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1.
Clin Exp Dermatol ; 48(5): 495-503, 2023 Apr 27.
Artigo em Inglês | MEDLINE | ID: mdl-36637147

RESUMO

BACKGROUND: The intestinal microbiota is altered in patients with atopic dermatitis (AD) when compared with those of the healthy population. Some interventions with specific probiotic preparations already demonstrate a change in composition of this microbiota accompanied by improvement in the disease. OBJECTIVES: This research work was designed to evaluate clinical efficacy of the probiotic preparation, and to measure the effect of the intervention on the total dose of corticosteroids administered to subjects. METHODS: This double-blind, randomized, placebo-controlled clinical trial including 70 participants with AD aged 4-17 years was designed to evaluate the clinical effect, compared with placebo, of a probiotic mixture of Bifidobacterium lactis, Bifidobacterium longum and Lactobacillus casei at a total daily consumption of 1 × 109 colony-forming units per capsule, over 12 weeks. After randomization and exclusion, 35 patients were allocated to probiotic and 35 to placebo. Clinical variables analysed were SCORAD (SCORing of Atopic Dermatitis) and Investigator Global Assessment (IGA) indices; effect on the amount of topical corticosteroids used; and assessment of safety. RESULTS: Mean SCORAD index at 12 weeks showed a statistically significant difference of -5.43 (95% confidence interval -10.65 to -0.21) between probiotic (SCORAD 13.52) and placebo groups (SCORAD 18.96); P = 0.04. Comparison between groups showed a statistically significant difference in the number of patients with IGA score improvement over the 12-week intervention: 29 of 32 (90.5%) in the probiotic group vs. 17 of 30 (56.7%) in the placebo group (P < 0.002). A comparison between groups of the proportions of days using corticosteroids and the total dose (g) of corticosteroids between baseline and end of study showed no significant difference, but between weeks 6 and 12 there was a statistically significant reduction in the probiotic group when compared with the placebo group in both variables. Numbers of adverse events were similar in both groups of treatment. CONCLUSIONS: The probiotic mix used in this clinical trial demonstrated efficacy on the change in activity index of AD compared with placebo. Furthermore, the total number of days and total amount of topical corticosteroids required by participants in the probiotic group showed a significant reduction compared with placebo between 6 and 12 weeks.


Assuntos
Dermatite Atópica , Fármacos Dermatológicos , Probióticos , Humanos , Criança , Adolescente , Dermatite Atópica/tratamento farmacológico , Dermatite Atópica/diagnóstico , Corticosteroides/uso terapêutico , Probióticos/uso terapêutico , Resultado do Tratamento , Glucocorticoides/uso terapêutico , Fármacos Dermatológicos/uso terapêutico , Método Duplo-Cego , Índice de Gravidade de Doença , Imunoglobulina A
3.
Rev. psiquiatr. Fac. Med. Barc ; 32(3): 120-132, jul.-sept. 2005. tab
Artigo em Es | IBECS | ID: ibc-047379

RESUMO

La psoriasis es un trastorno dermatológico inflamatoriocrónico. Se cree que es un proceso auto inmune. Diferentesinvestigaciones recientes sitúan a la inflamaciónneurogénica, un proceso proliferativo de fibras nerviosasno mielinizadas, como uno de los factores etiopatogénicoscomunes en la proliferación y mantenimiento de la placapsoriasica. El NGF (Factor de crecimiento Nervioso), unamolécula de la familia de las neurotrofinas, podría ser eliniciador, y perpetuar la señalización celular, mediantesegundos mensajeros, como los neuropéptidos(Substáncia P, Péptido del gen relacionado con lacalcitonina y Péptido Intestinal Vasoacitivo), de dichoproceso inflamatorio, lo que explicaría fenómenos comoel de Koebner o la simetría de las lesiones, en la Psoriasis.Por dicha razón, se comienza a observar a la enfermedad,como un proceso psicosomático. El cerebro generaríaseñalizaciones neuroquímicas, que modularían elproceso periférico, y viceversa. Se explicaría porqué elestrés es el factor de riesgo principal en la psoriasis. Laenfermedad mental, que produce estrés neuronal, pormedio de mecanismos neurobiológicos, podría generar,en el nervio periférico, mecanismos anti-apoptoticos, enpersonas genéticamente vulnerables. Se explicaría tambiénque la misma psoriasis produjera estrés psicosocial,por lo que se cerraría el círculo fisiopatologico


Psoriasis is a cronic inflamatory dermatologic disease.Scientific works believe that is an auto-inmune disease.Novel investigations describe Neurogenic Inflammation,a proliferative process into the unmielinized nervous fibers,like one of the most important common etiopathogenicfactor in the proliferation and maintenance of the psoriaticplaque. The Neural Grow Factor, a molecule of theneurotrophine familily, probably can act like aninicialization and maintenance of the molecular cellularsignaling, with the contribution of other second messengers(Substance P, Calcitonin-gene related peptide andVasoactive Intestinal Peptide), of the inflammatory process,that explain the Koebener phenomenon or the simmetryof the lesions of Psoriasis. For this reason, the disease is actually observed like a psicosomatic illnes. The brain,probably generates neurochemical signaling, thatmodulate the periferical process, and viceversa. Thisexplains the stress like the most important risk factor inthe development of Psoriasis. The mental disease, thatproduce neuronal stress, with neurobiologicalmechanims, probably generates, in the periferal nerve,antiapoptotic mechanims, in genetically vulnerablepatients. This explains, in the other hand, that psoriasisgenerates psicosocial stress, and close the vicious circleof the etiopathogenic mechanisms of Psoriasis


Assuntos
Humanos , Psoríase/fisiopatologia , Inflamação Neurogênica/fisiopatologia , Estresse Psicológico/complicações , Fator de Crescimento Neural/fisiologia , Neuropeptídeos/fisiologia
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