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Hepatitis D - Diagnosis

, medical expert
Last reviewed: 06.07.2025
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Viral hepatitis of mixed etiology can be assumed with the corresponding epidemiological history (blood transfusion, intravenous drug use, etc., multiple parenteral interventions, etc.), a more acute onset of the disease than with viral hepatitis B, fever, a short pre-icteric period with pain in the right hypochondrium and joints, a two-wave and more severe course of hepatitis, severe hyperfermentemia, an increase (not sharp) in the thymol test.

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Specific diagnostics of hepatitis D

It is based on detection of markers of active replication of both viruses: HBV, HDV. From the first days of jaundice onset, HBsAg, high titer anti-HBV IgM, HBe antigen, HDAg and/or anti-delta (anti-delta IgM) are detected in the blood serum. Anti-delta IgM are produced already in the acute period and serve as the main marker of delta infection. They can be determined in high titer for 1-3 weeks, then they cease to be detected, anti-delta IgG are detected already 1-3 weeks after the onset of the icteric period of the disease. However, anti-delta IgM cannot be detected in approximately 20% of patients, and detection of anti-HD IgG may be delayed for 30-60 days, and in this case, delta infection will not be diagnosed unless anti-HD IgG is re-tested in the blood serum. Using the PCR method, HDV RNA in blood serum is determined within 1-3 weeks from the onset of the icteric period.

In the blood serum of patients with superinfection, HBsAg, HBcAg or anti-HBe are detected in the prodromal period and from the first days of the icteric period, but anti-HBc IgM is absent. Anti-delta IgM is also detected and a little later (after 1-2 weeks) - anti-delta IgG. HDV RNA is detected in the blood of patients both in the prodromal period and from the first day of the icteric period, and then the blood is constantly tested during the development of chronic infection in isolation or along with HBV DNA. With the development of a severe course of hepatitis delta, HBsAg and HBV DNA often disappear from the blood, but HDV RNA is detected. Most researchers interpret this phenomenon as a consequence of the suppression of the replicative activity of HBV by the delta virus.

Acute viral hepatitis D should be suspected in the presence of a very short preicteric period, a combination of pronounced hepatosplenomegaly with pain in the right hypochondrium, edematous-ascitic syndrome, fever, hyperbilirubinemia, hyperenzymemia, low values of the sublimate test, an increase in the thymol test and the level of the y-globulin fraction in the blood serum. Acute hepatitis delta should also be suspected in the presence of jaundice in "healthy" HBsAg carriers or in the exacerbation of chronic hepatitis B.

Thus, in case of acute delta virus infection, it is necessary to conduct differential diagnostics, first of all, with acute and exacerbation of chronic viral hepatitis B.

Standard for diagnostics of hepatitis (inpatient care)

Diagnostic procedures

Frequency of examination

Notes

Bilirubin

Once every 10 days

In severe cases - as needed

ACT

ALT

Complete blood count

General urine analysis

HB s Ag

Prothrombin index

1

Repeated depending on the severity of hepatitis

Blood group and Rh factor analysis

1

Anti-HBc IgM

1

Anti-delta IgM

1

Criteria for the diagnosis of OGV with delta agent (coinfection) in combination with anti-HBV with IgM

Anti-HD-total

1

Criteria for the diagnosis of acute hepatitis B with delta agent (coinfection) in case of a negative test during the initial examination and detection during subsequent testing (seroconversion) in combination with anti-HBc IgM. Criteria for the diagnosis of acute delta (super) infection in the absence of anti-HBc IgM

Anti-HCV

1

Necessary to exclude mixed infection

Anti-HAV IgM

1

Anti-HIV

1

Management plan for a patient with icteric form of acute viral hepatitis B with delta agent (coinfection) and acute hepatitis delta in a hepatitis B virus carrier (superinfection)

Information about the patient: anamnesis data: intravenous administration of psychoactive drugs, parenteral interventions 1-6 months before the first signs of the disease, acute or subacute onset of the disease, the presence of symptoms of the pre-icteric period of viral hepatitis D (fever, abdominal pain, severe intoxication), short prodromal period, the appearance of jaundice, deterioration of the condition with the appearance of jaundice.

Biochemical blood test. Blood test for viral hepatitis markers:

  • increased ALT and AST activity (more than 30-50 norms), increased bound and free bilirubin fractions, normal prothrombin index values. Detection of acute phase markers of HBV in the blood serum - HBsAg and anti-HBV IgM, detection of anti-delta IgM and/or anti-delta IgG in the blood - diagnosis: "acute viral hepatitis B with delta agent (coinfection), icteric form, moderate severity" (see treatment tactics):
  • increased ALT and AST activity (more than 30-50 norms), increased bound and free bilirubin fractions, normal prothrombin index values. Absence of acute phase markers of HBV in the blood serum (anti-HBV IgM) in the presence of a positive test for HBsAg, detection of anti-delta IgM and/or anti-delta IgG in the blood - diagnosis: "acute viral hepatitis D in a carrier of viral hepatitis B (superinfection), icteric form, moderate severity" (see treatment tactics).

Information about the patient: significant deterioration of the condition with the appearance of jaundice (increased nausea, vomiting, increasing weakness).

Actions: daily monitoring of prothrombin index, unscheduled biochemical blood test

Information about the patient. Decrease in prothrombin index to 60-50%, increase in hyperbilirubinemia, increase in transaminase activity or a sharp decrease in their activity. Dizziness, decrease in liver size, pain during palpation of the liver, manifestations of hemorrhagic syndrome.

Diagnosis: “acute viral hepatitis B with delta agent (coinfection), icteric form, severe course” or “acute hepatitis delta in a carrier of viral hepatitis B (superinfection), icteric form, severe course”.

Actions: intensification of therapy.

Information about the patient. Further deterioration of the patient's condition, appearance of agitation or inhibition, decrease in the prothrombin index to less than 50%), appearance of symptoms of acute hepatic encephalopathy.

Actions: transfer to the intensive care unit (ward) (see treatment tactics); plasmapheresis, dehydration therapy (reduction of cerebral edema), relief of agitation, artificial ventilation if necessary.

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