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ORIGINAL ARTICLE
Year : 2014  |  Volume : 27  |  Issue : 2  |  Page : 453-457

Study of frequency of prediabetes in Egyptian patients with chronic hepatitis C virus infection


Tropical Medicine Department, Faculty of Medicine, Menoufia University, Menoufia, Egypt

Date of Submission17-Mar-2013
Date of Acceptance09-Oct-2013
Date of Web Publication26-Sep-2014

Correspondence Address:
Atef Abo El Soud Ali
MD, Tropical Medicine Department, Faculty of Medicine, Menoufia University, Menoufia
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1110-2098.141726

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  Abstract 

Objective
The aim of the study was to estimate the frequency of prediabetes in Egyptian patients with chronic hepatitis C virus (HCV) infection.
Background
Chronic HCV infection is an important risk factor for insulin resistance (IR) and prediabetes.
Patients and methods
This study was performed on 50 patients with chronic HCV infection. They included 38 men and 12 women; their age ranged from 20 to 61 years. They were categorized into two groups according to presence or absence of IR, and 25 healthy volunteers of matched age, sex, and BMI were enrolled as the control group. IR was measured by Homeostasis Model Assessment of Insulin Resistance (HOMA-IR).
Results
In all, 64% of HCV patients were prediabetic with HOMA-IR value greater than 2.
Conclusion
Chronic HCV patients should be screened regularly for IR.

Keywords: Hepatitis C virus, Homeostasis Model Assessment of Insulin Resistance, insulin resistance


How to cite this article:
Ali AA, El Deeb GS, Essa AA, Ahmed NS. Study of frequency of prediabetes in Egyptian patients with chronic hepatitis C virus infection. Menoufia Med J 2014;27:453-7

How to cite this URL:
Ali AA, El Deeb GS, Essa AA, Ahmed NS. Study of frequency of prediabetes in Egyptian patients with chronic hepatitis C virus infection. Menoufia Med J [serial online] 2014 [cited 2019 Nov 23];27:453-7. Available from: http://www.mmj.eg.net/text.asp?2014/27/2/453/141726


  Introduction Top


Hepatitis C virus (HCV) infection is one of the major causes of chronic liver disease. According to recent WHO estimates, the worldwide prevalence of HCV infection is 2.2%, affecting ~130 million people worldwide [1].

A number of studies have demonstrated a strong association between HCV infection and insulin resistance (IR), providing a possible link between this infection and diabetes mellitus [2].

Prediabetes mellitus is defined as a state of abnormal glucose homeostasis in which deficiency or resistance to insulin is the hallmark. Prediabetes mellitus precedes the development of overt type 2 diabetes mellitus (T2DM). It is associated with increased mortality and morbidity, and thus fits well with the criteria of a disease condition [3].

IR is defined as a condition in which higher insulin concentrations are needed to achieve normal glucose metabolism or in which normal insulin concentrations fail to achieve normal glucose metabolism [4].

The gold standard for the assessment of IR is the euglycemic hyperinsulinemic clamp technique. Another more practicable and also well-accepted method of measuring systemic IR is the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR). It is calculated by the following formula: fasting glucose (mmol/l) × fasting insulin (mIU/l)/22.5 [5].

In previous reports, HOMA less than 2 has been considered 'completely' normal and higher than 2 as prediabetic state [6].

The progression of prediabetes to T2DM has been examined in a number of populations with varying results. In general, epidemiological studies indicate that ~25% of individuals progress to T2DM in 5 years, whereas about 50% remain prediabetic and about 25% revert to normal [7].


  Patients and methods Top


The present study was performed on 50 patients with chronic HCV infection attending Mansoura General Hospital Outpatient Clinic for interferon therapy during the period from December 2011 to October 2012. They included 38 men and 12 women; their age ranged from 20 to 61 years with a mean age of 36.8 ± 8.5 years, and 25 healthy volunteers were enrolled as the control group. All patients and controls were classified into two groups.

Group I included HCV patients categorized into two groups according to presence or absence of IR:

Group 1A included chronic HCV patients with IR (HOMA-IR value > 2).

Group 1B included chronic HCV patients without IR (HOMA-IR value<2).

Group II included 25 healthy volunteers of matched age, sex, and BMI.

Exclusion criteria

  1. Diabetes mellitus.
  2. Family history of T2DM.
  3. Any associated liver disease (other than HCV) (e.g. HBV, hepatic schistosomiasis, autoimmune hepatitis, hemochromatosis, Wilson's disease, hepatocellular carcinoma).
  4. Any endocrinal disorders.
  5. Diabetogenic drugs (e.g. steroids).
  6. Severe systemic diseases: cardiac, respiratory, or renal diseases.
  7. Obese patients (BMI ≥ 30).


