ESTIMATION OF IMMUNOLOGICAL AND BIOCHEMICAL PARAMETERS IN HEPATITIS B POSITIVE PATIENTS

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J.K. Molade¹, A.A. Onifade¹, M.A. Jimoh², O.G. Oyero³, I.C. Ahube¹, O.K. Olawuyi¹ and I. Ayodeji¹

1. Department of Chemical Pathology, College of Medicine, University of Ibadan.
2. Department of Radiation Oncology, College of Medicine. University of Ibadan.
3. Insititute of Advanced Medical Research and Training, College of Medicine, University of Ibadan.

Abstract

Background: Changes in immunological response have been reported during HBV infections, and these changes can be markers for the diagnosis and prediction of the outcome of infection The aim of this study was to measure and correlate serum levels of interleukin-2 (IL-2), C-reactive protein (CRP) Alanine aminotransferase (ALT), Aspartate aminotransferase (AST) and HBV antigens and antibodies in a sample of patients with HBV infection and in healthy controls

Methods: The study population consisted of 26 patients with hepatitis B infection (HBsAg seropositive), and 26 apparently healthy (HBsAg seronegative) participants as controls. Biochemical markers of liver disease were evaluated by routine methods. Hepatitis B antigens (HBVsAg, HBeAg) and antibodies (HBsAb, HBeAb, HBcAb) were determined using immunochromatographic method. Serum concentrations of IL-2, and CRP were determined using ELISA method.

Results: IL-2 level in HBsAg seropositive patients was found to be lower than that of control with no statistical significance while CRP level in HBV positive patients was higher than that of control with no statistical significance. HBV patients showed statistically significant difference in AST and ALT levels, compared to healthy controls. A statistically significant value was also observed between IL-2 and CRP in HBV infected individuals.

Conclusion: The study concluded that deranged ALT and AST values correlate with HBV infection and may be a potential tool for disease diagnosis and progression.

Keyword: IL-2, C-reactive protein, Alanine transferase, Aspartate transaminase, Hepatitis B antigens, Hepatitis B antibodies.

Introduction

Hepatitis is inflammation of the liver and can be caused by a variety of different viruses. Since the development of jaundice is characteristic feature of many liver diseases, a correct diagnosis of underlying cause of liver diseases can be made by testing patients’ sera for the presence of specific anti-viral antigens or antibodies. Of the many viral causes of viral hepatitis, few are of great global importance than Hepatitis B virus (HBV). The HBV infection constitutes a serious public health problem, affecting approximately 240 million carriers worldwide. Chronic HBV infection had been found to significantly elevate the risk for developing liver cirrhosis and hepatocellular carcinoma¹. HBV is the most common pathogenic infective cause of hepatitis and affecting millions of people worldwide2.The virus is endemic throughout the world. It is shed in various body fluids of infected individuals².

Infection with HBV leads to a wide spectrum of clinical presentations ranging from an asymptomatic carrier state to self-limited acute or fulminant hepatitis to
chronic hepatitis with progression to cirrhosis and hepatocellular carcinoma. Infection with HBV is one of the most common viral diseases affecting man. Both viral factors and the host immune response have been implicated in the pathogenesis and clinical outcome of HBV infection³.

The HBV is an Hepadnavirus with a 42nm partially double stranded DNA composed of a 27nm nucleocapsid core (HBcAg), surrounded by an outer lipoprotein coat (also called envelope) containing the surface antigen (HBsAg). Hepatocytes that are infected in vivo by hepadnaviruses produce an excess of noninfectious viral lipoprotein particles composed of envelope proteins².The virus consists of a nucleocapsid and an outer envelope composed mainly of three Hepatitis B surface antigens (HBsAg) that play a central role in the diagnosis of HBV infection. The nucleocapsid contains hepatitis B core antigen (HBcAg), a DNA polymerase reverse transcriptase, the viral
genome as well as cellular proteins⁴.

HBV DNA can be detected in circulation (using PCR) within 1 month of infection, but it remains at the relatively low level of 102–104 genome equivalents per ml for about 6 weeks before the HBV DNA and the secreted HBV e Antigen (HBeAg) and HBsAg increase to their peak titres. HBV core antigen (HBcAg)- specific IgM appears early, and HBcAgspecific IgG persists for life, irrespective of the outcome of infection. Approximately 10–15 weeks after infection, serum Alanine Aminotransferase (ALT) levels begin to rise, which indicates T-cell-mediated liver injury⁵.

C-reactive protein (CRP) is an acute-phase protein that serves as an early marker of inflammation or infection. The protein is synthesized in the liver and it is normally found at concentrations of less than 10 mg/L in the blood. During infectious or inflammatory disease states, CRP levels rise rapidly within the first 6 to 8 hours and peak at levels of up to 350–400 mg/L after 48 hours⁶. When the inflammation or tissue destruction is resolved, CRP levels falls, making it a useful marker for monitoring disease activity⁷.

IL-2 has been known for many years as a T cell growthpromoting factor. The role of IL-2 in immune tolerance appears to be twofold⁸. First, it has been shown that IL-2 is critical in programming T cells for activation-induced cell death⁹. It is likely that this function of IL-2 is dependent on its ability to increase surface expression of Fas ligand (FasL) and suppress expression of the inhibitor of apoptosis¹⁰. The production of IL-2has been found to bereduced in chronic viral hepatitis B and this has been used to investigate its immunomodulatory and antiviral effects. However, the role of these important immunomodulators in hepatic injury due to HBV has not been evaluated in detail¹¹.