Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Más filtros

Métodos Terapéuticos y Terapias MTCI
Bases de datos
Tipo de estudio
Tipo del documento
País de afiliación
Intervalo de año de publicación
1.
Br J Dermatol ; 160(3): 534-9, 2009 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-19067714

RESUMEN

BACKGROUND: Photoadaptation to ultraviolet (UV) B phototherapy is due to both pigmentary and nonpigmentary influences. OBJECTIVES: To measure photoadaptation in vitiliginous skin and to compare it with normal pigmented skin. METHODS: Seventeen patients with Fitzpatrick skin phototypes III-VI with vitiligo received six to nine UVB treatments, two to three times weekly. Minimal erythema dose (MED) testing was done at baseline and after all treatments; the percentage change in MED was analysed as a measure of photoadaptation. The percentage decrease in cyclobutane pyrimidine dimers (CPDs) over 24 h after a single exposure of 1 MED was analysed on vitiliginous and normal skin. RESULTS: The mean +/- SD percentage change in MED from before to after treatments was: treated vitiliginous skin 28.5 +/- 39.9% (P = 0.015), treated normal skin 35.9 +/- 49.9% (P = 0.015), untreated vitiliginous skin 11.9 +/- 22.6% (P =0.070), untreated normal skin 25.1 +/- 41.3% (P = 0.041). Of these patients, two-thirds had a positive percentage change in MED (photoadaptation). The mean amount of CPDs induced per megabase of DNA immediately after exposure was significantly higher in vitiliginous skin. The mean +/- SD percentage decrease in CPDs (rate of repair) in 24 h was 35.7 +/- 26.8% in vitiliginous skin (P = 0.027) and 46.2 +/- 19.5% in normally pigmented skin (P = 0.001); no difference was noted in the repair in vitiliginous skin compared with normal skin (P = 0.4). CONCLUSIONS: Photoadaptation in vitiliginous and normal skin was observed in two-thirds of patients. Vitiliginous skin had significantly more CPDs following UVB exposure; the rate of repair of UVB-induced DNA damage was equivalent to that in normal skin.


Asunto(s)
Adaptación Fisiológica/efectos de la radiación , Terapia Ultravioleta/métodos , Vitíligo/radioterapia , Adaptación Fisiológica/genética , Adulto , Anciano , Daño del ADN , Reparación del ADN , Femenino , Humanos , Masculino , Persona de Mediana Edad , Tolerancia a Radiación/genética , Dosificación Radioterapéutica , Piel/efectos de la radiación , Pigmentación de la Piel , Vitíligo/genética , Vitíligo/fisiopatología
2.
Skin Therapy Lett ; 13(2): 1-6, 2008 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-18373041

RESUMEN

Vitiligo is an acquired leukoderma that results from the loss of epidermal melanocytes, and is characterized by macules and patches of depigmented skin. With a relatively high rate of prevalence, vitiligo occurs in localized, generalized, or segmental patterns; it can run a rapidly progressive course or remain stationary. The pathogenesis of vitiligo is not yet fully understood, but the autoimmune hypothesis is the most commonly accepted one, based on which, many treatment modalities have been described. Although many therapeutic options exist and new modalities are still emerging, treatment challenges persist, as not all patients respond to available therapies. Variables that affect the choice of treatment include the extent, distribution, and progression rate of the lesions. Another challenge is the lack of a standardized scoring system, which hampers the production of level 1a evidence studies for the treatment of this condition.


Asunto(s)
Corticoesteroides/uso terapéutico , Fármacos Dermatológicos/uso terapéutico , Inmunosupresores/uso terapéutico , Terapia por Luz de Baja Intensidad , Fototerapia , Vitíligo , Administración Cutánea , Calcitriol/análogos & derivados , Calcitriol/uso terapéutico , Terapia Combinada , Humanos , Tacrolimus/uso terapéutico , Vitíligo/tratamiento farmacológico , Vitíligo/radioterapia , Vitíligo/cirugía
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA