IJSRED-V2I1P1

International Journal of Scientific Research and Engineering Development-– Volume 2 Issue 1, Jan-Feb 2019
Available at www.ijsred.com
ISSN: 2581-7175 ©IJSRED: All Rights are Reserved Page 1
PREVALENCE OF TYPE 2 DIABETES AMONG
HEPATITIS C VIRUS SEROPOSTIVE SUBJECTS IN
DUTSE METROPOLIS, JIGAWA-NIGERIA
1
*Muhammad Y, 2
Anka UA, 3
Musa B, 4
Umar, FA, and 1
Mohammed Y.
1
*Chemical Pathology Unit, Laboratory Department, Rasheed shekoni Specialist Hospital Dutse.
2
Zamfara State Hospital Service Management Board.
3
Jigawa State Primary Healthcare Development Agency, Dutse.
4
Public Health and Diagnostic Institute, Northwest University Kano, Nigeria.
4
Medical microbiology Unit, Laboratory Department, Federal medical center Katsina.
Abstract:
The relationship between hepatitis C virus (HCV) and type 2 diabetes (T2DM) is still
unclear, but there are a lot of data hypothesizing the prevalence of T2DM among HCV
seropositive patients. The current research consisted of 62 HCV seropositive and 33 apparently
healthy subjects attending Rasheed shekoni specialist hospital Dutse. Serum biochemical
parameters were determined using chemistry analyzer (Selectra Pro). Results revealed a
statistical increase of all the liver enzymes of HCV subjects compared to controls, all parameters
for metabolic syndrome varies between HCV and controls, our findings also revealed that age
may be factor in developing type2 diabetes among HCV. A percentage prevalence of 16.1% and
19.4% in male and female respective HCV subjects have fasting sugar levels beyond 7.0 mmol/l.
conclusively, a high prevalence of type 2 diabetes was documented among HCV subjects.
Keywords — Hepatitis C Virus, Type 2 Diabetes, Prevalence, Metabolic syndrome.
Introduction:
HCV infection and T2DM are among the major public health threats with increasing
morbidity and mortality throughout the world (WHO, 2013). HCV infection is known to cause
chronic liver disease, cirrhosis, and hepatocellular carcinoma (HCC) Lonardo et al, (2009). HCV
infection afflicts more than 170 million individuals globally (Poynard et al., 2003; Afdhal, 2004;
Lonardo et al, 2009). Evidence is accumulating that both HCV and T2DM have the potential in
coexisting within an individual (Seeff and Hoofnagle, 2003). It’s reported that more than 412
million people have diabetes in 2015 and it is predicted that number will rise to 642million by
the year 2040 (IDF, 2015). The decreased mortality of people with diabetes, together with
increasing frequency of obesity and the sedentary lifestyle of the population point to a dramatic
increase in the prevalence rates of type 2 diabetes (Wild et al., 2004). Glucotoxicity due to
insulin resistance is the etiologic bases for complications in type 2 diabetic subjects (IDF, 2015).
Several mechanisms were hypothesized to induce T2DM in HCV infection such as increasing
mitochondrial reactive oxygen species by HCV non structural protein specifically NS3 through
oxidation of NADPH oxidase and nox2 (Bureau, 2001), others includes, TNFα and other
RESEARCH ARTICLE OPEN ACCESS

