is the high FreQUENCY of diabetes type 2 in chronic hepatitis c virus infection due to strong family history?

Fawad Qureshi, Faisal Qureshi, Qudsia Anjum Fasih and Sarwar Zuberi

Division of Medicine, Ziauddin Medical University and Hospitals, Karachi, Pakistan


Various epidemiological studies have suggested that hepatitis C virus (HCV) infection is a risk factor for the development of diabetes mellitus (DM) type 2.1-6 The etiological factors were initially thought to be cirrhosis but further studies differentiating between HCV and hepatitis B virus (HBV) related infection have shown that patient with HCV infection have a higher prevalence of Diabetes mellitus type-2.7

A retrospective analysis of 1117 patients with chronic viral hepatitis found that diabetes was present in significantly more patients with hepatitis C compared to hepatitis B virus (HBV) infection (21 versus 12 percent).2 HCV genotype 2a was over represented among the diabetic patients. In another case control trial, the prevalence of HCV infection was significantly higher among patients with diabe-tes mellitus compared to controls (4.2 versus 1.6 percent). Patients undergoing liver transplantation for HCV also appear to be at increased risk for developing diabetes mellitus following transplantation 8.

The cause of these associations is unknown, but their magnitude may be overestimated based upon the retrospective nature of the reports and due to some of the following factors.9

a.        Patients with diabetes have more parenteral exposures than the general population, placing them at increased risk for transmission of viruses.

b.       HCV infection becomes chronic more often than HBV infection.

c.        Not all studies are controlled for the presence of cirrhosis, which may be associated with impaired glucose tolerance.

Only one study that we came across which was from Saudi Arabia had mentioned other variables and showed that Anti-HCV-positive type-2 diabetics, when compared to non-diabetics, had a higher Body mass index (BMI), a frequent family history of DM, elevated serum transaminases, thrombocytopenia, and liver cirrhosis on biopsy.10 With this hypothesis in mind, we conducted the present study to determine other variables such as familial inheritance as the cause of higher frequency of DM type 2 among patients with HCV infection.


This was an analysis of cases seen in an outpatient department of a private medical university hospital between July 2002 - Jan 2003. Phone calls were made to the patients if data was not completely found in the charts. A total of 212 patients with DM type 2 were retrieved, out of which 100 were HCV positive and 112 were HCV negative. HCV was detected either by detection of antibodies to HCV or HCV RNA in the serum. Family trees were drawn on each patient with emphasis on history of DM type 2 in any family member. According to this, two groups: one with HCV positive and the other group with HCV negative patients were made. Each group was divided into five categories as follows. 2 patients from HCV negative group were excluded as their parents adopted them and therefore family history was not available.


Out of selected cases, 100 were HCV positive and 112 were HCV negative. In both the groups, 68% patients were males, and there was no significant difference between males and females (p=0.98) ratio in the two groups. Mean age was 46 years in both groups (range 30-74 years in group 1) vs (range 26-70 years in group 2).

There was no significant difference in history of DM among both or one parents in both the groups (p=0.18). On the other hand, a significant difference was observed in history of DM in siblings in the two groups (p=0.026) as shown in the table.

Table-1: Relationship of Diabetes mellitus type 2 and Hepatitis C Virus infection


HCV + DM +


History of DM type 2





In one parent





In both parents





In siblings





In relatives other than first degree





No family history







We found that DM type 2 occurred with increasing frequency among patients with Hepatitis C. In our group of patients, we explained that increased occurrence was associated with family history of DM. This variable effect may be one of the reasons of higher frequency of DM type 2 in this group of patients. A prospective study comparing the incidence and prevalence of DM type 2 in HCV infected and non-infected patients are warranted which may further detect other variables explaining this effect.


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2.        Mason AL, Lau JY, Hoang N, Qian K, Alexander GJ, Xu L, et al. Association of diabetes mellitus and chronic hepatitis C virus infection. Hepatology 1999;29:328-33.

3.        Simo R, Hernandez C, Genesca J, Jardi R, Mesa J. High prevalence of hepatitis C virus infection in diabetic patients. Diabetes Care 1996;19:998-1000.

4.        Caronia S, Taylor K, Pagliaro L, Carr C, Palazzo U, Petrik J, et al. Further evidence for an association between non-insulin-dependent diabetes mellitus and chronic hepatitis C virus infection. Hepatology 1999;30:1059-63.

5.        Okan V, Araz M, Aktaran S, Karsligil T, Meram I, Bayraktaroglu Z, et al. Increased frequency of HCV but not HBV infection in type 2 diabetic patients in Turkey. Int J Clin Pract 2002;56:175-7.

6.        Mehta SH, Brancati FL, Sulkowski MS, Strathdee SA, Szklo M, Thomas DL. Prevalence of type 2 diabetes mellitus among persons with hepatitis C virus infection in the United States. Ann Intern Med 2000;133:592-99.

7.        Fraser GM, Harman I, Meller N, Niv Y, Porath A. Diabetes mellitus is associated with chronic hepatitis C but not chronic hepatitis B virus infection. Isr J Med Sci 1996;32:526.

8.        Bigam DL, Pennington JJ, Carpentier A, Wanless IR, Hemming AW, Croxford R et al. Hepatitis C-related cirrhosis: A predictor of diabetes after liver transplantation. Hepatology 2000;32:87-90.

9.        Hadziyannis S, Karamanos B. Diabetes mellitus and chronic hepatitis C virus infection (editorial). Hepatology 1999; 29:604-5.

10.     Akbar DH, Siddique AM, Ahmed MM. Prevalence of Type-2 diabetes in patients with hepatitis C and B virus infection in Jeddah, Saudi Arabia. Med Princ Pract 2002;11:82-5.


Address for Correspondence:

Dr. Fawad Qureshi, Division of Medicine, Ziauddin Medical University and Hospitals, Karachi, Pakistan.