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Study of diabetes mellitus among patients with hepatitis C virusMona Abdel Raoufa, Zeinab A. Yousrya, Olfat M. Hindyb, Somayh S. Eissaa
and Dalia S. Solimanc
aDepartment of Internal Medicine, Faculty of Medicinefor Girls, AL-Azhar University, bDepartment of ClinicalPathology, National Liver Institute, El-MenoufyaUniversity and cDepartment of Internal Medicine,Police Authority Hospital
Correspondence to Somayh S. Eissa, 131 SakerQuriesh, New Maadi, Cairo, EgyptTel: + 01 113 754 668;e-mail: [email protected]
Received 1 February 2012Accepted 15 April 2012
The Egyptian Journal of Internal Medicine
2012, 24:17–23
Introduction
Hepatitis C virus (HCV) infection and type 2 diabetes are two common disorders with
high impact on health worldwide. There is growing evidence to support the concept
that HCV is associated with type 2 diabetes.
Purpose
This work aimed to study the clinical phenotype of type 2 diabetes in HCV patients.
Patients and methods
Our study was conducted upon 100 nonobese, noncirrhotic hepatitis C positive
patients who were classified into two groups according to homeostatic model
assessment (HOMA) test for insulin resistance (HOMA IR). This study also included
15 nonobese type 2 diabetic patients negative for HCV and hepatitis B virus infection
classified as control groups. We excluded alcoholics and drug addicts and patients
with conditions that affect blood glucose such as endocrine diseases associated with
disordered glucose metabolism and use of drugs. All participants were subjected to
full history taking and complete clinical examination including BMI and the following
early event in chronic HCV infection, occurring in 20% of
nonobese patients with minimal fibrosis. Metabolic
abnormalities further exacerbate insulin resistance and
contribute toward progression of fibrosis. In contrast,
there was no association between HOMA IR values and
the presence of advanced fibrosis or a faster progression of
fibrosis [24]. Our study showed that the clinical
phenotype associated with type 2 diabetes is character-
ized by higher blood pressure, older age, higher BMI,
serum triglycerides, and lower HDL cholesterol levels
than HCV-positive patients; similar results were obtained
by Antonelli et al. [2]. We found that patients with type 2Ta
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Figure 1
Number of patients HCV positive for diabetes and the number ofpatients HCV negative for diabetes. HCV, hepatitis C virus.
Figure 2
Comparison of steatosis between HCV + DM + patients (HOMAIRZ3) and among HCV + DM – patients (HOMA IRo3). HCV,hepatitis C virus; HOMA IR, homeostatic model assessment test forinsulin resistance.
Figure 3
Comparison of the stage of fibrosis between HOMA IRZ3 and HOMAIRo3. HOMA IR, homeostatic model assessment test for insulinresistance.
diabetes, noncirrhotic HCV positive (NC-HCV +), had
lower BMI than the type 2 diabetic control group; the
same result was obtained by Antonelli et al. [25]. In this
study, a highly significant positive correlation was found
between HOMA IR and BMI among HCV patients.
Negro et al. [23] reported that BMI is an independent
predictor of insulin resistance in HCV infection. Also, we
found a negative correlation between steatosis and BMI
in hepatitis C-positive patients, which is in agreement
with the findings of Lecube et al. [26]. Similar findings
were obtained by Castera et al. [27], who concluded that
mild steatosis may be associated with high BMI and
moderate to severe steatosis is more likely to be caused
directly by the virus, favoring liver fibrosis. We found a
significant positive correlation between HOMA IR and
steatosis and a nonsignificant positive correlation be-
tween HOMA IR and stage of fibrosis among HCV
patients, which is in agreement with the previous study
carried out by Albert et al. [1]. Also, we observed that
steatosis was higher in HCV + DM + patients (HOMA
IRZ3) than in HCV + DM – patients (HOMA IRo3).
A similar result was obtained by Machado and Cortez
Pinto [22]. Insulin resistance and diabetes can adversely
affect the course of chronic hepatitis C and lead to
enhanced steatosis, steatohepatitis, and liver fibrosis [1].
Both increased adipocity and the presence of steatosis
have been associated with a decreased rate of response to
antiviral treatment [19]. Clearance of HCV improves
insulin resistance [28]. Eradication of HCV infection
reduces the incidence of glucose abnormalities in chronic
HCV patients [29]. Insulin resistance and type 2 diabetes
not only accelerate the histological and clinical progres-
sion of chronic hepatitis C but also reduce the early and
sustained virological response to interferon-a (IFN-a)-
based therapy [23]. In contrast, IFN-a has been observed
Figure 4
Highly significant positive correlation between fasting insulin andHOMA IR HCV patients. HCV, hepatitis C virus; HOMA IR,homeostatic model assessment test for insulin resistance.
Figure 5
Significant positive correlation between fasting insulin and stage offibrosis in HCV patients. HCV, hepatitis C virus.
Figure 6
Negative correlation between steatosis and BMI in HCV patients.HCV, hepatitis C virus.
Figure 7
Correlation between HOMA IR and HCV RNA (PCR) among patients.
Figure 8
Section from liver tissue case no. 27 showing a preserved architecture(stage of fibrosis 0/6, negative steatosis) and a mild portal lymphocyticinfiltrate (Masson trichrome staining).
to be associated with the development of diabetes [30].
The acute administration of IFN-a may induce some
degree of insulin resistance in both healthy individuals
and in patients with chronic hepatitis C [31].
ConclusionHCV itself can contribute toward insulin resistance, as
evidenced by high HOMA IR among HCV patients.
Insulin resistance is a predictor of the stage of fibrosis and
the rate of fibrosis progression. Insulin resistance and
diabetes increase the risk of advanced liver disease,
including steatosis, fibrosis, cirrhosis, and hepatocellular
carcinoma. Diabetic HCV-positive patients had an inter-
mediate clinical phenotype (lower BMI and LDL)
compared with the control group (HCV–DM +). A
sustained response to IFN-a-based therapy may result
in improvements in blood glucose abnormalities, insulin
resistance, and diabetes. Early antiviral therapy decreases
the risk of type 2 diabetes and progression of fibrosis in
patients with chronic hepatitis C and insulin resistance.
AcknowledgementsConflicts of interestAll members of Internal Medicine Departments of Al-Zahraa UniversityHospital, National Liver Institute and Police Authority Hospital.
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