inflammatory cytokines pathway (Elsammak et al, 2005; Durante-Mangoni, et al, 2006), direct
alterations in insulin signaling by HCV (Banerjee et al, 2008; Bose, et al, 2012) and beta cell
dysfunction (Narita et al, 2004; Masini et al, 2005). It is documented that HCV infections
predisposes patients to increase risk of developing type 2 diabetes by interfering with normal
glucose homeostasis in the liver (Negro and Alaei, 2009; Negro, 2011). The current study aimed
at reporting the prevalence of type 2 diabetes among the HCV infected individuals in Dutse
metropolis Jigawa.
Materials and Methods:
Participants
The study population consisted of sixty two (62) confirmed HCV patients and thirty-three (33)
apparently healthy individuals as controls attending Rasheed shekoni specialist hospital general
outpatient department.
Blood Specimen Collection
Venous samples were collected from the test subjects and controls using standard venopuncture
and delivered into well labeled clean plain test tubes and EDTA container for biochemical and
molecular detection of HCV respectively. The blood samples were allowed to clot for 30minutes
and then centrifuged at 5,000 rpm for 5minutes to obtain the serum; the separated sera were
stored at -200
c
Detection of HCV using Rapid test strip
One drop about (30µl) of both serum and buffer were transferred onto the test strip using dropper
avoiding air bubbles. The results are read in 15 minutes time.
Determination of Liver enzymes.
Liver enzymes were determined using chemistry analyzer; Selectra Pro.
Statistical Analysis:
The results were presented as Mean±SD. One way analysis of variance (ANOVA) was
conducted, followed by Turkey Kramer multiple comparison test using SPSS Software 16.0.
Differences were considered as significant when P<0.05.
Results:
Mean Age, BMI and Serum biochemical parameters among HCV Subjects and Controls
All the results are presented as Mean ±SD. Mean average age, BMI, FBS, TG and HDL of test
and control groups were evaluated. The findings revealed no statistical difference between the
groups

Serum Levels of Some Liver Enzymes Among HCV Infected Patients Compared to Control
Groups
Of the ninety five (95) subjects recruited in this study, Liver enzymes (ALT, AST and ALP) of
HCV and control were determined, there is significant increase of all serum liver enzymes of
HCV compared to controls.
Age and Sex Distribution of Fasting Blood Sugar Among HCV and Control Subjects
Both HCV and Control subject`s fasting plasma glucose was evaluated, they were categorized
according to WHO standard for diabetes. Both male and females in HCV group are at increased
risk of developing type 2 compared to control group.
Table 1: Mean age, BMI and Serum biochemical parameters among HCV Subjects and
Controls
Parameters HCV Subjects (n=62) Control Subjects (n=33)
Mean Age (yrs) 39.4±8.9 29.7±8.3
BMI(kg⁄m2
) 23.4±2.4 21.1±2.0
FBS(mmol⁄l) 6.9±1.9 5.7±0.9
HDL(mmol⁄l) 0.74±0.16 0.82±0.10
TG(mmol⁄l) 1.07±0.15 0.94±0.14
KEY
BMI=Body mass index; FBS=Fasting blood sugar; HDL=High density lipoprotein; TG=Triglyceride; n=number of
subjects
Table 2: Serum Levels of Some Liver Enzymes HCV Infected Patients Compared to
Control Group
Parameters ALT(U/I) AST(U/I) ALP(U/I)
HCV Subjects(n=62) 52.1±19.9 67.5±26.7 113.8±8.6
Control (n=33) 15.6±8.6 21.5±9.0 47.0±12.4
KEY
HCV=Hepatitis C Virus; ALT=Alanine amino transferase; AST=Aspartate amino transferase; ALP= Alkaline
phosphatase; n=number of subjects.
Table 3: Sex Distribution of Fasting Blood Sugar Among HCV and Control Subjects
HCV CTRL
FBS (mmol⁄l) Male (n=31) Female (n=31) Male (n=19) Female (n=14)
< 7.0 21(33.9%) 19(30.6%) 18(54.5%) 12(36.4%)
>7.0 10(16.1%) 12(19.4%) 01(3%) 02(6.1%)
KEY
HCV=Hepatitis C Virus; n=number of subjects.
Discussion:
Both HCV and T2DM are among leading public health issue and the association between the two
has been documented for over 30 years ago (Allison et al., 1994). World health organization
(WHO) defined diabetes as FBS ≥7mmol/l for three consecutive days. According to the results

