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A case of Kaposi varicelliform eruption progressing to herpes simplex virus hepatitis in an immunocompetent patient

A 26-year-old Japanese woman presented with painful cutaneous vesicles and erosions, which were disseminated over her body, in association with fever and severe general fatigue (Fig. 1a,b). She had a history of atopic dermatitis (AD). Laboratory investigations revealed elevations of aspartate aminotransferase (AST) (324 U/L; normal range 13–33 U/L) alanine aminotransferase (ALT) (291 U/L; 8–42 U/L) and C-reactive protein (CRP) (23.86 mg/dL; < 0.2 mg/dL). Anti-herpes simplex virus (HSV) IgM (8.34; < 0.80) was detected in the acute-phase serum, and anti-HSV-IgG titres during the acute and recovery phases were significantly elevated (7.9 and 40.3, respectively; normal < 2.00 for both). There was no serological evidence of active infection caused by hepatitis viruses, Epstein–Barr virus, cytomegalovirus or varicella zoster virus. Exudate obtained from a skin erosion grew Streptococcus agalactiae and Staphylococcus aureus. We made a diagnosis of Kaposi varicelliform eruption (KVE) along with a secondary bacterial infection. The liver damage indicated by the raised AST and ALT titres was thought to be caused by HSV-induced hepatitis. The patient was treated with intravenous aciclovir and sulbactam–ampicillin, followed by oral valaciclovir (Fig. 2), which led to improvement in the patient’s skin and physical condition by day 2. The degree of liver damage also began to reduce, returning to normal levels 12 days after initiation of the antiviral therapy. Based on the clinical course and HSV antibody titres, we concluded that the liver dysfunction had been due to HSV hepatitis occurring in association with KVE. HSV causes a rare but severe hepatitis, mainly in immunocompromised patients, which accounts for < 2% of acute liver failure due to viral infection. Because 74% of HSV hepatitis cases rapidly progress to fulminant or acute liver failure, early diagnosis and treatment are crucial to improve prognosis. However, herpetic mucocutaneous manifestations are not found in 56% of HSV hepatitis cases, and most patients with herpetic rash commonly do not show hepatic dysfunction. Thus, the rarity of the disease and the absence of herpetic rash sometimes result in delayed diagnosis. In our case, laboratory investigations showed a moderate increase in AST and ALT, and these, together with the typical skin manifestations of KVE, led us to suspect HSV hepatitis. A diagnosis of HSV hepatitis was eventually made because the patient was not taking any systemic medication and there was no evidence of other viral infections that could cause liver dysfunction, and because the liver damage had occurred with the emergence of herpetic rash and then improved in conjunction with the improvement in cutaneous manifestations induced by antiviral therapy. Detection of HSV DNA in blood should have provided solid proof for HSV hepatitis, but when we tested the patient’s blood by PCR on the fourth day of antiviral therapy, we did not detect HSV DNA. This may have been because the HSV DNA had decreased to a level below the PCR detection limit at the time of blood collection, as the patient’s cutaneous and systemic manifestations were already improving with the aciclovir therapy. To our knowledge, there has only been one published case of KVE with fulminant hepatitis, which was reported by Min and Gnann, in a patient with bilateral malar crusted eruptions accompanied by fever, chills, fatigue and anicteric sclerae. In our case, the hepatitis was prevented from worsening by early Correspondence: Dr Michihiro Hide, Department of Dermatology, Institute of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8551, Japan E-mail: ed1h-w1de-road@hiroshima-u.ac.jp