Herpes zoster en la infancia y adolescencia / Herpes zoster in children and adolescents

El Herpes zoster (HZ) es la consecuencia clínicade la reactivación demorada del virus varicela-zoster(VVZ). La enfermedad es propia del adulto pero loscasos pediátricos no son infrecuentes. Afecta, principalmente,a niños inmunodeprimidos y a lactantespor reactivación del virus latente adquirido transplacentariamentedurante la vida intrauterina (varicelade la gestante). Rara vez sucede en niños normales.Su incidencia es mayor en niños que han padecidola infección varicelosa normal que en aquellosotros que han sido inmunizados activamente. Dadoque la vacunación contra la varicela se está extendiendorápidamente, el zoster podría llegar a seruna curiosidad en la infancia.La alteración de la inmunidad celular e inespecífica(células natural killer) parece jugar un papelesencial en su desarrollo. En el niño la enfermedadsuele ser benigna y el tratamiento se limita a medidasconservadoras. En los niños inmunodeficientesla infección puede ser severa requiriendo la administraciónintravenosa de antivirales de los que elaciclovir es el de elección

Herpes zoster (HZ) is the clinical consequence oflate reactivation of the varicella zoster virus (VZV). Itinfects mainly the elderly but pediatric cases are notuncommon. It occurs mostly in immunocompromisedchildren or in infancy after reactivation of latent VZVinfection acquired transplacentally during intrauterinelife. Rarely, HZ occurs in otherwise normal children.The incidence of HZ in children is higher afternatural varicella infection than after varicella vaccination.As the childhood population becomes increasinglyimmunized, zoster in children should becomea medical curiosity. The impairment of cellular andnon specific immunity (natural killer cells) appears tohave a particular role in the occurrence of HZ. Zosterin children typically runs a benign, mild course.Treatment of the usual form comprises antisepticmeasures and relief of pruritus. In immunocompromisedchildren, the infection is generally severe,thus requiring specific intravenous antiviral therapywith antiviral drugs without delay. Acyclovir is a firstlineagent

Ca2+ channels in clonal rat anterior pituitary cells (GH3/B6).

In clonal rat somatomammotroph cells (GH3/ B6) Ca2+ influx through voltage-dependent Ca2+ channels is important for regulating the Ca2+ concentration that mediates hormone secretion. To study the Ca2+ channel subtypes in GH3/B6 cells, Ca2+ channel currents were recorded with the whole-cell configuration of the patch-clamp technique using Ba2+ as the charge carrier. Forty-nine percent of the total Ba2+ current amplitude was mediated by a nifedipine-sensitive current (L-type). In addition, three other high-voltage-activated Ca2+ channel current components could be distinguished pharmacologically: 10 nM omega-agatoxin-IVA-sensitive current (22%; P-type), omega-conotoxin-MVIIC-sensitive current (18%; Q-type), and toxin-resistant current (24%). Since omega-conotoxin GVIA (2 microM) had no blocking effect, N-type Ca2+ channels are assumed not to be present in GH3/B6 cells. The T-type Ca2+ channel current was either absent or very small. Different pore-forming alpha1 subunits of Ca2+ channels were found to be expressed in GH3/B6 cells, which could be the molecular correlates of the different Ba2+ current subtypes: alpha1G of T-type, alpha1C, alpha1D and alpha1S of L-type, and alpha1A of P/Q-type current. In addition, transcripts for beta1, beta2 and beta3 subunits were detected. Blockage of L-type channels with 10 microM nifedipine or P/Q-type channels with 10 nM omega-agatoxin MVIIC + 200 nM omega-conotoxin blocked action potential firing in GH3/B6 cells and decreased basal prolactin secretion.