Hepatitis B infection

INTRODUCTION

        Hepatitis B is a viral disease process caused by the Hepatitis B virus (HBV). Hepatitis B virus is a major cause of acute and chronic hepatitis worldwide and is more prevalence in developing countries. More than 2 billion people are infected with HBV worldwide while some 280million are chronic carriers, harbouring the virus in their liver. The disease is responsible for 80% of all cases of primary liver cases, which is one of leading causes of death in Asia and Africa (Emechebe, et al, 2014).

      The infection can be acute or chronic, while adults that acquire acute infection usually recover or can be managed by supportive therapy. The chronic type is usually fatal. Diagnosis of HBV infection is usually through serological and virological markers. Hepatitis B surface antigen (HBsAg) is the hallmark of HBV infection and is the first serological marker to appear in acute HBV infection and persistence of HBsAg for more than 6 months suggest chronic HBV infection. Hepatitis B “e” antigen (HBeAg) is present only in HBsAg positive sea and its positivity denotes a high degree of viral replication, a disease activity and infectivity (Ignacio 2014).

      Hepatitis B virus is normally transmitted through blood or other body fluids (saliva, sweat, semen, breast milk, urine, faeces), and body contaminated equipment (including shared intravenous needles). The virus can also pass through the placenta to the foetus of an infected mother. (Joanne, et al, 2012).

        Hepatitis B virus (HBV) an envelope double stranded circular DNA virus of complex structure. HBV is classified as an orthohepadnavirus within the family hepatnaviridae. Serum from individuals infected with HBV contains three distinct antigenic particles: a spherical 22nm particle, a 42nm spherical particle   (containing DNA and DNA polymerase) called the Dane particle, and tubular or filamentous particles that vary in length. The viral genome is 3.2kb in length, consisting of four partially over-lapping, open-reading frames that encode viral proteins.  Viral multiplication takes place predominantly hepatocytes. The infecting virus encases its double-shelled Dane particles within membrane envelopes coated with hepatitis B surface antigen (HBsAg). The inner nucleocapsid core-antigen (HBcAg) encloses a single molecule of double-stranded HBV and an active DNA polymerase. (Joanne, et al, 2011).

       HBsAg in body fluid is (1) an indicator of hepatitis B infection (2) used in the large scale screening of blood for HBC, and (3) the bases for first the vaccine for human use developed by recombinant DNA technology Diagnosis of HBV is made by the detection of HBsAg in unimmunized individuals or HBsAg antibody, or detection of HBV nucleic acid by PRC. (Joanne et al, 2011).

      The clinical signs of hepatitis B vary widely. Most cases are asymptomatic. However, sometimes fever, loss of appetite, abdominal discomfort, nausea, fatigue and other symptoms gradually appear following an incubation period of 1 to 3 months.  The virus infects hepatic cells and causes liver tissue degeneration and the release of liver associated enzymes (transaminases) into the blood stream. This is followed by jaundice, the accumulation of bilirubin (a breakdown product of haemoglobin) in the skin and other tissues with a resulting yellow appearance. Chronic hepatitis B infection also causes the development of primary liver cancer, known as hepatocellular carcinoma. (Ott, et al, 2012).

1.1                                                                                                                                                 ACUTE HEPATITIS B

An acute infection may last up to six months (with or without symptoms) and infected persons are able to pass the virus to others during this stage. A patient will test positive for the hepatitis B virus (HBsAg), HBclgM, and possibly the HBs-antigen. Safe sex practices and vaccination of close household members should be recommended. (Lok, et al, 2010).

 Symptoms of an acute infection may include loss of appetite, myalgia, nausea, low-grade fever and possible abdominal pain. Although,most people do not experience symptoms such as nausea, Vomiting or jaundice (ie yellowing of the eyes and skin) that will require immediate medical attention. A small number of people have symptoms that last for months. They may have signs of abnormal liver function before they completely recover from the acute infection. Most infected persons do not require hospitalization, although some may require close medical attention.                   (Lok, et al,2010)

Treatment of acute hepatitis B is generally supportive, which may or may not require hospitalization. Rest and managing symptoms are the primary goals of therapy. Additional follow-up blood tests are needed to confirm recovery from an acute infection or progression to a chronic infection. (Waslkey, et al, 2010).

1.2                                                                                                                                                 CHRONIC HEPATITIS B

The risk of developing a chronic hepatitis B infection is directly related to the age at which one becomes infected with the virus 90% of infants exposed to the hepatitis B virus will develop chronic hepatitis B infections. Up to 50% of young children exposed to hepatitis B virus between the age of 1 and 5 years will develop chronic infections. 5-10% 0f healthy adults who are infected will develop chronic infection.  (Mc Hugh, et al, 2012).

 People who test positive for the hepatitis B virus (HBsAg) for more than six months are diagnosed as having a chronic infection.  This means that they were not able to get rid of the virus and it still remains in their liver and blood. Since chronically infected `individuals can pass the virus on, they should follow safe sex practices and avoid spreading their blood to others. Sex partners and close family household members should screen and vaccinated. (McHugh, et al,2011) .

Therapy is currently recommended for patients with evidence of chronic active hepatitis B disease (ie abnormal aminotransferase level, positive HBV DNA findings, positive or negative hepatitis B e-antigen (HBeAg). Various algorithms have seen proposed, such as that by the American Association for study of Liver Diseases (AASLD), the European Association for the study of the liver (EASL), the Asian Pacific Association of the study of the liver (APASL), the Canadian Association of the study of the liver (CASL), the National institute for Health and Clinical Excellence (NICE) Kuo and Kish, and Keeffe et al. (Weinbaum, et al, 2010).

The National Institute of Health (NIH) recommends nucleoside therapy for the treatment of patients with acute liver failure, as well as cirrhotic patients who are HBV DNA positive and those with clinical complications, cirrhosis or advanced fibrosis with positive serum HBV DNA, or reactivation of chronic HBV during or after chemotherapy or immune-suppression. In addition, immunoglobulin and vaccination should be administered to new born, to women positive for hepatitis B surface antigen (HBsAg).                             (Emechebe, et al, 2014).

In general, for HBeAg positive patients with evidence of chronic HBV disease, treatment is advised when the HBV DNA level is at or above 20,000 Iu/mI (105 copies /mI) and when serum alamine aminotransferase (ALT) is elevated for 3-6 months. For HBeAg-negative patients with chronic hepatitis B disease, treatment can be administered when the HBV DNA  is at or above 2000 Iu/,mI (104  copies/mI) and the serum ALT is elevated (ALT levels > 20 u/l for female; 30u/l for males) for 3-6 months. In patients with the NIH also indicates that immediate therapy is not routinely indicated for patients who have the following:

-          Chronic hepatitis B with high levels of serum HBV DNA but normal serum ALT levels or little activity on liver biopsy                (immune-tolerant phase).

-         Low levels of or no detectable serum HBV DNA and normal serum ALT levels (inactive chronically infected / low replicate phase).

-         Positive serum HBV DNA but not HBsAg (latent HBV infection), unless the patient is undergoing immune-suppression.