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A 51-year-old male with fulminating Hepatitis B secondary to a lifetime use of IV drug abuse - Research Paper Example

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This helps in identifying the initial treatment, as well as eliminating all contraindications to liver transplant. In addition, conducting proper prognosis helps…
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A 51-year-old male with fulminating Hepatitis B secondary to a lifetime use of IV drug abuse
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A 51-year-old male with fulminating Hepatitis B secondary to a lifetime use of IV drug abuse

Patients of such nature may spread the condition to others unknowingly (Vandevante et al, 2011).
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 such situations, (HbsAg) appears in patients’ blood in the form of small spheres. Apart from (HbsAg), patients with acute hepatitis also have HBeAg in circulation (Carey, 2009).
In hepatitis B virus infections, destruction of hepatocytes is not as a result of the virus, but it is caused by the host’s immune response to the viral antigens. The cellular immune response is the primary cause of pathogenesis, but the humoral immune response is less significant. Antigen presenting cells initiate the cellular immune response by presenting the viral epitopes to antigen specific T-lymphocytes. After production, the T cells go through a stage of maturation and expansion and then later migrate into the liver. 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 ... Read More
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