Diagnosing And Treating Hepatitis

Hepatitis A (HAV) Diagnosing HAV:

A blood test showing the presence of IgM anti-HAV in serum confirms the diagnosis of acute hepatitis A infection. Symptoms of this virus strain include nausea, vomiting, and diarrhea. Once infected and recovered, the antibodies to the virus provide protection from future infections with HAV. Following this, HAV blood tests will always return a positive result.

Diagnosing HBV:

Acute HBV infection is diagnosed by a simple blood test detecting the presence of hepatitis B surface antigen (HBsAg) and IgM antibody to hepatitis B core antigen (anti-HBc IgM). These antibodies develop in the blood in the early stages of infection at the time symptoms appear. The following antibody variations can occur, each having a specific implication: Antibody to HBsAg (anti-HBs): Develops after active infection and serves as an indicator of immunity.

•     Anti-HBs +: Indicates individual has been vaccinated, has received immune globulin, is immune, or is an infant who has received antibodies from its mother.
•     Anti-HBc +: Indicates past or present infection and lasts indefinitely. Also may be detected in someone who has received immune globulin or an infant who has received antibodies from its mother.
•     IgM anti-HBc +: Indicates recent infection with HBV, usually within 4-6 months.
•     HBeAg +: Indicates active viral replication and high infectivity.
•     HBsAg +: Indicates acute or chronic HBV. Persistence for 6 months after acute infection indicates progression to chronic HBV.

Treating HBV:

While there is no treatment for acute hepatitis B, there are two approved treatments for chronic hepatitis B – interferon alfa-2b and lamivudine. Only patients with active HBV replication are candidates. The drugs should not be given together.

About 35% of patients treated with injections of interferon for 4 to 6 months will have a long-term response. Interferon therapy often results in a number of side effects including flu-like symptoms, fatigue, headache, nausea and vomiting, loss of appetite, depression, and hair thinning. Because interferon may depress the bone marrow, blood tests are needed to monitor white blood cells, platelets.

The response to oral lamivudine, given for at least one year, may be somewhat lower. Lamivudine is very well tolerated but viral resistance to treatment may occur. Liver enzymes are monitored during treatment with both drugs. Patients with chronic hepatitis B should be vaccinated against hepatitis A.

Hepatitis C (HCV):

Infection by the hepatitis C virus can be determined by a blood test that detects HCV antibodies in the blood. This test is not a part of a routine physical, and people must ask their doctor for hepatitis C test. If the initial test is positive, a second test should be done to confirm the diagnosis and liver enzymes (a blood test) should be measured.

Anti-HCV (antibodies to the virus) may not be present in the first four weeks of infection in about 30% of patients. HCV infection may be identified by the presence of anti-HCV in approximately 60% of people as early as 5-8 weeks after exposure. In some individuals HCV antibodies may not be detected for 5-12 months. HCV-RNA and RT-PCR tests can determine HCV presence in as little as 1-2 weeks.

Over 80% of HCV infections become chronic, which means liver enzyme levels remain elevated for six months or more after the initial acute infection.

The enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are released when liver cells are injured or die, but they do not reliably predict the severity of the liver injury. Elevated ALT and AST levels may appear and disappear throughout the course of the infection. Current tests can indicate that the infection is chronic (infections that do not clear up within six months). High ALT and AST levels reveal ongoing liver damage.

A liver biopsy can identify the type and degree of damage (and can determine the severity of the disease). The disease may gradually progress over a period of 10-40 years.

Diagnosing hepatitis A :

If you have been in contact with someone with hepatitis A or you begin to have symptoms, see your GP.

Your GP will be able to diagnose hepatitis A with a blood test. If this shows a positive reaction to antibodies (proteins produced by your immune system to fight disease), it means your body is making antibodies to fight the hepatitis A virus present in your blood.

Background:

One of the more common causes of acute hepatitis is hepatitis A virus (HAV), which was isolated by Purcell in 1973. Humans appear to be the only reservoir for this virus. Since the application of accurate serologic investigations in the 1980s, the epidemiology, clinical manifestations, and natural history of hepatitis A have become apparent.

The relative frequency of HAV as a cause of acute hepatitis has declined in Western societies, while in contrast, notification of individual cases has increased, primarily as a result of improved reporting and diagnostic techniques. The nadir of reported cases was in 1987.

Improvements in hygiene, public health policies, and sanitation have had the greatest impact on hepatitis A, and vaccination and passive immunization have successfully led to some reduction in illness in high-risk groups.

Reduced encounters with HAV at a young age have resulted in both a decline in herd immunity and a change to the epidemiology of the illness, with increases in the mean age of occurrence of illness attributed to acute HAV infection in Western societies. Although this phenomenon may lay a framework for potential epidemics in the future, public health policies and newly implemented immunization practices are likely to reduce this potential.

Type A viral hepatitis: epidemiology, diagnosis, and prevention:

Five very different viruses make up the “classical” etiological agents responsible for acute or chronic viral hepatitis in humans. For the most part, these viruses share only a common tropism for the liver, with the hepatocyte representing the dominant site of viral replication and either acute or chronic forms of hepatitis representing the major clinical manifestations associated with infection. These viruses can be considered as two distinct groups, based on several clinically and epidemiologically important characteristics: those viruses that possess a lipid-containing outer viral envelope (hepatitis B, C, and D viruses: HBV, HCV, HDV)1 and those that do not (hepatitis A and E viruses: HAV, HEV).

HAV and HEV, which lack a lipid envelope, are stable when they are secreted from infected liver cells into the bile, and they gain entry to the intestinal tract via this route. Thus, these viruses typically spread by a fecal–oral mode of transmission, and they can cause extensive common-source outbreaks of disease. However, neither of these viruses causes persistent infection, and neither has been identified as a cause of chronic viral hepatitis. In contrast, HBV, HCV, and HDV all possess lipid envelopes and are likely to be rapidly inactivated by bile. Thus, these viruses are not shed in feces in biologically significant amounts. Their transmission occurs by several other routes, most often involving virus shed from a mucosal surface or by direct percutaneous exposures. In addition, HBV, HCV, and HDV may each cause persistent infection, and each has been shown to be an important etiological agent of chronic viral hepatitis and cirrhosis. Infection with HBV or HCV may lead ultimately to the development of primary hepatocellular carcinoma, often after many years of persistent infection and chronic hepatitis. Although chronic viral hepatitis is not associated with HAV infection, acute hepatitis due to HAV is nonetheless an important public health problem, both in the US and overseas.