The two distinctive clinical features of varicella-zoster virus (VZV) are varicella (chickenpox) by primary infection and zoster (singles) by the reactivation of latent infection. In addition to the two typical clinical symptoms mentioned above, diverse clinical manifestations have been reported as a result of VZV reactivation, including chronic radicular pain without rash, visual loss, facial palsy, dysphagia, sore throat, odynophagia, otalgia, hearing loss, dizziness, headache, hemiplegia, etc. Most of these symptoms are derived from neuropathy and vasculopathy of affected nerves and arteries. Diagnosis of VZV disease can be difficult if there is no appearance of a skin rash during development of atypical symptoms. In addition to natural infection, vaccination and anti-viral agent treatment have influenced the changes of epidemics and clinical presentations of varicella and zoster. In this article, diverse clinical manifestations caused by VZV reactivation, particular without skin rash, are reviewed.
Valaciclovir is metabolized to acyclovir after ingestion and thereafter exerts its antiviral activity. Because of its superior pharmacokinetic profile, it has quickly replaced acyclovir in the treatment of herpesvirus infection. Neurotoxicity caused by valaciclovir has been reported, however, among patients with pre-existing impaired renal function. This paper reports a case of neurotoxicity of valaciclovir in a patient with end-stage renal disease who was undergoing continuous ambulatory peritoneal dialysis (CAPD). A 67-year-old female on CAPD took 500 mg of valaciclovir twice for herpes zoster. After she took her second dose orally, she developed confusion and disorientation, along with involuntary movements. Her mental confusion progressed to a coma. Discontinuation of valaciclovir showed no rapid improvement. There- fore, hemodialysis was started. After two sessions of hemodialysis, the patient became alert; and after four sessions of hemodialysis, her neurological abnormalities were completely reversed. In conclusion, valaciclovir can induce life-threatening neurotoxicity, especially in CAPD patients, even with appropriate dose reduction, which can be effectively managed by hemodialysis.
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