obtained from the current study, 16.1% and 19.4% of male and female HCV subjects have
fasting blood glucose above 7mmol/l, while only 3% and 6.1% of male and female control
subjects reported to have fasting sugar levels beyond 7mmol/l, this is indicating the likelihood of
developing T2DM by HCV patients compared to apparently healthy group. Serum liver enzymes
namely ALT, AST and ALP were determined for both HCV and control. The results showed a
statistical difference (p<0.005) of all the enzymes in HCV patients compared to the control
group, the increase may be signifying the degree of liver injury. Some of the parameters for
diagnosis of syndrome X which are also risk factors for T2DM were evaluated for both groups.
HCV subjects have abnormal results compared to controls, although the derangement is not
statistically significant (p>0.005). Ageing may be a factor in the development of T2DM among
HCV infected patients as it was reported by Thuluvath and John (2003) and Butt et al., (2004).
The average mean age of HCV subjects in the present research is higher than controls. This is in
accordance with report of National Health and Nutrition Examination Survey (NHANES III)
which stated that HCV subjects ≥40 years are three times more likely to develop T2DM than
normal individuals (Mehta et al., 2001). Our findings revealed a higher prevalence of T2DM in
HCV infected individuals than that of control and this is in line with several authors (Özyilkan et
al. 1994; Mason et al. 1999; Ryu et al., and Garrido et al., 2001; Lecube et al., 2004 and Parolin
et al., 2004), the results are also in contrast to that of Balogun et al. (2006).
Conclusion:
In conclusion, as it was documented previously, regarding relationship between existence of
T2DM in HCV infection, the current research revealed a higher prevalence of type 2 diabetes
among the HCV seropositive patients in Dutse metropolis, while factors such as age, BMI,
Triglyceride and HDL may play an important role in the process.
REFERENCES
1) Afdhal, N. H., The natural history of hepatitis C. In: 2004. Copyright© 2004 by Thieme
Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. 24, 3–8
2) Allison, M. E. D., Wreghitt, T., Palmer, C. R. & Alexander, G. J. M.(1994). Evidence for
a link between hepatitis C virus infection and diabetes mellitus in a cirrhotic
population. J Hepatol 21, 1135–1139
3) Balogun, W. O., Adeleye, J. O., Akinlade, K. S., Kuti, M. & Otegbayo, J. A. (2006).Low
prevalence of hepatitis-C viral seropositivity among patients with type-2 diabetes mellitus
in a tertiary hospital. J Natl Med Assoc 98, 1805.
4) Banerjee S, Saito K, Ait-Goughoulte M, Meyer K, Ray RB, Ray R. (2008) Hepatitis C
virus core protein upregulates serine phosphorylation of insulin receptor substrate-1 and
impairs the downstream akt/protein kinase B signaling pathway for insulin resistance. J
Virol 82(6):2606–2612.
5) Bose SK, Shrivastava S, Meyer K, Ray RB, Ray R. (2012) Hepatitis C virus activates the
mTOR/S6K1 signaling pathway in inhibiting IRS-1 function for insulin resistance. J
Virol 86(11):6315–6322.

