Postherpetic Neuralgia in Patients With Acute Herpes Zoster
Graeme M. Lipper, MD

Postherpetic neuralgia (PHN) is a painful and often debilitating complication of acute herpes zoster virus infection that is characterized by intense neuropathic pain. Victims typically describe their pain as a relentless stabbing, throbbing, or burning that often keeps them awake at night. The disorder, thought to occur due to inflammatory nerve injury during infection, may last months to years and causes intractable pain and morbidity. Risk factors for developing PHN include older age (> 50 years), worse pain associated with the acute viral infection, extensive cutaneous involvement (eg, widespread blistering), and severe prodromal pain.[1] Acyclovir and its analogues (ie, valacyclovir, famciclovir) speed the resolution of herpetic skin lesions and acute pain while reducing viral shedding. However, it remains unclear whether these antiviral drugs reduce the true incidence or severity of PHN.[2-4] In contrast, the herpes zoster vaccine may decrease the incidence of PHN by up to 66.5%.[5]

Tricyclic antidepressants and the anticonvulsant drug gabapentin may reduce the pain of PHN, but few data exist to support their use during the acute phase of zoster to prevent PHN.[6,7] To address this important question, Lapolla and colleagues conducted an open-label study assessing the incidence of PHN after therapy with both valacyclovir and gabapentin (300 mg/day, titrated up to a maximum dose 1200 mg orally 3 times a day as tolerated). Investigators enrolled 133 patients with acute zoster who had moderate to severe pain (mean age, 64.6 years; 67% women, 82% non-Hispanic whites). All patients received both valacyclovir (1000 mg orally 3 times a day x 7 days) and gabapentin (300 mg/day, titrated upward weekly as tolerated to a maximum dose of 3600 mg divided 3 times a day) at the onset of acute zoster. Gabapentin was discontinued for patients who reported mild to no pain over 1 week.

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La enfermedad de Fabry es una enfermedad genética extremadamente rara, se cree que afecta a 1/117.000 nacidos vivos, que se incluye dentro del grupo de enfermedades metabólicas hereditarias de depósito lisosomal.

Enfermedad de Fabry

Sinónimos:
Angioqueratoma Difuso
Ceramida Trihexosidasa, Déficit de
Alfa Galactosidasa A, Déficit de
Lipidosis Glucolipídica
Angioqueratoma Corporal Difuso
Anderson Fabry, Enfermedad de
Lipidosis Hereditaria Distópica

Descripción de la enfermedad:
http://iier.isciii.es/er/prg/er_bus2.asp?cod_enf=973

La enfermedad de Fabry es una enfermedad genética extremadamente rara, se cree que afecta a 1/117.000 nacidos vivos, que se incluye dentro del grupo de enfermedades metabólicas hereditarias de depósito lisosomal.
Esta enfermedad está causada por el déficit de alfa galactosidasa A (gal A) , presente en muchos tipos de células del organismo, implicada en la rotura de la globotriaosilceramida (Gb3).
En la enfermedad de Fabry, la enzima gal A esta parcial o totalmente inactiva. El resultado es que la Gb3 se acumula en las células del organismo y altera las funciones de diferentes órganos diana, siendo riñones, corazón, sistema nervioso y piel, los más afectados.
La tríada clínica característica que define la enfermedad de Fabry es neuropatía distal, dolorosa, angioqueratomas, e hipohidrosis.

Clínicamente el primer síntoma suele ser el dolor, en forma de crisis agudas y lacerantes de dolor abdominal difuso, refractario al tratamiento, que pueden duran 2 ó 3 semanas o incluso más y desaparecer bruscamente. Las crisis dolorosas pueden desencadenarse por fiebre, fatiga, ejercicio, estrés, o cambios de temperatura. Estas crisis son más comunes en la infancia y una vez que el paciente alcanza la edad adulta, dichas crisis pueden llegar a desaparecer, o por el contrario, el dolor puede agravarse a medida que pasan los años.

