Hepatitis D is an infectious liver lesion, coinfection or superinfection of viral hepatitis B, which significantly worsens its course and prognosis. Disease belongs to the group of transfusion hepatitis, a prerequisite for infection with hepatitis D is the presence of an active form of hepatitis B. Detection of hepatitis D virus is carried out by PCR. A liver examination is required: biochemical tests, ultrasound, MRI, rheohepatography. The treatment is similar to the treatment of hepatitis B, but requires large dosages of drugs and their longer intake. In most cases, there is a chronization of the disease with a subsequent outcome in cirrhosis of the liver.
Hepatitis D is caused by an RNA-containing virus, which is the only representative of the “wandering” genus Deltavirus known to date, which is characterized by the inability to independently form a protein for replication and uses a protein produced by the hepatitis B virus for this purpose. Thus, the causative agent is a sattelite virus and occurs only in combination with the hepatitis B virus.
Disease is extremely resistant in the external environment. Heating, freezing and thawing, exposure to acids, nucleases and glycosidases do not significantly affect its activity. The reservoir and source of infection are patients with a combined form of hepatitis B and D. Contagiousness is especially pronounced in the acute phase of the disease, but patients pose an epidemic danger throughout the entire period of circulation of the virus in the blood.
The mechanism of transmission of hepatitis D is parenteral, a prerequisite for virus transmission is the presence of an active hepatitis B virus. The hepatitis D virus integrates into its genome and enhances the ability to replicate. The disease can be a co-infection when the hepatitis D virus is transmitted simultaneously with B, or a superinfection when the pathogen enters an organism already infected with the hepatitis B virus. The most significant risk of infection is during blood transfusion from infected donors, surgical interventions, traumatic medical manipulations (for example, in dentistry) have a noticeable epidemiological significance.
Disease is able to overcome the placental barrier, can be transmitted sexually (the spread of this infection is high among people prone to promiscuous sexual relations, homosexuals), having in some cases a family spread of the virus suggests the possibility of its transmission by contact and household means. Patients with viral hepatitis B, as well as carriers of the virus, are susceptible to viral hepatitis D. In particular, the susceptibility of persons with chronic HBsAg carrier is high.
Hepatitis d symptoms
Hepatitis D complements and aggravates the course of hepatitis B. The incubation period of coinfection is significantly reduced, it is 4-5 days. Incubation of superinfection lasts 3-7 weeks. The pre-jaundice period of hepatitis B proceeds similarly to that of hepatitis B, but has a shorter duration and a more violent course. Superinfection can be characterized by the early development of edematous ascitic syndrome. The jaundice period proceeds in the same way as with hepatitis B, but bilirubinemia is more pronounced, signs of hemorrhage are more common. Intoxication in the jaundice period of hepatitis D is significant, prone to progression.
Coinfection proceeds in two phases, the interval between the peaks of clinical symptoms of which is 15-32 days. Superinfection is often difficult to diagnose differentially, since its course is similar to that of hepatitis B. A characteristic difference is the speed of the clinical picture, rapid chronization of the process, hepatosplenomegaly, disorder of protein synthesis in the liver. Recovery takes much longer than in the case of hepatitis B, residual asthenia can persist for several months.
Chronic viral hepatitis D does not differ in specific symptoms, it manifests itself similarly to chronic hepatitis of another etiology. Patients are concerned about general weakness and fatigue, “causeless” episodes of fever with chills without catarrhal symptoms may occur periodically, accompanied by sub-jaundice and jaundice. Secondary hepatic signs are formed on the skin (erythema palmar, vascular asterisks), the liver and spleen are enlarged, hepatic edema and ascites often develop. The course of chronic viral hepatitis D is undulating, periods of exacerbations are replaced by remissions. In 15% of patients with delta hepatitis, cirrhosis of the liver develops quite quickly, within one and a half to two years.
In the acute phase of the disease, specific IgM antibodies are detected in the blood, and only IgG is detected over the next few months. In general practice, diagnosis is carried out using the PCR method, which allows to isolate and identify the RNA virus.
To study the condition of the liver in viral hepatitis D, liver ultrasound, rheohepatography, MRI of the liver and biliary tract are performed. In some cases, a puncture liver biopsy may be performed to clarify the diagnosis. Non-specific diagnostic measures are similar to those for hepatitis of a different etiology and are aimed at dynamic control of the functional state of the liver.
Hepatitis d treatment
Hepatitis D is treated by a gastroenterologist according to the same principles as the treatment of viral hepatitis B. Since the hepatitis D virus is more resistant to interferon, basic antiviral therapy is adjusted towards increasing dosages, and the duration of the course is 3 months. If there is no effect, the dosages are doubled, the course is extended to 12 months. Since the hepatitis D virus has a direct cytopathic effect, drugs of the corticosteroid hormone group are contraindicated in this infection.
Prognosis and prevention
The prognosis in the case of mild and moderate coinfection is more favorable, since a complete cure is noted much more often than with superinfection. However, the combined defeat of hepatitis B and D viruses often occurs in severe form with the development of life-threatening complications. Chronic coinfection develops in 1-3% of cases, while superinfection develops into a chronic form in 70-80% of patients. Chronic hepatitis D leads to the development of cirrhosis. Recovery in the case of superinfection is extremely rare.
Prevention of hepatitis D is similar to that of viral hepatitis B. Preventive measures are of particular importance for people suffering from hepatitis B and having a positive reaction to the presence of the HBsAg antigen. Specific vaccination against viral hepatitis B effectively protects against delta hepatitis.