Diagnosis | Hepatitis A

Diagnosis

In the patient interview (anamnesis), the path-breaking symptoms and causes can be identified or other causes can be excluded. For example, specific questions can be asked about previous hepatitis A vaccinations or recent trips abroad. During the physical examination, an acute hepatitis A infection often reveals a painful pressure in the right upper abdomen and a palpable enlargement of the liver.

In the blood, parameters can be collected that indicate an inflammation of the liver. The liver enzymes (transaminases or “liver values”) GOT (glutamate-oxalacetate transferase or ASAT = aspartate aminotransferase) and GPT (glutamate-pyruvate transferase or ALAT = alanine aminotransferase) are localized in different cell organelles in a liver cell. In the event of liver cell destruction, these and other enzymes are released and can be detected in the blood.

Depending on the constellation of the enzymes, the extent of the liver cell damage can be determined. The first possibility to confirm the diagnosis by a blood test is about 14 days after the infection, because then the first antibodies against the hepatitis virus A are produced by the body. These are the antibodies of immunoglobulins M (IgM).

IgM is an immunoglobulin that is produced as the earliest antibody in the course of an immune response (the body’s own defense reaction). An elevated IgM antibody level indicates acute infection by HAV. A few days later, the B lymphocytes or plasma cells produce the permanent immunoglobulin G (IgG).

These are the most important antibodies with the strongest defence effect. They are the second most important antibodies after IgM and increase in number in the blood to fight the infection. After an infection has been overcome, they are permanently detectable in the blood and, in the case of hepatitis A, they guarantee lifelong immunity.

The detection of viral DNA in the stool of the infectious patient is also possible for diagnosis. Sonography: In an ultrasound examination, the abdominal cavity (abdomen) and the abdominal organs are visualized with the help of ultrasound waves. The transducer emits ultrasound waves that are absorbed or reflected by the various tissues it encounters.

The transducer receives the reflected waves, which are converted into electrical impulses and displayed on a screen in different shades of grey. In symptomatic acute hepatitis A, the liver may be enlarged and appear slightly less echoic (i.e. darker) due to an accumulation of fluid in the liver (edema). Sonography is not used to make a diagnosis but can be helpful in assessing the extent of the disease.

If the liver is attacked by a hepatitis A infection, an increase of the so-called transaminases occurs in the blood. Transaminases are enzymes that accelerate important reactions in the conversion of amino acids. They are localized in large numbers in the cells of the liver, among other places, where they exert their effect.

If liver cells are destroyed, as in liver inflammation, these enzymes are released into the blood. If newly formed antibodies (class IgM) against hepatitis A viruses can also be detected in the blood, these in combination with the laboratory value changes are evidence of a hepatitis A infection. In acute infections, which an organism undergoes for the first time, certain specific antibodies are formed against the invading virus.

IgM means immunoglobulin of type M, which represents an antibody that is only produced during the initial infection. These can fight the virus while at the same time the body produces IgG type antibodies, which will provide a more targeted and effective defence when the virus re-infects the body. If IgM-type antibodies are produced during a hepatitis A infection, the person affected knows that his or her body is affected by an acute infection.

Approximately 4 months after the initial infection, immunoglobulins M are no longer detectable. Immunoglobulins of the IgG type are the specific antibodies that provide the organism with lifelong immunological protection against a specific antigen. They are formed during the initial infection with the virus and circulate permanently in the blood from the 6th week after infection.