HEPATITIS B ( Health tips)

 1. Mode of spread:

• Intravenous route: Transfusion of infected blood or blood products. Contaminated needles used by drug addicts, tattooists or acupuncturists.
• Sexual intercourse with infected person because virus is present in salvia, semen and vaginal secretions.
• From infected mother to child at the time of delivery.

2. High risk persons are IV drug abusers, patients and staff and hemodialysis centers,    homosexuals physicians, dentists, nurses and persons working in pathological laboratory and blood bank.

3. The risk of fulminant hepatitis is in 1-2% of persons with acute disease.

4. Can lead to chronic hepatitis, carrier state or hepatocellular carcinoma.

5. Perinatally infected infants generally have no clinical signs or symptoms, and infection produces typical illness in only 5-15% of children aged 1-5 years.

6. Incubation period: 1-6 months.

HEPATITIS B VIRUS (HBV)

Hepatitis B virus is a DNA virus also called Dane partcle; it consist of an inner core and an outer surface capsule.

The inner core is formed of core protein (hepatitis B core antigen-HBcAg). Core protein contains DNA and DNA polymerase. The capsule protein is referred to as hepatitis B surface antigen (HBsAg). Hepatitis B virus also contains e antigen (BHeAg).

VIRAL MARKERS

The hepatitis B virus proteins act as antigens to which infected person can make antibodies. These antigens an their antibodies are important in identifying hepatitis B virus infection; these are called viral markers.

1. Hepatitis B surface antigen (HBsAg).

• It is located in the capsular material of virus and is the first viral marker detectable after infection with hepatitis B.
• It appear in the blood in late incubation period before the elevation of aminotransferases and development of clinical features hepatitis.
• If becomes undetectable usually after 1-2 month after the onset of jaundice and rarely persists beyond 6 months. In chronic hepatitis it remains detectable beyond 6 months.

5. Antibodies to hepatitis B surface antigen (anti-HBs)

• Anti-HBs usually appear after clearance of surface antigen and persist for many years or perhaps permanently. Occasionally appearance of anti-HBs is delayed for several weeks of disappears of surface antigen (i.e. no antigen and no antibody detectable); this is called window period. During this period patient is infectious, therefore negative surface antigen does not rule out infection. If doubt is there, perform anti-HBc 1gM to confirm the infection.
• Presence of these antibodies indicates previous infection or vaccination.
• Disappearance of HBsAg and appearance of anti-HBs indicate recovery from HBV infection.

3. Hepatitis B core antibodies (anti-HBc)

• Hepatitis B core antigen (HBcAg) is located in the central part of the virus but it does not appear in the blood.
• Anti-HBc is the first antibody to appear, it appears shortly after HBsAg is detected. 1 gM type of Anti-HBc is a definitive evidence of acute infection and is predominant in first 6 months. 1 gG type of anti-HBc appear during acute hepatitis and is predominant beyond 6 months and persist indefinitely, whether the patient recovers (in which anti-HBsAg is also present) or develop chronic hepatitis (in which HBsAg is also present).

4. Hepatitis B 2 antigen (HBcAg).

• HBeAg appears during incubation period shortly after detection of HBsAg. It indicates viral replication and infectivity.
• Persistence of HBeAg in serum beyond 3 months suggests and increased likelihood of chronic hepatitis-B and presence of HBeAg during chronic hepatitis B is associated with ongoing viral replication, infectivity and inflammatory liver injury.
• Disappearance of HBeAg is followed by the appearance of anti-HBe indicating diminished viral replication and decreased infectivity.
• Some rare mutant forms of virus cannot synthesize the “e” antigen (pre-core mutant) and PCR for HBV DNA is required to confirm viral replication. Majority of hepatitis B virus is “wild type” that synthesizes ‘e’ antigen (HBeAg).
• HBsAg-positive serum containing HBeAg is more likely to be highly infectious. For example mothers with HBsAg and HBeAg transmit hepatitis B infection to their offspring in more than 90% while mothers with HBsAg with anti-HBe rarely infect their offspring.

5. Hepatitis B virus DNA (PCR for hepatitis B)

The presence of hepatitis B virus DNA in serum is a more sensitive marker of viral replication and infectivity. It can be detected by polymerase chain reaction (PCR) method.

Significance of viral markers in hepatitis B

• HBeAg: present in acute or chronic infection.
• HBeAg: rises early and fall rapidly in acute hepatitis, persistence indicates development of chronic hepatitis and increased sensitivity.
• HBV DNA (PCR): implies viral replication.
• Anti-HBe: indicates previous exposure and immunity to HBV.
• Anti-HBe: indicates diminished viral replication and low infectivity.
• Anti-HBc:

IgM: high titer in acute and low titer in chronic infection.

      IgG: indicates past exposure to hepatitis B.

      Patient may be recovered or developed chronic hepatitis.

Clinical application to viral markers.

·         Identify hepatitis B infection (HBsAg).

·         Identify either acute or chronic infection (anti-HBc antibodies).

·         Identify virus replication (HbeAg) that is required for treatment with interferon.

CLINICAL FEATURES

• Clinical features are similar to hepatitis A although the illness may be more sever; however infection may be asymptomatic.
• In addition, a serum sickness-like immunological syndrome may be seen in acute hepatitis during prodromal stage in up to 25% of cases. This consists of rashes (e.g. urticaria, maculopapular rash, Henoch-Schonlein purpura and polyarthritis affecting small joints.
• Fever is usually present.

Extrahepatic immune complex-mediated conditions such as polyarteritis nodosa, or glomerulonephritis are occasionally seen.

INVESTIGATIONS

Non-specific

LFTs, complete blood count, urine analysis, PT and blood sugar-as performed in  hepatitis A.

Specific

• HBsAg and anti-HBc 1gM should be performed. If HBsAg is positive, a full viral profile is then performed.
• In routine HBsAg is performed but it may be profile is then performed.
• In routine HBsAg is performed but it may be cleared rapidly or titer is very low, therefore anti-HBc IgM should also be performed simultaneously.
• HBV DNA (PCR) is the most sensitive test of viral replication.

COMPLICATIONS

1. Fulminant hepatic failure.
2. Post hepatitis syndrome: fatigue, fat intolerance and right upper quadrant pain.
3. Chronic hepatitis.
4. Cirrhosis.
5. Hepatocellular carcinoma.
6. Rare complications of viral hepatitis are as follows:
• Pancreatitis, myocarditis
• Atypical pneumonia
• Aplastic anemia
• Transverse myelitis
• Peripheral neuropathy