[Herpes zoster].
This paper summarizes present knowledge on pathogenesis and therapy of herpes zoster. Formerly, zoster was considered a reinfection of a partly immune individual by the varicella-zoster virus localized into a body segment of lowered resistance. Recent epidemiological and virological evidence, however, suggests a different mode of pathogenesis: in the course of varicella, VZV migrates via the sensory nerves to the dorsal root ganglia where it remains in an inactive form. It may be reactivated in response to a local or systemic lowering of the level of host resistance, resulting in painful ganglionitis and, by descension, in the characteristic segmental skin lesions of herpes zoster. Treatment with systemic corticosteroids in the early stages of zoster helps to decrease the frequency and severity of postzosteric neuralgias. Corticosteroids ought to be given at a relatively high dosage and be tapered only slowly in the course of a few weeks. They are particularly useful in older individuals, who constitute a population prone to postzosteric neuralgias. In severe cases of generalized zoster, corticosteroids should not be given to avoid further lowering of host resistance. Recently, antiviral drugs have been developed which combine high effectiveness with very tolerable side effects, namely vidarabine and acyclovir.
D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D005727:Ganglia, Spinal; D006562:Herpes Zoster; D014645:Herpesvirus 3, Human / Q000472:pathogenicity; D006801:Humans; D009437:Neuralgia / Q000517:prevention & control; D014740:Vidarabine / Q000627:therapeutic use
D000305:Adrenal Cortex Hormones; D014740:Vidarabine
Herpes zoster.