Chronic hepatitis B
After acute hepatitis B in 5-10% of cases, the disease can persist. Three methods are possible:
- Single of the HBsAg s Portage these patients are still infected with the virus and they can contaminate their surroundings. However, the liver is normal. The assay is also normal transaminases.
- Chronic hepatitis weakly active: in the space door liver inflammatory infiltration of mononuclear cells persists for more than 6 months. Transaminases are high but there is little or no clinical signs. S The HBsAg is present in serum associated once every two to HBsAg e. This form can heal or become CHRONIC HEPATITIS ACTIVE.
- Chronic active hepatitis is characterized by a greater liver damage. There periportal and lobular NECROSIS. Fibrosis appears whose intensity is a reflection of cirrhosis. The clinical signs are: fatigue, an enlarged liver, an enlarged spleen. In terms of the laboratory, TRANSAMINASES are increased and gamma globulin.
Cirrhosis may appear 10 to 30 years with all the serious consequences it entails: hepatic failure, ASCITES, encephalopathy.
Finally, liver cancer affects about one quarter of the holders of a post-hepatitis B cirrhosis. This cancer can be revealed by an ultrasound but the achievement of the general condition is important and is accompanied by loss of appetite, and a dull pain in the right subcostal region.
Ascites may appear as well as jaundice. The prognosis is poor.
TREATMENT
Lamivudine is the first oral antiviral indicated for the treatment of chronic hepatitis B in adults with evidence of viral replication.
This treatment at a dose of 100 mg / day is recommended in patients with decompensated liver disease.
Lamivudine is incorporated into the genome of the virus, blocks the formation of DNA (see this term) and subsequent replication.
Treatment should be continued for many months. (Most often several years).
This treatment causes a slowing of liver fibrosis.
The benefit of treatment seems to be greater in patients with a high rate of aminotransferases prior to initiation of treatment.
Combination therapy with alpha interferon is possible but does not seem more effective than lamivudine monotherapy.
Since April 2003 a new molecule is available.
It is the first anti-HBV nucleoside analogue.
This is adefovir dipivoxil (Hepsera).
This treatment is indicated in patients suffering from chronic hepatitis B with high viral replication, continuous elevation of ALT (transaminases), active liver inflammation and fibrosse histologically proven.
Ainsiqu'une decompensated liver disease.
The dosage is one tablet per day.
A new therapeutic hope is based on results VITRO (see this term).
A cellular protein, 3G Apobec seems capable of inhibiting the replication of HBV.
It will cause the inactivation of the DNA (see DNA (DEOXYRIBONUCLEIC ACID) by incorporating viral during reverse transcription.
This molecule could control viral replication chronically ill and perhaps eradicate the virus during the acute phase of infection.
Another molecule appears to inhibit specifically the viral polymerase. it is endecavir
dose appears to be 0.5 mg per day.
Another molecules seems to be very effective, it is tenofovir.
this molecule normalize transaminases in three quarters of cases and negativity of HBsAg was found in about 10% of cases.
After acute hepatitis B in 5-10% of cases, the disease can persist. Three methods are possible:
- Single of the HBsAg s Portage these patients are still infected with the virus and they can contaminate their surroundings. However, the liver is normal. The assay is also normal transaminases.
- Chronic hepatitis weakly active: in the space door liver inflammatory infiltration of mononuclear cells persists for more than 6 months. Transaminases are high but there is little or no clinical signs. S The HBsAg is present in serum associated once every two to HBsAg e. This form can heal or become CHRONIC HEPATITIS ACTIVE.
- Chronic active hepatitis is characterized by a greater liver damage. There periportal and lobular NECROSIS. Fibrosis appears whose intensity is a reflection of cirrhosis. The clinical signs are: fatigue, an enlarged liver, an enlarged spleen. In terms of the laboratory, TRANSAMINASES are increased and gamma globulin.
Cirrhosis may appear 10 to 30 years with all the serious consequences it entails: hepatic failure, ASCITES, encephalopathy.
Finally, liver cancer affects about one quarter of the holders of a post-hepatitis B cirrhosis. This cancer can be revealed by an ultrasound but the achievement of the general condition is important and is accompanied by loss of appetite, and a dull pain in the right subcostal region.
Ascites may appear as well as jaundice. The prognosis is poor.
TREATMENT
Lamivudine is the first oral antiviral indicated for the treatment of chronic hepatitis B in adults with evidence of viral replication.
This treatment at a dose of 100 mg / day is recommended in patients with decompensated liver disease.
Lamivudine is incorporated into the genome of the virus, blocks the formation of DNA (see this term) and subsequent replication.
Treatment should be continued for many months. (Most often several years).
This treatment causes a slowing of liver fibrosis.
The benefit of treatment seems to be greater in patients with a high rate of aminotransferases prior to initiation of treatment.
Combination therapy with alpha interferon is possible but does not seem more effective than lamivudine monotherapy.
Since April 2003 a new molecule is available.
It is the first anti-HBV nucleoside analogue.
This is adefovir dipivoxil (Hepsera).
This treatment is indicated in patients suffering from chronic hepatitis B with high viral replication, continuous elevation of ALT (transaminases), active liver inflammation and fibrosse histologically proven.
Ainsiqu'une decompensated liver disease.
The dosage is one tablet per day.
A new therapeutic hope is based on results VITRO (see this term).
A cellular protein, 3G Apobec seems capable of inhibiting the replication of HBV.
It will cause the inactivation of the DNA (see DNA (DEOXYRIBONUCLEIC ACID) by incorporating viral during reverse transcription.
This molecule could control viral replication chronically ill and perhaps eradicate the virus during the acute phase of infection.
Another molecule appears to inhibit specifically the viral polymerase. it is endecavir
dose appears to be 0.5 mg per day.
Another molecules seems to be very effective, it is tenofovir.
this molecule normalize transaminases in three quarters of cases and negativity of HBsAg was found in about 10% of cases.
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