What is Hepatitis B?
Hepatitis B is a viral infection of the liver that causes inflammation of the liver and death of hepatocytes (liver cells). It can occur as an acute infection that in 5% -10% of cases becomes chronic (when the infection is maintained for more than 6 months). Chronic infection can progress to liver cirrhosis and even liver cancer.
Causes of Hepatitis B
It is caused by hepatitis B virus (HBV). The VBH belongs to the family of viruses called Hepadnaviridae and its genetic material is a DNA of 3,200 base pairs in length that has a circular shape. Occasionally, VBH infection is associated with another virus called hepatitis Delta virus. When this occurs, the damage to the liver is much greater, which worsens the prognosis of the disease.
Hepatitis B virus seen under a microscope.
Hepatitis B infection can be prevented with a very effective vaccine.
Pathways of Hepatitis B infection
VBH is transmitted through blood and other body fluids such as saliva and semen that may contain traces of blood. Another important route of transmission of hepatitis B is the vertical route from the infected mother to the child during delivery. The virus can also be transmitted from mother to child through breast milk.
Taking into account the routes of transmission of the virus, are practices of risk performing tattoos or piercings, acupuncture, sharing syringes and objects that may have traces of blood such as toothbrushes, razors or nail clippers and maintaining relationships sexual without protection.
Most people infected acutely with the hepatitis B virus have no symptoms. Occasionally these people may present with yellowing of the skin (jaundice), dark urine, tiredness, loss of appetite, nausea, vomiting and abdominal pain.
The chronic infection does not produce symptoms in the majority of the cases and the disease usually is discovered during routine analyzes of blood when being observed that the levels of the hepatic enzymes (transaminases) are elevated. To confirm that this transaminase elevation is caused by HBV, the presence of the protein that forms the outer coat of the virus called surface antigen (HBsAg) and virus DNA (VBH-DNA) is detected in blood. Other markers of HBV infection that are detected in blood are the antibodies against the protein that forms the inner core of the virus (anti-HBc) of both IgM and IgG, another viral protein called “e” antigen (AgHBe) and the antibodies against it (anti-HBe).
Hepatitis B infection can be prevented by a specific vaccine. This vaccine is very effective and generates antibodies that protect against infection in up to 90% of the people who receive it. The protection lasts at least 20 years and it is very likely that it can protect for life although this has not been proven yet.
The goals of hepatitis B treatment are:
- Avoid inflammation and destruction of liver cells.
- Try to eliminate the virus (loss of VBH-DNA and HBsAg in blood).
All patients with hepatitis B and increased transaminases should be treated. However, 20% of patients with HBV infection have normal transaminase levels and should only be treated if they have a high viral load (levels of VBH-DNA in blood).
There are several drugs that are useful for the treatment of hepatitis B virus that can be divided into two groups:
- Immunomodulators (Interferón alfa pegilado -PEG-IFN-).
- Nucleoside analogs.
PEG-IFN is administered by a weekly subcutaneous injection and results in the normalization of transaminase levels (objective 1) in 39% of chronic hepatitis B viruses and the loss of VBH-DNA in 25% and Ag HBs in 6% of the cases (objective 2). However, PEG-IFN produces important side effects (flu syndrome, joint pain, etc).
With respect to nucleoside analogs, they achieve normalization of transaminase levels in 40% -80% of patients (objective 1) and the loss of VBH-DNA in 40% -90% and AgHBs in 3 % -6% of cases (objective 2). Treatment with nucleoside analogues is well tolerated without significant side effects and is administered orally (one tablet per day).
There are several nucleoside analogues currently available: Lamivudina, Adefovir, Telbivudina, Entecavir y Tenofovir.
Lamivudine and Adefovir produce resistance (mutations in the DNA of B virus that make the drug ineffective) with a frequency of 70% after 5 years of treatment, so they are generally not used.
Entecavir and Tenofovir produce hardly any resistance and are the drugs of choice. The drawback is that they must be administered for years because if the treatment is interrupted before the HBsAg is lost, most patients relapse.
Most people infected acutely with the hepatitis B virus have no symptoms.
How aggression and evolution can be predicted
By means of a liver biopsy, the degree of inflammation of the liver and the level of destruction of the hepatocytes can be determined.
In recent years it has been proven that the evolution of liver damage in chronic hepatitis B can be predicted by determining a polymorphism (variant) of the human PNPLA3 gene. To study this polymorphism, a puncture is performed on the patient’s fingertip (similar to that done to determine glucose levels) and the drop of blood is deposited on a special card that absorbs and preserves human DNA. The analysis can give the following results.
- Homozygous CC: Low risk of progression of liver damage.
- Heterozygous CG: Low risk of progression of liver damage.
- Homozygous GG: High risk of progression to more severe forms of liver damage (increased liver fibrosis).
Other useful techniques to know the aggressiveness of liver disease in chronic hepatitis B are ultrasound of the liver and Fibroscan.
- McMahon BJ. Epidemiology and natural history of hepatitis B. Semin Liver Dis 2005;25(Suppl 1):3-8.
- Pardo M, et al. Current therapy of chronic hepatitis B. Arch Med Res 2007;38:661-77.
- Dienstag JL. Hepatitis B virus infection. N Engl J Med 2008;359:1486–1500.
- Gill US, Kennedy PT. New insights in the management of chronic hepatitis B. Clin Med 2015;15:191-196.
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