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| ORIGINAL ARTICLE |
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| Year : 2017 | Volume
: 8
| Issue : 1 | Page : 36-41 |
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Lipid profile pattern in chronic viral hepatitis C in Makurdi, Nigeria
Ayu Agbecha1, Chinyere Adanna Usoro2, Maisie Henrietta Etukudo2
1 Department of Chemical Pathology, Federal Medical Centre, Makurdi, Nigeria
2 Department of Medical Laboratory Science, Chemical Pathology Unit, University of Calabar, Calabar, Nigeria
| Date of Web Publication | 2-Feb-2017 |
Correspondence Address:
Ayu Agbecha
Department of Chemical Pathology, Federal Medical Centre, Makurdi
Nigeria
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0975-9727.199375
Context: Hepatitis C virus (HCV) infection with a worldwide distribution causes liver disease. The liver is the principal site for formation and clearance of lipoproteins. Aim: The purpose of this study is to assess the influence of HCV on lipid metabolism and the effect of the stages of this disease on lipid pattern in infected patients. Materials and Methods: The study involved the selection of 36 chronic hepatitis C (CHC) patients attending the clinic at a tertiary hospital in Makurdi, Nigeria. After fulfilling the inclusion criteria, 36 anthropometrically matched apparently healthy individuals were selected as a control to the CHC group. CHC is defined as patients, who continuously tested positive for anti-HCV antibody for up to 1 year during their periodic visit to the clinic. Results: There was no significant (P > 0.05) difference between the mean systolic blood pressure (BP), diastolic BP, age, waist circumference, body mass index of chronic HCV, (CHCV) and controls. There was a significantly lowered total cholesterol (P = 0.029) and high-density lipoprotein cholesterol (HDL-C) (P = 0.000) in CHCV patients compared to the matched controls. There was a significantly lowered total cholesterol (P = 0.004) and HDL-C (P = 0.000) in asymptomatic CHC compared to the matched controls. Conclusion: Lipid profile monitoring may help in the diagnosis of hepatic infection severity and may also act as a good prognostic sign, so it must be analyzed in all advanced hepatic infection cases. Keywords: Cholesterol, chronic hepatitis C, lipids
How to cite this article:
Agbecha A, Usoro CA, Etukudo MH. Lipid profile pattern in chronic viral hepatitis C in Makurdi, Nigeria. Muller J Med Sci Res 2017;8:36-41 |
How to cite this URL:
Agbecha A, Usoro CA, Etukudo MH. Lipid profile pattern in chronic viral hepatitis C in Makurdi, Nigeria. Muller J Med Sci Res [serial online] 2017 [cited 2023 Jun 6];8:36-41. Available from: https://www.mjmsr.net/text.asp?2017/8/1/36/199375 |
| Introduction | |  |
Hepatitis C virus (HCV) causes hepatitis C disease with a worldwide distribution, varied broadly among geographic areas.[1] Available data put the prevalence of HCV infection at approximately 2.2%–3.3% globally (130–170 million people), the highest prevalence reported in Africa (5.3%) and the Eastern Mediterranean regions.[1],[2] Majority (70%–90%) of individuals with HCV fail to spontaneously clear the virus in the acute phase and become chronically infected.[3],[4],[5] Chronic hepatitis C (CHC) disease is defined as nonremission of the disease after testing positive for over 6 months.[5] About 150 million people of the world were estimated to have chronic hepatitis C viral (CHCV) infection, which could progress to liver cirrhosis or cancer.[6] CHCV disease is a disease with varying stages of liver damage, with varying prognoses, and response to treatment. CHCV disease has prolonged periods of absent symptom.[4] About 27% of liver cirrhosis and 25% liver cancer globally occur in HCV-infected persons.[7]
The liver is the principal site for formation and clearance of lipoproteins. It receives fatty acids and cholesterol from peripheral tissues and diet, packages them into lipoprotein complexes, and releases these complexes back into the circulation.[8],[9] Thus, in severe liver disease, lipid metabolism is profoundly disturbed.[10],[11],[12] CHCV disease has been linked with dyslipidemia.[13],[14],[15],[16],[17] Majority of studies specifically showed lowered plasma cholesterol in CHC disease.[18],[19],[20]
The purpose of this study was to assess the influence of HCV on lipid metabolism by observing the variations in serum lipoproteins (total cholesterol, low-density lipoprotein [LDL], high-density lipoprotein [HDL], very LDL [VLDL], and triglycerides [TGs]) in CHCV patients.
| Materials and Methods | | |
Ethical clearance was sought and obtained from the Ethical Board of a Tertiary Hospital in Makurdi, Nigeria, to allow the participation of viral hepatitis C patients attending clinic. A total of 72 participants comprising 36 CHC patients and 36 apparently healthy controls aged 18–55 years were selected for the study. The CHC patients were anthropometrically matched with the controls to eliminate interferences of anthropometric parameters on the lipid profile pattern. Informed consent was sought from the individual patients by educating them on the need and relevance of the study. A structured questionnaire was administered to the consented patients, who answered the questions and returned same.
