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Certain behaviors put a person at risk of contracting hepatitis D. Avoiding these high-risk behaviors is another approach to hepatitis D prevention. Following are some recommendations for avoiding these types of high-risk behaviors:

1.If you are a healthcare or public safety worker, get vaccinated against hepatitis B and always follow routine barrier precautions. Handle needles and other sharp objects in a safe manner.

2.Consider the risks if you are thinking about getting a tattoo or body piercing. You might get infected if the tools have someone else’s blood on them or if the artist or piercer does not follow good health practices.

3.Don’t share toothbrushes, razors, nail clippers, washcloths, or anything else that could have an infected person’s blood on it.

4.Do not shoot drugs. If you shoot drugs, stop and get into a treatment program. If you can’t stop, never share drugs, needles, syringes, water, or “works” — and be sure to get vaccinated against hepatitis A and hepatitis B.

5.If you are having sex, but not with one steady partner, use latex condoms correctly every time you have sex. Using condoms may lower your risk of getting hepatitis D.

Hepatitis D or delta virus (HDV) is an infection of the liver caused by a defective virus (delta agent). Delta agent can cause infection only in those individuals who have an active hepatitis B infection or who are a hepatitis B carrier.

The delta hepatitis virus (HDV) is an RNA virus, meaning that its genetic material is made up of ribonucleic acid. It is a small virus that requires the HBV to survive. HDV cannot survive on its own because it requires the HBV envelope (HBsAg) to enable it to infect the liver cells. The ways in which HDV is transmitted (spread), that is, by exposure to contaminated blood, especially intravenous drug use, and by sexual contact, are essentially the same as for HBV.

Acute HBV and acute delta hepatitis can be acquired at the same time, which results in a more severe form of acute hepatitis. Most of these patients, however, will subsequently clear both the HBV and delta hepatitis virus. Individuals who already have chronic hepatitis B also can acquire acute delta hepatitis. These individuals, however, usually will go on to develop chronic delta hepatitis infection on top of their chronic hepatitis B infection. Furthermore, individuals who have chronic delta hepatitis infection (and, by definition, chronic HBV infection) will almost always develop cirrhosis (severe liver scarring) rapidly. Chronic delta hepatitis with chronic HBV co-infection is very difficult to treat. These patients require at least one year of interferon therapy. Still, most treated patients will have a relapse after interferon is discontinued. Furthermore, lamivudine (3TC) has no effect on the delta hepatitis virus.

HDV is transmitted percutaneously or sexually through contact with infected blood or blood products. Blood is potentially infectious during all phases of active hepatitis D infection. Peak infectivity probably occurs just before the onset of acute disease. HDV has a worldwide distribution. It is endemic in the developing world, with a high prevalence in South America. HDV infection is limited to individuals who have HBV infection, and like hepatitis B is acquired parenterally. Worldwide about 5% of HBV carriers are anti-HDV positive. Delta hepatitis remains a common problem among intravenous drug users.

The clinical course is influenced by several factors, including the HDV genotype. This issue is discussed in detail elsewhere but a brief review is warranted to provide the rationale for antiviral therapy. (See “Pathogenesis and clinical manifestations of hepatitis D virus infection”.)

The predominant genotype in the Western world is genotype I. Once chronic HDV infection is established, it usually exacerbates the preexisting liver disease due to HBV. Progression towards cirrhosis may be rapid, but does not occur in all patients. HDV-associated chronic liver disease may run an indolent course and asymptomatic HDV carriers have been found in some geographical areas.

Patients who are currently referred for HDV infection appear to represent cohorts infected many years ago in whom the HDV-related disease rapidly developed to cirrhosis, but whose subsequent disease progression has been slow. This was illustrated in a report from Italy in which the estimated 5- and 10-year probability of survival free of liver transplantation in patients who had already developed clinically overt cirrhosis was 49 and 40 percent, respectively. A more ominous course toward liver decompensation has been documented in patients with active HBV and HDV replication. In the Far East, where the predominant genotype is genotype II, there is a less frequent association of chronic HDV infection with progressive liver disease.