Role of HDV in differential diagnosis
Upon admission of a patient with prominent clinical symptoms of acute liver injury, the physician is required to perform a comprehensive differential workup. According to the algorithms outlined in clinical case studies, the baseline serological panel must include screening for markers of major viral hepatitides: A, B, C, and D (as well as screening for HIV infection).
If a patient's serological profile shows a complete absence of markers for both acute and chronic forms of hepatitis A, B, C, and D, the clinical and epidemiological investigation shifts toward other etiological factors. For instance, in the presence of epidemiological risks (waterborne transmission, history of travel to endemic regions) and a specific clinical presentation (severe course in pregnant women), a negative test for HDV and other viruses provides a valid reason to suspect hepatitis E virus infection.
General syndromes requiring the exclusion of hepatitis D
Suspicion of a viral etiology of hepatitis (including the potential involvement of hepatitis D virus) arises when a patient exhibits a characteristic cyclic progression of disease stages and the development of several key syndromes:
- Cytolytic syndrome: a manifold elevation of reference values for hepatic transaminases (ALT and AST). The de Ritis ratio is typically less than 1, which is considered a hallmark of viral hepatocyte damage.
- Jaundiced syndrome and cholestasis: a significant increase in total bilirubin levels (primarily due to the direct, or conjugated, fraction), the presence of bile pigments in the urine (bilirubinuria), and a moderate rise in alkaline phosphatase.
- Hepatomegaly: enlargement of the liver, which may feel elastic and tender upon palpation (due to capsule stretching).
Additionally, the protein-synthetic function of the liver is assessed (via the prothrombin index) to rule out severe hepatocellular insufficiency.
Laboratory dynamics and severe forms
When massive hepatic necrosis and acute liver failure develop (which can occur in various viral hepatitides, including coinfections), a sharp negative trend is observed. In such cases, the following are noted:
- Worsening cytolytic syndrome (ALT rising to critical values).
- Total hyperbilirubinemia.
- Critical drop in the prothrombin index (PI).
- Onset of hemorrhagic syndrome and hepatic encephalopathy (appearance of a specific musty breath odor — foetor hepaticus).
Therefore, to precisely determine the cause of such severe conditions, it is critically useful to perform a complete early screening, including the detection or exclusion of HDV markers.
Briefly: answers to topical questions
What specific markers (antibodies, antigens, nucleic acids) are used to confirm hepatitis D virus infection?
Serological and molecular genetic markers are used to confirm hepatitis D virus infection. Specific markers include:
- Antigens — viral antigen (HDAg), detected during the acute phase or in liver tissue via biopsy.
- Antibodies — early antibodies (anti-HDV-IgM) and IgG antibodies (anti-HDV-IgG) that rise in titer and predominate in chronic infection.
- Nucleic acids — viral RNA (HDV-RNA), detected by qualitative and quantitative PCR to confirm active replication.
The presence of HBV infection markers is a mandatory prerequisite.
The presence of which helper virus is obligatory for hepatitis D virus replication?
Replication of the hepatitis D virus obligatorily requires a helper virus — hepatitis B virus (HBV). HDV is a defective virus and utilizes the hepatitis B virus surface antigen (HBsAg) as its outer envelope (supercapsid) to form a complete viral particle and penetrate hepatocytes.
What are the main transmission routes of hepatitis D virus?
The primary mechanism of hepatitis D virus transmission documented in sources is parenteral.
HDV infection can only occur in the presence of HBV infection: either as a coinfection via simultaneous transmission of HBV and HDV, or as a superinfection in a patient with chronic HBV infection / HBsAg carrier state.
What are the clinical and laboratory differences between B+D coinfection and hepatitis D superinfection in a patient with chronic hepatitis B?
HBV+HDV coinfection and HDV superinfection in chronic hepatitis B differ in the patient's baseline status, clinical course, laboratory findings, and outcomes.
| Sign | HBV + HDV Coinfection | HDV Superinfection in Chronic Hepatitis B |
|---|---|---|
| Conditions of occurrence | Simultaneous infection with HBV and HDV | HDV infection in a patient who already has chronic HBV infection or an HBsAg carrier state |
| Clinical course | Debut is identical to acute hepatitis B; characterized by a biphasic course with a clinical and enzymatic exacerbation in the 2nd–4th week of the icteric period | Prognosis is unfavorable; the majority present with a wave-like course with recurrent exacerbations, and in 25–27% with a progressive course characterized by rapid liver shrinkage, massive necrosis, and severe acute hepatic encephalopathy |
| Laboratory findings | Characterized by AST predominating over ALT; possible decrease in prothrombin index and detection of acute phase markers anti-HBc IgM and anti-HDc IgM | Diagnosis is based on detecting markers of acute viral hepatitis D against the background of chronic viral hepatitis B markers |
| Outcomes | Recovery is reported in 75% of cases; progression to chronic infection in 5–10% of cases | Approximately 30% fatal outcome; approximately 70% progression to chronic infection with high activity and rapid development of liver cirrhosis |
Class and exam questions
Why is testing for hepatitis D markers prescribed?
Screening for HDV markers (along with viruses A, B, and C) is a mandatory step to rule out coinfections and accurately verify the diagnosis of acute viral liver damage.
Which laboratory parameters indicate the need to screen for hepatotropic viruses?
First and foremost, a pronounced cytolytic syndrome (multiplefold increase in ALT and AST, de Ritis ratio < 1) and cholestatic syndrome with jaundice.
What else to study on this topic
- Acute viral hepatitis E: clinical features in pregnant women
- Criteria for the development of fulminant hepatic failure
- Marker diagnostics of acute viral hepatitis B
- Cytolytic and cholestatic syndromes: laboratory differentiation
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