The inclusion criteria comprised patients who continuously tested positive for anti-HCV antibody for up to 1 year during their periodic visit to the clinic, apparently healthy individuals with the desired blood pressure (BP), and anthropometric indices. The exclusion criteria comprised participants with conditions that predispose to dyslipidemia.
The lipid profile of CHC patients (n = 36) was compared with anthropometrically matched controls (n = 36). Using a cutoff alanine aminotransferase value of greater and <36 U/L, the CHC patients (n = 36) were subgrouped into symptomatic (n = 10) and asymptomatic (n = 26) CHC, respectively. The plasma lipids of the symptomatic (n = 10) and asymptomatic (n = 26) CHC patients were statistically compared with that of their anthropometrically matched controls (n = 13 and n = 26, respectively).
The anti-HCV antibody ELISA kit, obtained from DIA.PRO Diagnostic BioProbes Srl, Milano-Italy, was used for the assay of anti-HCV antibody. The determination of anti-HCV antibody was based on the ELISA sandwich principle. Immobilized recombinant HCV antigens coated onto the walls of microtiter plate wells bind anti-HCV antibody in the sample. The addition of a second polyclonal specific anti-human IgG/IgM antibody (anti-hIgG/M) conjugated to horseradish peroxidase (HRP-conjugate), bind to any HCV antigen–antibody complexes previously formed. The amount of anti-human IgG/IgM antibody-horseradish peroxidase-conjugate bound is proportional to HCV antigen–antibody complexes formed, which is proportional to the amount of anti-HCV antibody in the serum. On addition of enzyme substrate, products are formed which react with the chromogen tetramethylbenzidine to yield a colored solution, whose intensity is proportional to the anti-HCV antibody present in the serum.
The reagent kit for the determination of cholesterol, HDL-cholesterol (HDL-C), and TG was obtained from Randox laboratories Limited, United Kingdom. Total cholesterol was determined by the cholesterol esterase method. Free cholesterol is liberated from cholesterol esters by cholesterol esterase. The free cholesterol is oxidized by cholesterol oxidase to yield a ketone and hydrogen peroxide. The hydrogen peroxide is converted into water and oxygen, which is immediately used for the oxidation of para Aminophenazone in a phenol solution giving rise to a pink-colored solution. The intensity of the colored solution is directly proportional to the concentration of cholesterol in the sample. The HDL-C was determined by the cholesterol esterase method after fractional separation from other lipids. The HDL-C reagent is a mixture of cholesterol esterase, cholesterol oxidase, and catalase. These enzymes eliminate chylomicrons, VLDL-cholesterol (VLDL-C), and LDL-cholesterol (LDL-C). HDL-C is released into the supernatant mixture of detergent and serum after centrifugation. The HDL-C fraction extracted is measured by the cholesterol esterase method used in cholesterol determination. TGs were determined using the lipase method. Lipase hydrolyzes TG into hydrogen peroxide, subsequently acted upon by peroxidase to produce water and oxygen. Oxygen is immediately used for the oxidation of para Aminophenazone which in the presence of phenol yields a pink-colored quinoneimine dye, whose color intensity is directly proportional to the concentration of TG in the serum. LDL cholesterol and VLDL-C were estimated using the Friedewald equation.[21]
The IBM Armonk, New York, United States SPSS version 21 was used in analyzing the data generated. Descriptive statistics were used in determining the means and standard deviations of the parameters measured. Student's t-test was used in comparing the means of parameters in CHCV and control groups. A two-tailed P < 0.05 was indicative of statistical significance.
