Hepatitis B

Overview

HBV infection is parenterally transmitted i.e.:

1. Firstly, In babies born to HBV infected mothers, after transfusion of blood and blood products.
2. Secondly, IV drug use
3. Thirdly, Sexual contact
4. Lastly, HDV infection only in HBV-infected individuals

The hepatitis B virus consists of a core containing DNA and a DNA polymerase enzyme needed for virus replication. The core of the virus is surrounded by surface protein (Fig. 23.23). The virus, also called a Dane particle, and an excess of its surface protein (known as hepatitis B surface antigen) circulate in the blood. Humans are the only source of infection.

Spread of infection

Hepatitis B is one of the most common causes of chronic liver disease and hepatocellular carcinoma worldwide. Approximately one-third of the world’s population have serological evidence of past or current infection with hepatitis B and approximately 350–400 million people are chronic HBsAg carriers.

Hepatitis B may cause an acute viral hepatitis; however, acute infection is often asymptomatic, particularly when acquired at birth. Many individuals with chronic hepatitis B are also asymptomatic.

Hepatitis B infection is caused by the hepatitis B virus (HBV). The virus pass from person to person through blood, semen or other body fluids. It does not spread by sneezing or coughing.

• Injection drug use
• Infected unscreened blood products
• Tattoos/acupuncture needles
• Sexual (homosexual and heterosexual)
• Close living quarters/playground play as a toddler (may contribute to high rate of horizontal transmission in Africa)
• HBsAg-positive mother

Signs and symptoms of hepatitis B range from mild to severe. They usually appear about one to four months after you’ve infected, although you could see them as early as two weeks post-infection. Some people, usually young children, may not have any symptoms.

Hepatitis B signs and symptoms may include:

• Abdominal pain
• Dark urine
• Fever
• Joint pain
• Loss of appetite
• Nausea and vomiting
• Weakness and fatigue
• Yellowing of your skin and the whites of your eyes (jaundice)

On exposure to Hepatitis B virus, the spectrum of clinical presentation depends on the immune status of the individual.

Acute hepatitis B—

appropriate immune response in majority of adults leads to acute hepatitis within 5 weeks to 5 months of exposure to infection but resolves within 6 months after the onset. No treatment require as the body is able to clear the virus with the resolution of hepatitis, and clearance of virus markers and development of immunity.

Acute and sub acute

liver failure is a severe form of acute hepatitis that complicate by liver failure. Paradoxically hepatitis B virus may present in extremely Low quantity or undetectable due to profound and inappropriate immune response. Antiviral therapy indicate but liver transplant may require if the condition does not stabilise.

Chronic hepatitis B—

Persistence of Hepatitis B infection for more than 6 months seen when the body has either inadequate or no response to HBV and is unable to clear the virus resulting in chronic inflammation of the liver of variable intensity.

Investigation

Interpretation of various serological markers in hepatitis B, clinical situations in hepatitis B infection and serological markers and transaminase levels.

HBV contains several antigens to which infected persons can make immune responses, these antigens and their antibodies are important in identifying HBV infection, although the widespread availability of polymerase chain reaction (PCR) techniques to measure viral DNA levels in peripheral blood means that longitudinal monitoring now also frequently guide by direct assessment of viral load. Hepatitis B surface antigen (HBsAg).

HBsAg

HBsAg is an indicator of active infection, and a negative test for HBsAg makes HBV infection very unlikely. In acute liver failure from hepatitis B, the liver damage mediate by viral clearance and so HBsAg negative, with evidence of recent infection shown by the presence of hepatitis B core IgM. HBsAg appears in the blood late in the incubation period, but before the prodromal phase of acute type B hepatitis; it may present for a few days only, disappearing even before jaundice has developed, but usually lasts for 3–4 weeks and can in the illness and rapidly reaches a high titre, which subsides gradually but then persists.

Anti-HBc is initially of IgM type, with IgG antibody appearing later. Anti-HBc (IgM) can sometimes reveal an acute HBV infection when the HBsAg has disappeared and before anti-HBs has developed. Hepatitis B e antigen (HBeAg). HBeAg is an indicator of viral replication. In acute hepatitis B it may appear only transiently at the outset of the illness; its appearance follow by the production of antibody (anti-HBe). The HBeAg reflects active replication of the virus in the liver.

Chronic HBV infection mark by the presence of HBsAg and anti-HBc (IgG) in the blood. Usually, HBeAg or anti-HBe is also present; HBeAg indicates continued active replication of the virus in the liver. The absence of HBeAg usually implies low viral replication; the exception is HBeAg-negative chronic hepatitis B, in which high levels of viral replication, serum HBV-DNA and hepatic necroinflammation seen, despite negative HBeAg.

Treatment

In hepatitis B, among previously healthy adults who present with clinically apparent acute hepatitis, recovery occurs in ~99%; therefore, antiviral therapy is not likely to improve the rate of recovery and not require. In rare instances of severe acute hepatitis B, treatment with a nucleoside analogue at oral doses used to treat chronic hepatitis B has attempted successfully.

Although clinical trials have not done to establish the efficacy or duration of this approach, most authorities would recommend institution of antiviral therapy with a nucleoside analogue (entecavir or tenofovir, the most potent and least resistance-prone agents) for severe, but not mild–moderate, acute hepatitis B. Treatment should continue until 3 months after HBsAg seroconversion or 6 months after HBeAg seroconversion.

Fulminant hepatitis

In fulminant hepatitis, the goal of therapy is to support the patient by maintenance of fluid balance, support of circulation and respiration, control of bleeding, correction of hypoglycemia, and treatment of other complications of the comatose state in anticipation of liver regeneration and repair. Protein intake should restrict, and oral lactulose or neomycin administered. Glucocorticoid therapy has shown in controlled trials to ineffective.

Likewise, exchange transfusion, plasmapheresis, human cross-circulation, porcine liver cross-perfusion, hemoperfusion, and extracorporeal liver-assist devices have not proven to enhance survival. Meticulous intensive care that includes prophylactic antibiotic coverage is the one factor that does appear to improve survival. Orthotropic liver transplantation is resort to with increasing frequency, with excellent results, in patients with fulminant hepatitis.

Frequently Asked Questions

What is Hepatitis B?

Hepatitis B is a viral infection caused by Hepatitis B virus affecting Liver. HBV is a DNA virus with a remarkably compact genomic structure; despite its small, circular, 3200-bp size, HBV DNA codes for four sets of viral products with a complex, multiparticle structure.

Homeopathic Medicines used by Homeopathic Doctors in treatment of Hepatitis B?

• Aconite
• Belladonna
• Chamomilla
• Cornus cer
• China
• Nitric Acid
• Kali carb

What causes Hepatitis B?

Hepatitis B virus (HBV)

What are the symptoms of Hepatitis B?

• Abdominal pain
• Dark urine
• Fever
• Joint pain
• Loss of appetite
• Nausea also vomiting
• Weakness also fatigue
• Yellowing of your skin and
• Whites of your eyes (jaundice)