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J Am Acad Dermatol. 2011 Oct 5. [Epub ahead of print]
Childhood- and later-onset vitiligo have diverse epidemiologic and clinical characteristics.
Nicolaidou E, Antoniou C, Miniati A, Lagogianni E, Matekovits A, Stratigos A, Katsambas A.
Source

First Department of Dermatology, University of Athens School of Medicine, «Andreas Sygros» Hospital for Skin and Venereal Diseases, Athens, Greece.
Abstract
BACKGROUND:

Vitiligo onset during childhood is common. There are limited data regarding childhood-onset vitiligo.
OBJECTIVE:

We sought to provide an epidemiologic and clinical comparison between childhood- and later-onset vitiligo.
METHODS:

Two groups of patients were included in this cross-sectional study. Consecutive patients examined at the Vitiligo Clinic of Andreas Sygros Hospital for Skin and Venereal Diseases, Athens, Greece, from January 2005 to December 2009 with a disease onset before the age of 12 years were included in the childhood-onset group. The later-onset group included randomly selected patients who were examined at the same period and had a disease onset after the age of 12 years. After clinical examination, a standardized questionnaire was completed for each patient.
RESULTS:

In all, 126 patients were included in the childhood-onset and 107 patients in the later-onset group. Childhood-onset vitiligo: (1) involved different sites at initial presentation, (2) included more cases of segmental type, and (3) was characterized by a higher prevalence of allergic diseases and a lower prevalence of thyroid diseases. Longer duration of disease and a positive family history of thyroid disease were associated with the presence of thyroid disease only in the childhood-onset group. In the later-onset group, only female sex was associated with the presence of thyroid disease.
LIMITATIONS:

The study was conducted in a hospital specializing in skin diseases and a selection bias toward more severe vitiligo cases is possible.
CONCLUSIONS:

Childhood-onset vitiligo had distinct epidemiologic and clinical characteristics, compared with later-onset disease.

Copyright © 2011 American Academy of Dermatology, Inc. Published by Mosby, Inc. All rights reserved.

PMID:
21982634
[PubMed – as supplied by publisher]

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Dres. Judith Domínguez- Cherit, Rodrigo Roldan-Marin, y col.
Journal American Academy of Dermatology, Nov 2008

La melanoniquia longitudinal (ML) es una pigmentación negro-amarronada en el plato ungueal, definida como una banda pigmentada que se extiende longitudinalmente desde el extremo proximal o la lúnula al borde libre del plato ungueal.  Si se afecta toda la uña se la llama melanoniquia completa profunda.  La pigmentación del plato ungueal puede ser causada por depósito de melanina, o por otras sustancias como sangre, pigmentos internos o externos (argiria, enfermedad de Addison, porfiria), drogas (minociclina, psoralenos, ciclofosfamida, zidovudina), infección bacteriana o fúngica (Proteus mirabilis, especies de Aspergillus, especies de Cándida, Trichophyton rubrum), o tumores subungueales diferentes del melanoma subungueal.

En éste estudio se focalizó en la melanoniquia secundaria a deposición de melanina.

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Dres. V De Giorgi, S Sestini, N Bruscino y col.
JEADV 2009, 23, 1320–1323.

Este estudio incluyó a 265 pacientes, que concurrieron al Departamento de Dermatología de la Universidad de Florencia entre Marzo del 2006 y Julio del 2007.

A todos los pacientes un dermatólogo le realizaba un examen de piel total, quién detallaba el número de características clínicas (típicas o atípicas) y sitios de nevos melanocíticos.  Todas las lesiones maculares o sobrelevadas marrones mayores de 2 mm consideradas como nevos melanocíticos se contaban en todos los sitios incluyendo piel de pliegues, palmas, plantas y área genital.  Se definía a un nevo clínicalmente atípico si era mayor a 5 mm con un borde irregular y/o pigmentación irregular.  A todos los pacientes se les realizó un exámen de la cavidad oral, las lesiones pigmentadas de éstas áreas se contaban en 11 sitios anatómicos diferentes: borde del bermellón (inferior y superior), mucosa labial (superior e inferior), gingiva (mandíbula y maxilar), paladar, mucosa bucal, lengua, retromolar y piso de la boca.

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