| Results | | |
[Table 1] shows BP, age, waist circumference (WC), body mass index (BMI), fasting total cholesterol, HDL-C, LDL-C, VLDL-C, and TG in chronic seropositive HCV and seronegative patients. There was no significant (P > 0.05) difference between the mean systolic BP, diastolic BP, age, WC, and BMI of chronic seropositive HCV and seronegative patients. There was a significantly lowered total cholesterol (P = 0.029) and HDL-C (P = 0.000) in chronic seropositive HCV patients compared to the matched seronegative controls. Whereas no significant (P > 0.05) difference in mean fasting serum LDL-C, VLDL-C, and TG was observed between chronic seropositive HCV and matched seronegative patients. | Table 1: Blood pressure, anthropometric, lipid profile, and liver function parameters in chronic hepatitis C virus and controls
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[Table 2] shows the BP, anthropometric parameters, and lipid profile of asymptomatic CHC and controls. There was no significant (P > 0.05) difference between the mean systolic BP, diastolic BP, age, WC, and BMI of asymptomatic CHC and controls. There was a significantly lowered total cholesterol (P = 0.004) and HDL-C (P = 0.000) in asymptomatic CHC compared to the matched controls. Whereas no significant (P > 0.05) difference in mean fasting serum LDL-C, VLDL-C, and TG was observed between asymptomatic CHC and matched controls. | Table 2: Blood pressure, anthropometric, lipid profile, and liver function parameters in asymptomatic chronic hepatitis C virus patients (with alanine aminotransferase value <36 U/L) and controls
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[Table 3] shows the BP, anthropometric parameters, and lipid profile of symptomatic CHC and controls. There was no significant (P > 0.05) difference between the mean systolic BP, diastolic BP, age, WC, and BMI of symptomatic CHC and controls. Whereas no significant difference in mean fasting serum LDL-C, VLDL-C, and TG was observed between symptomatic CHC and matched controls. There was a significantly lowered total cholesterol (P = 0.003) and HDL-C (P = 0.031) in symptomatic CHC compared to the matched controls. Whereas no significant (P > 0.05) difference in mean fasting serum LDL-C, VLDL-C, and TG was observed between symptomatic CHC and matched controls. | Table 3: Blood pressure, anthropometric, lipid profile, and liver function parameters in symptomatic chronic hepatitis C virus patients (with alanine aminotransferase value>36 U/L) and controls
Click here to view |
| Discussion | | |
Interactions between CHCV infection and lipid metabolism have been described in some studies.[13],[14],[15],[16],[17] Although changed serum lipids have been reported to be commonly found in patients with chronic liver disease of any etiology,[22] the relationship between HCV and lipid metabolism seems to be more specific. In a bid to establish dyslipidemia in CHCV infection independent of liver involvement, this study compared ungrouped, asymptomatic, and symptomatic CHC disease with their matched controls.
Our study found a statistically low total and HDL-C in the ungrouped, asymptomatic, and symptomatic CHC disease compared with their matched controls. Low LDL-C was also observed in all the groups compared with their matched controls, the decrease was, however, not statistic.
The study observed no disparity in the levels of VLDL-C and TG of the groups compared with their controls.
Our study is consistent with the works of Maggi et al., Fabris et al., and Serfaty et al., who reported a higher prevalence of hypocholesterolemia and low LDL levels in HCV-infected patients compared to control groups.[14],[16],[17] The results of the study are also in agreement with the studies of Floris-Moore et al., Marzouk et al., and Corey et al., who observed the frequency of hypocholesterolemia in noncirrhotic HCV-infected patients has been five times higher compared to their reference population.[18],[19],[20]
The low HDL-C observed in our study is consistent with a study led by Li et al., reporting LDL and HDL values to be lower in HCV-infected patients.[23] The study is also in line with that of Nogueira et al., which evaluated 150 HCV-infected patients' genotypes 1, 2, and 3, showed that serum HDL values were lower in genotype 2 HCV-infected patients.[24] An Egyptian study, carried out on 150 genotype 4 HCV-infected patients, revealed a lower total, LDL, and HDL-C in HCV patients compared to the controls.[25]
Marzouk et al., showed decrease levels of TGs among CHCV patients, in disagreement with our study.[19] However, our result of no statistical difference in TG level of CHCV and controls is in line with that of Corey et al.[20]
The binding of viral particles to LDL and HDL then LDL receptor (LDLr) could partly explain the low serum cholesterol and lipoprotein level observed in the asymptomatic CHC. A large amount of literature data emphasize the complex interactions between HCV and different parts of the host lipid metabolism, which are used in several steps of the viral lifecycle. The virus adheres and enters the hepatocyte through numerous receptors including CD81, scavenger receptor B type 1 (SR-B1), glycosaminoglycans, claudin 1, occludin, and the LDLr. The SR-B1 is a lipoprotein part of the hepatocyte membrane that has a physiological role as an HDL, VLDL, and LDL receptor, to extract cholesterol from these lipoproteins for subsequent cell internalization.[26],[27] The LDL receptor is the ligand for LDL on the surface of the hepatocyte and has a role in the endocytosis of these particles. HCV circulates in blood as two types of particles, which are classified based on their densities: high-density particles which are associated to immunoglobulins and are less infective, and low-density particles, associated with lipids and lipoproteins, highly infective.[26] These lipoviral particles contain HCV RNA, core protein, LDL, VLDL, and apolipoproteins B and E.[28]
Impairment of hepatic secretion of lipoproteins could account for the low lipid levels in the symptomatic CHC patients. The liver plays a key role in regulating lipid homeostasis representing an obvious target of lipid disorders. Liver steatosis is reported in 31%–72% of patients with CHC.[29] The replication of HCV has been shown to decrease intrahepatic cholesterol synthesis.[30]
| Conclusion | | |
Lipid profile monitoring may help in the diagnosis of hepatic infection severity and may also act as a good prognostic sign, so it must be analyzed in all advanced hepatic infection cases.
Financial Support and Sponsorship
Nil.
Conflicts of Interest
There are no conflicts of interest.
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[Table 1], [Table 2], [Table 3]
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