Herpetic Hepatitis
Pathogeny
Electron micrograph of herpes simplex virus particles (photograph of Dr. Frederick Murphy).
The virus is often acquired in childhood through contact with discharge from the vesicles or saliva of an infected person. The initial infection causes a fever and malaise accompanied by pain and blistering, redness and swelling at the site of inoculation.
This table is self-limiting, but the virus can infect the sensory and autonomic neurons, remaining dormant in the ganglia (trigeminal ganglia frequently), where it can reactivate and infect epidermal cells again. Reactivations may triggered by psychological stress. The elevation of prostaglandins have also been associated with reactivation, which may explain the reactivation associated with febrile illness.
The HSV-1 is a double-stranded DNA virus that belongs to the herpesvirus family. The replication cycle takes 24 hours. The HSV-1 is a direct cytopathic virus, destroying the infected cell either keratinocytes or hepatocytes specifically.
Immunocompromised host
The HSV-1 infection in patients with some degree of immunosuppression may be associated with the most severe, specifically hepatitis. Conditions that are associated with increased risk of disseminated infection are:
Infection with human immunodeficiency virus (HIV, AIDS), particularly with CD4 counts below 200 per mm3.
Organ transplant recipients: In 60 to 80% of patients previously infected organ recipients is possible to detect the virus in pharyngeal secretions during the first weeks post-transplant. Is seen in both bone marrow transplants in solid organ transplantation.
Burns and other skin diseases (pémfigo, eczema).
Cancer patients on chemotherapy or myelodysplasia.
Use of corticosteroids (steroids).
Newborns.
Pregnancy.
Clinical Manifestations
Fulminant hepatitis HSV-1 is a rare manifestation of this infection. Herpetic hepatitis has also been associated with infection by herpes type 2 virus. Clinical manifestations include:
Fever (82%)
Leukopenia (43%)
Abdominal pain (33%)
Coagulopathy (20%)
Anorexia, nausea and vomiting (18%)
The other clinical features are usually seen in acute liver failure. The typical oral or genital lesions are present in only 30% of cases. There may be simultaneous commitment of other organs (lungs, adrenals, etc.). Herpes hepatitis can be a cause of fulminant hepatitis post-transplant early, earlier than the cytomegalovirus (CMV).
Diagnosis
When skin or oral lesions are present, the virus can be searched directly by viral culture, polymerase chain reaction (PCR) or Tzanck staining secretion. When there is suspicion of this infection in the absence of skin lesions the diagnosis is made by using immunofluorescence in liver tissue obtained by biopsy usually shows transjugular.
Treatment
Early treatment with intravenous acyclovir (5 mg/kg every 8 hours for 7 to 14 days iv) can avoid the high mortality associated with herpes simplex virus hepatitis. Valacyclovir is also probably useful. In cases of suspected resistance to acyclovir, vidarabine or foscarnet can be used.
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