Fulminating Hepatitis B secondary to a lifetime use of IV drug abuse Research Paper

Fulminating Hepatitis B secondary to a lifetime use of IV drug abuse - Research Paper Example This helps in identifying the initial treatment, as well as eliminating all contraindications to liver transplant. In addition, conducting proper prognosis helps in identifying patients who need a transplant and those who will survive without a liver transplant. Symptoms presented by fulminant hepatitis B require immediate medical interventions to prevent further damage on liver cells. However, in some patients, the condition is asymptomatic, which makes it difficult to detect. Patients of such nature may spread the condition to others unknowingly (Vandevante et al, 2011). Hepatitis B virus This paper looks into a case of a 51 year old patient suffering from fulminating Hepatitis B as a result of prolonged intravenous drug abuse. The fulminant condition under consideration is as a result of hepatitis B virus. Currently, hepatitis B virus (HBV) is the leading cause of fulminant hepatitis compared to other viral hepatitis. Hepatitis B virus attacks and replicates within hepatocytes. In terms of structure, hepatitis B virus has an outer shell and an inner core. The inner core bares the viral DNA, enzymes and proteins including hepatitis B virus core antigen (HBcAg) and HBVe antigen (HBeAg). The outer shell has the hepatitis B virus surface antigen (HbsAg), which is produced in excess by hepatocytes replicating the hepatitis B virus. ... In cases of acute HBV, a bigger number of viral DNA is cleared from liver cells through a non-cytocidal process caused by inflammatory byproducts derived from CD8+ T lymphocytes. The release of inflammatory products occurs once CD+ T cells are stimulated by interferon-gamma and tumor necrosis factor-alfa, which are products of CD4+ T cells (Gish, 2009). The inflammatory byproducts lead to down regulation of viral replication as well as triggering direct lysis of infected liver cells. The destruction of infected hepatocytes through lysis occurs due to action of HBV specific CD8+ cytotoxic T cells. Major destruction of hepatocytes in fulminant viral hepatitis is also as a result of host immune factors. HumoralAb response in fulminant hepatitis B is usually enhanced (Gish, 2009). This leads to an increased rate of HBsAG clearance from the liver. High level of anti-HBsAb is evident in patients with fulminant hepatitis B on admission. Fulminating hepatitis B may either be hyperacute, acut e, and subacute. In hyperacute, features present include encephalopathy within 7 days after the appearance of jaundice, and an increased rate of getting cerebral oedema (Aspinal at al., 2011). Acute condition presents itself with jaundice to encephalopathy within8-28 days and a high risk of cerebral oedema. In subacutecondition, development of jaundice to encephalopathy may occur within 5-26 wks, and there is a minimal risk of cerebral oedema. Main clinical features in fulminating hepatitis B include encephalopathy, jaundice, and hepatocellular carcinoma. The liver may appear enlarged during the initial stages, but later reduces in size. Other conditions include cerebral oedema, renal failure, and