Nerdy Science Blog

As the name denotes, Hepatitis B is a disease caused by Hepatitis B virus. It causes inflammation to take place in the liver, thus the name of hepar (liver) and –itis (inflammation). The Hepatitis B virus is composed of a surface protein coat, a nucleocapsid and internal proteins and nucleic acid. It has three antigens, the surface, core and the ‘e’ antigens. The surface antigen is found in an excessive amount during infection while the core antigen is found only in the blood as an internal part of a complete Hepatitis B virion. The ‘e’ antigen is associated with complete infectious Hepatitis B virion, thus the existence of such antigen in the blood denotes the infectivity of a person.

Hepatitis B is a serious endemic disease throughout the world. Today, at least 280 million cases had been recorded. The natural reservoirs of this virus are humans and probably chimps and monkeys.

Hepatitis B virus is transmitted parenterally by needles and intravenous equipment, sexually, unscreened blood products and perinatally. Thus, risk factors include: spouse of an acutely infected person, individuals who have unprotected sex, health care workers exposed to blood, drug abusers who share needles, recipients of repeated transfusions, patients on hemodialysis, recipients of a transplanted organ and children born to an infected mother.

Once the virus enters the body, the virus will first infect the liver cells (hepatocytes). Their nucleocapsid proteins will invite cytolitic T cells to destroy the infected liver cells. The differences of T cell responsiveness in a patient determine two outcomes – those who recover after acute hepatitis and those who progress to chronic hepatitis.

One of the main sequels of Hepatitis B infection is hepatocellular carcinoma, which is a major health problem worldwide. 80% of the world’s hepatocellular carcinoma is caused by Hepatitis B virus.

Most primary Hepatitis B infections are self-limiting and resolve by itself within 3 to 6 months. Most infections are asymptomatic. Prodromal symptoms (before the acute onset of the disease) includes – anorexia, nausea, vomiting, fatigue, malaise, arthralgias, myalgias, headache, photophobia, pharyngitis, cough and low-grad fever. When the liver is damaged to certain degree, symptoms related to liver dysfunction present themselves. This include – jaundice, dark urine, clay-colored stools, tender hepatomegaly and right upper-quadrant pain.

In the diagnostic laboratory tests, changes in serum alanine aminotransferase and aspartate aminotransferase levels are expected. Jaundice is usually visible in the sclera or on the skin when the serum bilirubin is more than 2.5mg/dl. There will also be changes in Prothrombin time and albumin level. Liver biopsy is usually unnecessary.

With the help of the results from laboratory tests, physicians could differentiate Hepatitis B with other diseases which could also cause inflammation of the liver for example infectious mononucleosis, cytomegalovirus, herpes simplex and other diseases which could produce similar presentations, signs and symptoms; for example toxoplasmosis, leptospirosis, alcoholic hepatitis, acute cholecystitis, common duct stone, ascending cholangitis and carcinoma of the pancreas. Other diseases which could cause metabolic liver disorders include Wilson disease, alpha1-antitrypsin deficiency, hemochromatosis, and sometimes a doctor would even need to rule out metastasis to the liver from another cancer site, which could also produce similar clinical presentations.

All patients with suspected hepatitis should undergo serologic tests such as – Serum HBsAg, Serum IgM anti-HBc, Serum immunoglobulin G anti-HBc, HBeAg, Serum anti-HBs and quantitative HBV DNA. The positive tests could proves that the patient is infected by Hepatitis B virus instead of all the other diseases stated above. In a patient infected with Hepatitis B, HBsAg presents except in patients without ongoing viral activity. Immunoglobulin G anti-hepatitis B core antigen is also present. The immunoglobulin M anti-HBc is present with acute or recent infection. It is useful for distinguishing acute from chronic infection in patients found to be HBsAg positive for unknown during (for example blood donors). HBeAg and HBV DNA are qualitative markers for active Hepatitis B virus replication.

Putting the result of serological tests and other additional laboratory findings of elevated ALT and AST level, elevated alkaline phosphatase level, elevated serum bilirubin level, hypoalbuminemia and prolonged prothrombintime, a doctor could end up with the diagnosis of chronic Hepatitis B.

Treatment of acute Hepatitis B includes:

1. Supportive care – high-calorie diet, intravenous hydration and parenteral nutrition if patients are vomiting or unable to maintain oral intake. Avoid alcohol and drugs metabolized by the liver. Bile-salt sequestrant resins can be given if there is severe itch, for example Cholestyramine.
2. Antiviral therapy – in rare instances, treatment with Lamivudine (antiviral medication) has been successful.
3. Liver transplantation for fulminant hepatic failure and grade III or IV encephalopathy.

Future care of the patient includes

1. Monitor for clinical and biochemical recovery – disappearance of HBsAg after apparent clinical recovery from acute Hepatitis B. Those who failed to be HBsAg-negative could be inactive carriers. Such patients are the source of infection and should take good care of their conduct so that the virus could not be spread to other people around them. The likelihood of becoming a HBsAg carrier is high among neonates, patients who receive hemodialysis and immunosuppressed patients.
2. Monitor for possible complications such as – serum sickness-like syndrome which includes arthralgia, arthritis, rash, angioedema, hematuria and proteinuria. Other comaplications are glomerulonephritis, nephrotic syndrome, polyarteristis nodosa, fulminant hepatitis, chronic hepatitis and last but not least, hepatocellular carcinoma.

The treatment for chronic Hepatitis B.

Five medications are approved for treatment. They are interferon alpha, pegylated interferon alpha, Lamivudine, Adefovir dipivoxil and Entecavir. Among these five available drugs, PEG IFN (pegylated interferon alpha) has supplanted standard IFN (interferon).

Researches show that PEG IFN benefits by achieving the highest rate of HBeAg responses after a year of therapy and does not readily induce viral mutations. It requires finite-duration of therapy. While the disadvantages of PEG IFN is that it is administered through subcutaneous injections, associated with inconvenience and intolerability and not safe in patients with cirrhosis. Thus, oral antiviral is better tolerated by the patients even though it requires long-term therapy in most patients.

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