6) Bureau C, Bernad J, Chaouche N, Orfila C, Beraud M, Gonindard C, et al. (2001)
Nonstructural 3 protein of hepatitis C virus triggers an oxidative burst in human
monocytes via activation of NADPH oxidase. J Biol Chem 276(25):23077–23083.
7) Butt AA, Fultz SL, Kwoh CK, Kelley D, Skanderson M, Justice AC (2004). Risk of
diabetes in HIV infected veterans pre- and post-HAART and the role of HCV
coinfection. Hepatology 40: 115 –119.
8) Durante-Mangoni E, Zampino R, Marrone A, Tripodi MF, Rinaldi L, Restivo L, et al.
(2006) Hepatic steatosis and insulin resistance are associated with serum imbalance of
adiponectin/tumour necrosis factor-alpha in chronic hepatitis C patients. Aliment
Pharmacol Ther 24(9):1349–1357.
9) Elsammak M, Refai W, Elsawaf A, Abdel-Fattah I, Abd EE, Ghazal A. (2005) Elevated
serum tumor necrosis factor alpha and ferritin may contribute to the insulin resistance
found in HCV positive Egyptian patients. Curr Med Res Opin 21(4):527–534.
10) Garrido Serrano A, Guerrero Igea FJ, Lepe Jiménez JA, Palomo Gil S, Grilo Reina A
(2001)Hyperinsulinemia in cirrhotic patients infected with hepatitis C virus infection.
Gastroenterol Hepatol 24 : 127 –131.
11) Hepatitis C. World Health Organization Media Center; (2013). Available from:
http://www.who.int/mediacentre/factsheets/fs164/en/
12) International Diabetes Federation. IDF Diabetes Atlas Seventh Edition. 2015. Available
online: http://www.diabetesatlas.org/resources/2017-atlas.html (accessed on 15
November 2017).
13) Lecube A, Hernández C, Genescà J, Esteban JI, Jardí R, Simó R(2004). High prevalence
of glucose abnormalities in patients with hepatitis C virus infection: a multivariate
analysis considering the liver injury. Diabetes Care 27 : 1171 –1175.
14) Lonardo, A., Adinolfi, L. E., Petta, S., Craxì, A. & Loria, P. (2009). Hepatitis C and
diabetes: the inevitable coincidence? Expert Rev. Anti Infect. Ther. 7, 293–308
15) Masini M, Campani D, Boggi U, Menicagli M, Funel N, Pollera M, et al. Hepatitis C
virus infection and human pancreatic beta-cell dysfunction. Diabetes Care (2005)
28(4):940–941
16) Mason, A. L. et al. (1999). Association of diabetes mellitus and chronic hepatitis C virus
infection. Hepatology 29, 328–333.
17) Mehta SH, Brancati FL, Sulkowski MS, Strathdee SA, Szklo M, Thomas DL (2001).
Prevalence of type 2 diabetes mellitus among persons with hepatitis C virus infection in
the United States (Letter). Hepatology 33 : 1554.
18) 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(1):132–138.
19) Negro, F. (2011).Mechanisms of hepati-tis C virus-related insulin resistance. Clin. Res.
Hepatol. Gastroenterol.35, 358–363.
20) Negro, F., and Alaei, M. (2009). Hepati-tis Cvirus and type 2 diabetes. World J.
Gastroenterol.15, 1537–1547.
21) Özyilkan, E. et al. (1994). Increased prevalence of hepatitis C virus antibodies in patients
with diabetes mellitus. J Intern Med 235, 283–284.
22) Parolin MB, Zaina FE, Araujo MV, Kupka E, Coelho JC (2004). Prevalence of type 2
diabetes mellitus in Brazilian liver transplant candidates: negative association with HCV
status. Transplant Proc 36 : 2774 –2775.

23) Poynard, T., Yuen, M. F., Ratziu, V., and Lai, C. L. (2003). Viral hepatitis C.Lancet362,
2095–2100
24) Ryu JK, Lee SB, Hong SJ, Lee S. (2001). Association of chronic hepatitis C virus
infection and diabetes mellitus in Korean patients. Korean J Intern Med 16 : 18 –23
25) Seeff, L. B. & Hoofnagle, J. H. (2003). National Institutes of Health consensus
development conference: management of hepatitis C: 2002. Hepatology 36, s1–s2
26) Thuluvath PJ, John PR: Association between hepatitis C, diabetes mellitus, and race: a
case-control study. Am J Gastroenterol 98 : 438 –441,2003.
27) Wild S, Roglic G, Green A, Sicree R, King H (2004). Global prevalence of diabetes:
estimates for the year 2000 and projections for 2030. Diabetes Care 27: 1047 –1053,

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