All participants were subjected to the following:

  1. Detailed history taking.
  2. Full clinical examination.
  3. Complete blood count.
  4. Liver function tests.
  5. Renal function tests.
  6. Fasting blood glucose.
  7. Fasting insulin using Active Insulin Enzyme-Linked Immunosorbent Assay (ELISA, DSL-10-1600; Diagnostic Systems Laboratories Inc., Webster, Texas, USA).


Methods

Collection of samples

After 10 h overnight fasting, venous blood sample was collected from each patient using a sterile plastic syringe. Serum was separated and stored in storage tubes in deep freeze at −20°C until tested.

Principle of the test

The DSL-10-1600 Active Insulin ELISA is an enzymatically amplified 'one-step' sandwich-type immunoassay. In the assay, standards, controls, and unknown serum samples are incubated with anti-insulin antibody in microtitration wells that have been coated with another anti-insulin antibody. After incubation and washing, the wells are incubated with the substrate tetramethylbenzidine. An acidic stopping solution is then added and the degree of enzymatic turnover of the substrate is determined by dual-wavelength absorbance measurement at 450 and 620 nm.

The absorbance measured is directly proportional to the concentration of insulin present. A set of insulin standards is used to plot a standard curve of absorbance versus insulin concentration from which the insulin concentrations in the unknowns can be calculated.

(8) HCV markers (HCV Ab using third-generation ELISA test and HCV RNA by quantitative PCR).

(9) Liver biopsy.

(10) HOMA equation.



With such method, the high HOMA score denotes high IR [8].


  Results Top


  1. Statistical analysis revealed no significant difference between the studied groups with respect to age, BMI, and sex distribution [Table 1].
  2. Statistical analysis revealed significant difference between the studied groups with respect to fasting blood glucose; it was higher in group 1A than in group 1B and in controls, and there was no significant difference between group 1B and controls [Table 2].
  3. Statistical analysis revealed high significant difference between the studied groups with respect to fasting insulin; it was higher in group 1A than in group 1B and in controls, and there was no significant difference between group 1B and controls [Table 3].
  4. Statistical analysis revealed significant difference between the studied groups with respect to HOMA-IR; it was higher in group 1A than in group 1B and in controls, and there was no significant difference between group 1B and controls [Table 4].
  5. Statistical analysis revealed that 64% of patients are prediabetic with HOMA-IR value greater than 2 [Table 5] and [Figure 1],[Figure 2],[Figure 3] and [Figure 4].
Figure 1:

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Figure 2:

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Figure 3:

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Figure 4:

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Table 1: Distribution of the studied groups regarding their age, BMI, and sex

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Table 2: Distribution of the studied groups regarding fasting blood glucose level

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Table 3: Distribution of the studied groups regarding fasting insulin levels

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Table 4: Distribution of the studied groups regarding Homeostasis Model Assessment of Insulin Resistance levels

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Table 5: Frequency of prediabetes among the studied groups

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  Discussion Top


A number of studies have demonstrated a strong association between HCV infection and IR, providing a possible link between this infection and diabetes mellitus [2].

The prevalence of T2DM in patients with CHC was higher than that in the general population and chronic hepatitis B patients [9].

IR was the best predictor for the development of T2DM, and it played a primary role in the development of T2DM [10].

In this study, statistical analysis revealed significant difference between the studied groups with respect to fasting blood glucose; it was higher in group 1A than in group 1B and in controls, and there was no significant difference between group 1B and controls.

In addition, in this study, statistical analysis revealed high significant difference between the studied groups with respect to fasting insulin; it was higher in group 1A than in group 1B and in controls, and there was no significant difference between group 1B and controls. This is consistent with the study by Souza et al. [11] who found that IR patients had higher levels of blood glucose, fasting insulin, and HOMA-IR.

In addition, Fartoux et al. [12] found that HCV patients had higher levels of fasting insulin and fasting blood sugar than controls, which could promote fibrogenesis by causing upregulation of connective tissue growth factor and directly by stimulating hepatic stellate cells to proliferate and secrete extracellular matrix.

In the present study, statistical analysis revealed significant difference between the studied groups with respect to HOMA-IR; it was higher in group 1A than in group 1B and in controls, and there was no significant difference between group 1B and controls. This is consistent with the study by Souza et al. [11] who found that patients with chronic hepatitis C and IR had higher levels of blood glucose, fasting insulin, and HOMA-IR compared with patients without IR.

Serum HOMA-IR has been used as an indirect way to measure IR, and it correlates well with insulin sensitivity using the euglycemic hyperinsulinemic clamping technique [12].

