Changes in Serum Lipid Profile among Patients Suffering from Chronic Liver Disease Secondary to Hepatitis C
- 1 Departement of Medicine, Section of Gastroenterology, The Aga Khan University Hospital, Karachi, Pakistan
- 2 Departement of Medicine, Jinnah Postgraduate Medical Centre, Karachi, Pakistan
- 3 Departement of Medicine, Jinnah Postgraduate Medical Centre, Karachi, Pakistan
- 4 Departement of Medicine, Jinnah Postgraduate Medical Centre, Karachi, Pakistan
- 5 Departement of Medicine, Jinnah Postgraduate Medical Centre, Karachi, Pakistan
Abstract
Objective: To find out the changes in lipid metabolism among patients suffering from chronic liver disease secondary to hepatitis C. Study Design: Hospital based observational study. Setting: Medical Unit-I, Ward–5, Jinnah Postgraduate Medical Centre, Karachi. Duration: July 2013 to December 2013. Patients and Methods: About 110 patients admitted in Medical Unit-I with a diagnosis of chronic liver disease were included in the study. Patients suffering from DM, HTN, CKD were excluded from the study. Fasting lipid profile was done in all cases. Results and Observations: There were 44 (40%) male and 66 (60%) female patients. Mean age of the patients was 50.18 (±11.7) years. Total cholesterol was decreased in 76 (69.09%) patients. Normal range was present in 34 (30.91%) patients. None of the patient had hypercholesterolemia. Serum triglyceride levels were low in 14 (12.72%) patients, normal in 82 (74.54%), borderline high in 7 (6.36%) and hypertriglyceridemia was seen in 7 (6.36%). HDL-c was below normal in 26 (23.63%) cases, normal in 78 (70.91%), and high in 6 (5.45%). LDL was near optimal/above optimal in only 5 (4.5%) patients. Mean TC/HDL ratio was 2.53 (±1.02). Mean LDL/HDL ratio was 1.23 (±0.73). Mean TC of HCV +ve patients was 130.5 mg/dl as compared to that of HCV –ve patients which was 82.85 mg/dl (P-value: 0.011). Mean TGs of HCV +ve group was 151.5 mg/dl while that of HCV –ve was 79.9 mg/dl (P-value: 0.025). Mean HDL & LDL levels were 43.67 mg/dl and 39.78 mg/dl in HCV group while 34.83 mg/dl & 64.67 mg/dl in the other group with P-value of 0.026 and 0.081 respectively. Conclusion: When it comes to its relationship with lipid metabolism, HCV is a remarkable virus. Its interaction with lipoproteins and its ability to induce massive steatosis are quite unique and idiosyncratic. Despite of causing hepatic steatosis, chronic HCV infection is associated with a paradoxically favorable lipid profile, although its reason cannot be enlightened precisely. There is a need for very well settled molecular and genetic studies to well understand HCV infection and lipid metabolism.
- Mohd Hanafiah, K., Groeger, J., Flaxman, A.D. and Wiersma, S.T. (2013) Global Epidemiology of Hepatitis C Virus Infection: New Estimates of Age-Specific Antibody to HCV Seroprevalence. Hepatology, 57, 1333-1342. https://doi.org/10.1002/hep.26141
- Lauer, G.M. and Walker, B.D. (2001) Hepatitis C Virus Infection. New England Journal of Medicine, 345, 41-52. https://doi.org/10.1056/NEJM200107053450107
- Zein, N.N., Rakela, J., Krawitt, E.L., Reddy, K.R., Tominaga, T. and Persing, D.H. (1996) Hepatitis C Virus Genotypes in the United States: Epidemiology, Pathogenicity, and Response to Interferon Therapy. Annals of Internal Medicine, 125, 634-639. https://doi.org/10.7326/0003-4819-125-8-199610150-00002
- Idrees, M. and Riazuddin, S. (2008) Frequency Distribution of Hepatitis C Virus Genotypes in Different Geographical Regions of Pakistan and Their Possible Routes of Transmission. BMC Infectious Diseases, 8, 1. https://doi.org/10.1186/1471-2334-8-69
- Fabris, C., Federico, E., Soardo, G., Falleti, E. and Pirisi, M. (1997) Blood Lipids of Patients with Chronic Hepatitis: Differences Related to Viral Etiology. Clinica Chimica Acta, 261, 159-165. https://doi.org/10.1016/S0009-8981(97)06532-7
- Serfaty, L., Andreani, T., Giral, P., Carbonell, N., Chazouillères, O. and Poupon, R. (2001) Hepatitis C Virus Induced Hypobetalipoproteinemia: A Possible Mechanism for Steatosis in Chronic Hepatitis C. Journal of Hepatology, 34, 428-434. https://doi.org/10.1016/S0168-8278(00)00036-2
- Diaz, O., Delers, F., Maynard, M., Demignot, S., Zoulim, F., Chambaz, J., et al. (2006) Preferential Association of Hepatitis C Virus with Apolipoprotein B48-Containing Lipoproteins. Journal of General Virology, 87, 2983-2991. https://doi.org/10.1099/vir.0.82033-0
- Andre, P., Komurian-Pradel, F., Deforges, S., Perret, M., Berland, J., Sodoyer, M., et al. (2002) Characterization of Low- and Very-Low-Density Hepatitis C Virus RNA-Containing Particles. Journal of Virology, 76, 6919-6928. https://doi.org/10.1128/JVI.76.14.6919-6928.2002
- Dubuisson, J., Penin, F. and Moradpour, D. (2002) Interaction of Hepatitis C Virus Proteins with Host Cell Membranes and Lipids. Trends in Cell Biology, 12, 517-523. https://doi.org/10.1128/JVI.76.14.6919-6928.2002
- Perlemuter, G., Sabile, A., Letteron, P., Vona, G., Topilco, A., Chrétien, Y., et al. (2002) Hepatitis C Virus Core Protein Inhibits Microsomal Triglyceride Transfer Protein Activity and Very Low Density Lipoprotein Secretion: A Model of Viral-related Steatosis. The FASEB Journal, 16, 185-194. https://doi.org/10.1096/fj.01-0396com