparison to HIV+ controls (OR(unadjusted)=1.82, 95% CI 1.27-2.38). Our finding of excess DM risk with HCV infection in comparison to non-infected controls is strengthened by consistency of results from both prospective and retrospective studies. The excess risk observed in comparison to HBV-infected controls suggests a potential direct viral role in promoting DM risk, but this needs to be further examined.
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              Prevalence of type 2 diabetes mellitus among persons with hepatitis C virus infection in the United States.

              Shruti Mehta, S Strathdee, Chris Thomas … (2000)
              Hepatitis C virus (HCV) infection may contribute to the development of diabetes mellitus. This relationship has not been investigated at the population level, and its biological mechanism remains unknown. To examine the prevalence of type 2 diabetes among persons with HCV infection in a representative sample of the general adult population of the United States. Cross-sectional national survey. The Third National Health and Nutrition Examination Survey, 1988-1994. 9841 persons older than 20 years of age for whom data on HCV infection and diabetes were complete. The presence of diabetes was ascertained by using American Diabetes Association guidelines based on fasting plasma glucose measurement and medication history. Presence of HCV infection was assessed by testing for serum HCV-specific antibodies (anti-HCV). Of the 9841 persons evaluated, 8.4% had type 2 diabetes and 2.1% were anti-HCV positive. Type 2 diabetes occurred more often in persons who were older, were nonwhite, had a high body mass index, and had low socioeconomic status. Type 2 diabetes was less common in persons who acknowledged previous illicit drug use. After adjustment for these factors, persons 40 years of age or older with HCV infection were more than three times more likely than those without HCV infection to have type 2 diabetes (adjusted odds ratio, 3.77 [95% CI, 1.80 to 7.87]). None of the 19 persons with type 1 diabetes were anti-HCV positive. In the United States, type 2 diabetes occurs more often in persons with HCV infection who are older than 40 years of age.
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                Author and article information

                Journal
                Journal ID (nlm-ta): World J Gastroenterol
                Journal ID (iso-abbrev): World J. Gastroenterol
                Journal ID (publisher-id): WJG
                Title: World Journal of Gastroenterology
                Publisher: Baishideng Publishing Group Inc
                ISSN (Print): 1007-9327
                ISSN (Electronic): 2219-2840
                Publication date (Print): 7 March 2017
                Publication date (Electronic): 7 March 2017
                Volume: 23
                Issue: 9
                Pages: 1697-1711
                Affiliations
                Anne-Claire Desbois, Patrice Cacoub, Inflammation-Immunopathology-Biotherapy Department, Sorbonne Universités, 75005 Paris, France
                Anne-Claire Desbois, Patrice Cacoub, UMR_S 959, French National Institute of Health and Medical Research, 75013 Paris, France
                Anne-Claire Desbois, Patrice Cacoub, FRE3632, The French National Center for Scientific Research, 75005 Paris, France
                Anne-Claire Desbois, Patrice Cacoub, Department of Internal Medicine and Clinical Immunology, Groupe Hospitalier Pitié-Salpêtrière, AP-HP, 75013 Paris, France
                Author notes

                Author contributions: Desbois AC and Cacoub P designed research, contributed to new reagents or analytic tools, analyzed data, and wrote the paper; Desbois AC performed research.

                Correspondence to: Patrice Cacoub, MD, PhD, professor, Department of Internal Medicine and Clinical Immunology, Groupe Hospitalier Pitié-Salpêtrière, AP-HP, 83 boulevard de l'hôpital, 75013 Paris, France. patrice.cacoub@ 123456aphp.fr

                Telephone: +33-1-42178009 Fax: +33-1-42178033

                Article
                Other ID: jWJG.v23.i9.pg1697
                DOI: 10.3748/wjg.v23.i9.1697
                PMC ID: 5340821
                PubMed ID: 28321170
                SO-VID: c17c1832-5f90-448b-8bc3-16b9444f91ee
                Copyright © ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
                License:

                This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

                History
                Date received : 3 October 2016
                Date revision received : 10 November 2016
                Date accepted : 7 February 2017
                Categories
                Subject: Systematic Reviews

                Keywords: hepatitis c virus,diabetes mellitus,insulin resistance,liver fibrosis,treatment
                Data availability:
                Keywords: hepatitis c virus, diabetes mellitus, insulin resistance, liver fibrosis, treatment

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