Varicella-Zoster Hepatitis
Last reviewed: 23.04.2024
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Elementary corpuscles of the virus were first discovered by N. Argao in 1911. The virus of varicella was cultivated for the first time by T.N. Weller in tissue culture in 1953. The virus is a spherical particle with a diameter of 150-200 nm containing DNA; by properties close to the virus of herpes simplex and indistinguishable from the causative agent of herpes zoster, which is therefore designated as a virus of chicken pox-zoster or in abbreviated form - VZV. According to modern classification, it is a human herpesvirus type 3 (HHV 3).
The virus is less stable in the environment and is not pathogenic for animals. Well cultivated in human cultures and monkeys. The best culture for VZV replication is human hepatocytes, followed by lung fibroblasts.
Epidemiology of varicella-zoster of hepatitis
Virtually the entire population is suffering from chicken pox by the age of 10-14 years. The only source of infection is a sick person. The source of infection can be and patients with herpes zoster.
Infection is transmitted by airborne, less often by contact, with the possibility of infection at a great distance. Transplacental transfer from mother to fetus has been proven.
[Pathogenesis of varicella-zoster of hepatitis
The pathogenesis of VZV-hepatitis has not been studied. For the first time the idea of hepatitis of the herpesvirus type 3 virus originated in the development of a live vaccine against varicella, when it was convincingly shown that he had a marked tropism for hepatocytes. This property of the virus was successfully used by Japanese scientists for its cultivation. The best culture for replication was hepatocytes, followed by lung fibroblasts.
Generalized forms of varicella and isolated varicella-zoster hepatitis are extremely rare, mainly in children with altered immunological status.
Pathomorphology
The virus affects the nuclei of cells, with the formation of eosinophilic intranuclear inclusions. Can cause the formation of giant multinucleated cells.
In internal organs, mainly in the liver, kidneys, lungs, small foci of necrosis with hemorrhages along the periphery are revealed in the central nervous system.
Symptoms of varicella-zoster of hepatitis
Currently, varicella-zoster hepatitis is described mainly in immunocompromised patients. In this case, it can occur both in the generalized infection and in isolation. The spectrum of VZV lesions of the liver varies from mild and subclinical to severe and fulminating forms of hepatitis. In this case varicella-zoster hepatitis always has an acute course. Chronic course of the disease is not observed.
The lethality for disseminated VZV infection in adult kidney transplant recipients is 34%. At the same time, 82% have primary chicken pox, and 18% have reactivation of the infection. The main clinical manifestations are hepatitis, pneumonitis, DIC syndrome. At the same time, there was no specific cytostatic drug with which the risk of disseminated infection would be associated. VZV-hepatitis can also occur in HIV-infected patients.
Isolated varicella-zoster hepatitis can develop in immunocompromised patients (liver transplant recipients, patients with acute lymphoblastic leukemia, and so on). The defeat of the liver is not accompanied by vesicular eruptions on the skin and mucous membranes.
Very rarely acute varicella-zoster hepatitis develops in immunocompetent children and adolescents. In addition, a typical clinical-biochemical picture of hepatitis can be observed in 3-5% of patients with chicken pox. In this case, the activity of hepatic-cellular enzymes in the blood serum exceeds 100 U / l.
Treatment of varicella-zoster of hepatitis
The use of high doses of acyclovir in combination with the reduction of immunosuppressive therapy leads to a reduction in mortality from disseminated VZV infection in immunocompromised patients.
With disseminated VZV infection, which occurs with involvement in the liver process, therapy with acyclovir and ganciclovir can only bring temporary improvement. However, the number of copies of VZV DNA in the blood serum is often kept at a high level, and the manifestations of hepatitis usually do not disappear. The appointment of sodium foscarnet in these cases can lead to a decrease in the level of viremia and normalization of liver function.
The use of acyclovir in immunocompetent children and adolescents with acute VZV-hepatitis facilitates the course of chickenpox, but does not have a significant effect on the course of hepatitis. Hepatitis has an acute course, resulting in recovery. More than 80% of patients with serum transaminase activity normalize to the 25-30th day of treatment.
Prevention of varicella-zoster of hepatitis
For the purpose of specific prevention of VZV infection, including accompanied by liver damage, a live vaccine is used.
Summarizing the above, we can say that varicella-zoster hepatitis has an acute course and is a relatively rare manifestation of VZV infection, developing mainly in immunocompromised patients. However, given the proven hepatotropic VZV and the fact that most patients with chicken pox and herpes zoster have no functional liver function, some cases of VZV-hepatitis may remain undiagnosed. The question needs further study.