Provoke of Viral Hepatitis on the Lipid Indices Among the Eastern Sudanese Patients
[1]
Maisa Ahmed Badneen Maki, Department of Postgraduate Studies, Faculty of Medical Laboratory Sciences, Alzaiem Alazhari University, Khartoum, Sudan.
[2]
Bashir Abdrhman Bashir, Department of Hematology, Faculty of Medical Laboratory Sciences, Port Sudan Ahlia College, Port Sudan, Sudan.
[3]
Amna Othman Alzain, Department of Postgraduate Studies, Faculty of Medical Laboratory Sciences, Alzaiem Alazhari University, Khartoum, Sudan.
Background: Globally, about 325 million people are surviving with hepatitis B virus (HBV) and hepatitis C virus (HCV) infection, with the highest infection rates of HBV recorded in Sudan. Despite the HBV or HCV infections linked to morbidity and mortality, the lipid indices could reflect the clinical course of liver impairment. Objective: This study elucidated the provoke of viral hepatitis on lipid indices among eastern Sudanese hepatitis patients. Material and Methods: Overnight fasting blood specimens were collected from HBV/HCV casualty patients who admitted to Port Sudan teaching hospital during March to July 2019. 80 subjects were enrolled in this work. 42 diagnosed with seropositive HBV or HCV, along with 38 healthy appearing adults as a control. Body mass index and lipid indices were determined. HBV and HCV were confirmed by enzyme linked immunosorbent assay (ELISA). Result: HBV was observed in 36 (45%) and HCV was noted in 6 (7.5%). Total cholesterol, triglyceride, very low-density lipoprotein-cholesterol (VLDL-c), low density lipoprotein-cholesterol (LDL-c), risk factor 2 index were significantly higher in patients with hepatitis, whereas high density lipoprotein-cholesterol (HDL-c) and risk factor 1 index were significantly lower in patients with viral hepatitis than in normal subjects (P < 0.000). Conclusion: HBV or HCV contributes to hyperlipidemia among eastern Sudanese populations. HDL-c and risk factor 1 index could be best evidence of liver trauma.
Lipid Indices, Viral Hepatitis, HDL, Risk Factor, Port Sudan
[1]
WHO. Hepatitis B: fact sheet. http://www.who.int/news-room/fact-sheets/ detail/hepatitis-b. Up-dated 2018. Accessed July 18, 2018.
[2]
Bashir Abdrhman Bashir, Maisa Ahmed Badneen, Mohammed Omer Gibreel, Suhair Abdrahim Othman. Prevalence of Transfusion Transmissible Infections among Blood Donors in Port Sudan. Egypt J Hematol. 2019; 44 (1): 72-76.
[3]
Luo L, Pu X, Wang Y, Xu N. Impaired plasma lipid profiles in acute hepatitis. Lipids in Health and Disease 2010 9: 5.
[4]
Plauth M, Bernal W, Dasarathy S, Merli M, Plank LD, Schutz Tet al. ESPEN guideline on clinical nutrition in liver disorder. Clinical Nutrition. 2019; 38: 485–521.
[5]
Agbecha A, Usoro CA, Etukudo MH. Serum lipids in chronic viral hepatitis B patients in Makurdi, Nigeria. CHRISMED J Health Res 2017; 4: 81-6.
[6]
Qazi Arisar FA, Khan SB, Umar A, Shaikh NS, Choudhry F. Changes in Serum Lipid Profile among Patients Suffering from Chronic Liver Disease Secondary to Hepatitis C. Open Journal of Gastroenterology. 2016; 6: 333–342.
[7]
Sarin SK1, Choudhury A2, Sharma MK2, Maiwall R2, Al Mahtab M3, Rahman S3, Acute-on-chronic liver failure: consensus recommendations of the Asian Pacific association for the study of the liver (APASL): an update. Hepatol Int. 2019; 13 (4): 353-390.
[8]
Bhattacharya A, Pal B, Mukherjee S, Roy SK. Assessment of nutritional status using anthropometric variables by multivariate analysis. BMC Public Health. 2019; 19: 1045.
[9]
Ofori EK, Intiful FD, Asante M, Asare GA, Adjei PK, Steele‐Dadzie RK, et al. Prevalence of cardiovascular disease risk factors among students of a tertiary institution in Ghana. Food Sci Nutr. 2018; 6 (2): 381–387.
[10]
González-Aldaco K, Torres-Reyes LA, Ojeda-Granados C, José-Ábrego A, Nora A. Fierro, Román S. Immunometabolic Effect of Cholesterol in Hepatitis C Infection: Implications in Clinical Management and Antiviral Therapy. Annals of Hepatology. 2018; 17 (6): 908 – 919.
[11]
Gavito AL, Bautista D, Suarez J, Badran S, Arco R, Pavón FJ, et al. (2016) Chronic IL-6 Administration Desensitizes IL-6 Response in Liver, Causes Hyperleptinemia and Aggravates Steatosis in Diet-Induced-Obese Mice. PLoS ONE. 2016; 11 (6): e0157956.
[12]
Quaye O, Amuzu1 BG, Adadey SM, Tagoe AE. Effect of Hepatitis B Virus (HBV) Infection on Lipid Profile in Ghanaian Patients. Virology: Research and Treatment. 2019; 10: 1–5.
[13]
Kuo Y-H, Tsai M-C, Kee K-M, Chang K-C, Wang J-H, Lin C-Y, et al. Associated Factors for Metabolic Syndrome in the Older Adults with Chronic Virus Hepatitis in the Community. PLoS ONE. 2016; 11 (5): e0155544.
[14]
Francque SM, van der Graaff D, Kwanten WJ. Non-alcoholic fatty liver disease and cardiovascular risk: Pathophysiological mechanisms and implications. J Hepatol. 2016; 65 (2): 425-43.
[15]
Pisto P, Santaniemi M, Bloigu R, Ukkola O, Kesäniemi YA. Fatty liver predicts the risk for cardiovascular events in middle-aged population: a population-based cohort study. BMJ Open 2014; 4: e004973.
[16]
Lu J, Hou X, Tu H, Tang Z, Xiang Y, Bao Y, Li-Ng M, Tropp S, Danoff A, Bini EJ. Chronic hepatitis B virus infection status is more prevalent in patients with type 2 diabetes. J Diabetes Investig 2017; 8: 619–625.
[17]
Kong F, Hongjuan You H, Delong Kong D, Zheng K, Tang R. The interaction of hepatitis B virus with the ubiquitin proteasome system in viral replication and associated pathogenesis. BMC Virol J. 2019; 16: 73.
