Association between Hepatitis C Virus Infection and Diabetes Mellitus

Mehta, Shruti H.; Strathdee, Steffanie A.; Thomas, David L.

doi:10.1093/oxfordjournals.epirev.a000808

Cited by 40 publications

(22 citation statements)

References 65 publications

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“…Experiments on transgenic mice have provided evidence for the contribution of HCV in the development of insulin resistance in HCV infection, which eventually leads to type II diabetes (Shintani et al, 2004). Overall, epidemiologic and biological data both suggest that the association between HCV infection and diabetes is real and appears to be causally linked, at least in predisposed individuals (older and overweight), as recently reviewed (Mehta et al, 2001;. However, few data are available on the interaction between diabetes and HCV infection in HCC risk.…”

Section: Diabetes and Hepatocellular Carcinomamentioning

confidence: 96%

Southern Europe as an example of interaction between various environmental factors: a systematic review of the epidemiologic evidence

et al. 2006

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Hepatitis B virus (HBV), hepatitis C virus (HCV) and alcohol consumption are major causes of hepatocellular carcinoma (HCC) worldwide. We performed a systematic review of epidemiologic studies carried out on HCC aetiology in Southern Europe, an area with an intermediatehigh prevalence of these agents as well as of putative risk factors such as tobacco smoking, diabetes and obesity. To retrieve the articles, we performed a Medline search for titles and abstracts of articles. After the Medline search, we reviewed the papers and reference lists to identify additional articles. A synergism between HCV infection and HBV infection, overt (hepatitis B virus antigen (HbsAg) positivity) or occult (HBsAg negativity with presence of HBV DNA in liver or serum), is suggested by the results of some studies. The pattern of the risk for HCC due to alcohol intake shows a continuous dose-effect curve without a definite threshold, although most studies found that HCC risk increased only for alcohol consumption above 40-60 g of ethanol per day. Some evidence supports a positive interaction of alcohol intake probably with HCV infection and possibly with HBV infection. A few studies found that coffee has a protective effect on HCC risk due to various risk factors. Some data also support a role of tobacco smoking, diabetes and obesity as single agents or preferably cofactors in causing HCC. In countries with a relatively high alcohol consumption and intermediate levels of HCV and HBV infections (1-3% of population infected by each virus), such as Mediterranean countries, the three main risk factors together account for about 85% of the total HCC cases, leaving little space to other known risk factors, such as haemochromatosis, and to new, still unrecognised, factors as independent causes of HCC.

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Section: Diabetes and Hepatocellular Carcinomamentioning

confidence: 96%

Southern Europe as an example of interaction between various environmental factors: a systematic review of the epidemiologic evidence

et al. 2006

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“…Chronic HCV infection has been associated with a number of extrahepatic manifestations including mixed cryoglobulinemia and glomerulonephritis. A high prevalence of diabetes mellitus (DM) among nontransplant patients with hepatitis C (50 -62%) was first reported in 1994 by Allison et al (2) and has since been corroborated by multiple studies (3)(4)(5). In addition, a higher prevalence of HCV antibodies has also been found among type 2 diabetic patients when compared with normal controls (6,7).…”

mentioning

confidence: 90%

Hepatitis C virus is independently associated with increased insulin resistance after liver transplantation

et al. 2004

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“…1,5,6 Some individuals with chronic HCV develop a number of extrahepatic comorbidities, ranging from autoimmune manifestations to disorders such as diabetes. [7][8][9][10] A geographic gradient with respect to autoimmune manifestations in HCV may exist. For example, the presence of cryoglobulins and autoantibodies is largely a southern European phenomenon.…”

Section: Introductionmentioning

confidence: 99%

Host genetic determinants in hepatitis C virus infection

2004

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In addition to viral and environmental/behavioural factors, host genetic diversity is believed to contribute to the spectrum of clinical outcomes in hepatitis C virus (HCV) infection. This paper reviews the literature with respect to studies of host genetic determinants of HCV outcome and attempts to highlight trends and synthesise findings. With respect to the susceptibility to HCV infection, several studies have replicated associations of the HLA class II alleles DQB1*0301 and DRB1*11 with selflimiting infection predominantly in Caucasian populations. Meta-analyses yielded summary estimates of 3.0 (95% CI: 1.8-4.8) and 2.5 (95% CI: 1.7-3.7) for the effects of DQB1*0301 and DRB1*11 on self-limiting HCV, respectively. Studies of genetics and the response to interferon-based therapies have largely concerned single-nucleotide polymorphisms and have been inconsistent. Regarding studies of genetics and the progression of HCV-related disease, there is a trend with DRB1*11 alleles and less severe disease. Studies of extrahepatic manifestations of chronic HCV have shown an association between DQB1*11 and DR3 with the formation of cryoglobulins. Some important initial observations have been made with respect to genetic determinants of HCV outcome. Replication studies are needed for many of these associations, as well as biological data on the function of many of these polymorphisms.

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Association between Hepatitis C Virus Infection and Diabetes Mellitus

Cited by 40 publications

References 65 publications

Southern Europe as an example of interaction between various environmental factors: a systematic review of the epidemiologic evidence

Southern Europe as an example of interaction between various environmental factors: a systematic review of the epidemiologic evidence

Hepatitis C virus is independently associated with increased insulin resistance after liver transplantation

Host genetic determinants in hepatitis C virus infection

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