The present study showed that the prevalence of prediabetes among nondiabetic chronic HCV infection is 64%. This high percentage is consistent with the study by Delagado-Borrego et al. [13],[14] who found that the presence of HCV is associated with 62% increase in IR, which provides a possible pathogenic basis for the association of DM with HCV.


  Conclusion Top


From the results of the present study, we can conclude that frequency of prediabetes among nondiabetic chronic HCV patients was 64%, which denotes that HCV infection could be a significant risk factor for development of T2DM.

Recommendations

  1. Chronic HCV patients should be screened regularly for IR.
  2. Once IR is recognized in chronic HCV patients, lifestyle modifications including diet control, weight loss, and suitable physical exercise should be suggested to address IR effectively in the long run.
  3. Further work-up should be performed to evaluate the role of IR in the progression of the liver disease.
  4. Further studies should be conducted to evaluate the role of insulin-sensitizing drugs to modulate the progression of the liver disease in chronic HCV patients with IR.



  Acknowledgements Top


Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.Alter MJ. Epidemiology of hepatitis C virus infection. World J Gastroenterol 2007; 13 :2436-2441.  Back to cited text no. 1
    
2. Narita R, Abe S, Kihara Y, Akiyama T, Tabaru A, Otsuki M. Insulin resistance and insulin secretion in chronic hepatitis C virus infection. J Hepatol 2004; 41 :132-138.  Back to cited text no. 2
    
3. Eldin WS, Emara M, Shoker A. Prediabetes: a must to recognise disease state. Int J Clin Pract 2008; 62 :642-648.  Back to cited text no. 3
    
4. Kahn CR. Insulin resistance, insulin insensitivity, and insulin unresponsiveness: a necessary distinction. Metabolism 1978; 27 :1893-1902.  Back to cited text no. 4
    
5. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985; 28 :412-419.  Back to cited text no. 5
    
6. Romero-Gómez M, Del Mar Viloria M, Andrade RJ, Salmerón J, Diago M, Fernández-Rodríguez CM, et al. Insulin resistance impairs sustained response rate to peginterferon plus ribavirin in chronic hepatitis C patients. Gastroenterology 2005; 128: 636-6641.  Back to cited text no. 6
    
7. Larson H, Lindgarde F, Berglund G, Ahren B. Prediction of diabetes using ADA or WHO criteria in post-menopausal women: a 10-year follow up study. Diabetologia 2004; 43: 1224-1228.  Back to cited text no. 7
    
8. Bonora E, Saggiani F, Targher G. Homeostasis model assessment closely mirrors the glucose clamp techniques in the assessment of insulin sensitivity. Diabetes Care 2000; 28: 57-63.  Back to cited text no. 8
    
9. Lecube A, Hernandez C, Genesca J, Esteban JI, Jardi R, Simo R. High prevalence of glucose abnormalities in patients with hepatitis C virus infection: a multivariate analysis considering the liver injury. Diabetes Care 2004; 27: 1171-1175.  Back to cited text no. 9
    
10.Lillioja S, Mott DM, Howard BV, Bennett PH, Yki-Jarvinen H, Freymond D. Impaired glucose tolerance as a disorder of insulin action: longitudinal and cross-sectional studies in Pima Indians. N Engl J Med 1988; 318: 1217-1225.  Back to cited text no. 10
    
11.Souza AF, Pace FH, Chebli JM, Ferreira LE. Insulin resistance in non-diabetic patients with chronic hepatitis C what does it mean? Arq Bras Endocrinol Metabol 2011; 55 :412-4418.  Back to cited text no. 11
    
12.Fartoux L, Poujol-Robert A, Guechot J, Wendum D, Poupon R, Serfaty L. Insulin resistance is a cause of steatosis and fibrosis progression in chronic hepatitis C. Gut 2005; 54 :1003-1008.  Back to cited text no. 12
    
13.Emoto M, Nishizawa Y, Maekawa K, Hiura Y, Kanda H, Kawagishi T. Homeostasis model assessment as a clinical index of insulin resistance in type 2 diabetic patients treated with sulfonylureas. Diabetes Care 1999; 22: 818-8122.  Back to cited text no. 13
    
14.Delagado-Borrego A, Casson D, Schoenfeld D, Somsouk M. HCV is independently associated with increased insulin resistance after liver transplantation. Transplantation 2004; 77 :703-710.  Back to cited text no. 14
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]


This article has been cited by
1 Insulin Resistance and Prediabetes in Hepatitis C Virus Patients
Dalia E. Desouky,Zaynab Kasemy,Alaa E. Abdel-Hamid,Mohamed S. Omar
The American Journal of the Medical Sciences. 2015; 350(2): 77
[Pubmed] | [DOI]



 

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Abstract
Introduction
Patients and methods
Results
Discussion
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Acknowledgements
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