RESUMO
A dermatoporose é a síndrome de fragilidade cutânea. Acomete principalmente indivíduos acima de 60 anos, com maior prevalência no sexo feminino. Os principais fatores de risco são: envelhecimento, exposição solar intensa e uso de corticoterapia tópica e sistêmica. Se manifesta clinicamente por atrofia cutânea, púrpuras senis, pseudo cicatrizes estrelares e lacerações, podendo evoluir com hematomas dissecantes e infecções graves. Trata-se de uma doença com grande impacto na qualidade de vida dos pacientes e, até o presente momento, não há terapias com resultados satisfatórios. Hidratação, vitamina C tópica e oral, luz intensa pulsada foram algumas das terapêuticas estudadas. A hidroxiapatita de cálcio é um bioestimulador de colágeno composto por microesferas em um veículo de carboximetilcelulose (Radiesse®). Tem sido usada para estimular a produção endógena de colágeno e consequentemente melhorar a qualidade e espessura da pele. Este efeito do produto poderia melhorar o quadro clínico da dermatoporose. O estudo teve como objetivo avaliar a melhora das lesões purpúricas e da atrofia da pele após aplicação de Radiesse® no antebraço de 5 pacientes portadores de dermatoporose no setor de Dermatologia do Hospital do Servidor Público Municipal de São Paulo. Os 5 pacientes foram submetidos a aplicação de Radiesse® nos antebraços e foram avaliadas 45 e 90 dias após o procedimento, o número de lesões purpúricas, grau de atrofia da pele através do teste de pinçamento e realizado comparação fotográfica. Após o tratamento, observou-se melhora do número das lesões purpúricas, melhora da atrofia da pele e melhora da qualidade de pele quando comparada fotograficamente. Dessa forma, o tratamento com Radiesse® mostrou-se promissor, com resultados satisfatórios e com um bom perfil de segurança. Palavras-chave: Dermatoporose. Púrpura senil. Radiesse. Bioestimulador. Tratamento.
Assuntos
Púrpura/tratamento farmacológico , Atrofia/diagnóstico , Pele/efeitos dos fármacos , Dermatopatias/diagnóstico , Envelhecimento/efeitos dos fármacos , Carboximetilcelulose Sódica/administração & dosagem , Envelhecimento da Pele/efeitos dos fármacos , Corticosteroides/efeitos adversos , Desidroepiandrosterona/fisiologia , Durapatita/administração & dosagem , Durapatita/uso terapêutico , Terapia com Luz de Baixa IntensidadeRESUMO
Abstract The transforming growth factor-beta 1 (TGFβ1) promotes fibrosis, differentiating epithelial cells and quiescent fibroblasts into myofibroblasts and increasing expression of extracellular matrix. Recent investigations have shown that PPAR (peroxisome proliferator-activated receptor*) is a negative regulator of fibrotic events induced by TGFβ1. Dehydroepiandrosterone (DHEA) is an immunomodulatory hormone essential for PPAR functions, and is reduced in some processes characterized by fibrosis. Although scarring alopecia characteristically develops in the female biological period in which occurs decreased production of DHEA, there are no data in the literature relating its reduction to fibrogenic process of this condition. This article aims to review the fibrogenic activity of TGFβ1, its control by PPAR and its relation with DHEA in the frontal fibrosing alopecia.
Assuntos
Humanos , Feminino , Desidroepiandrosterona/fisiologia , Alopecia/fisiopatologia , Alopecia/patologia , Fibrose , PPAR gama/fisiologia , Alopecia/etiologia , Alopecia/terapia , Fator de Crescimento Transformador beta1/fisiologia , Fibroblastos/fisiologia , Fibroblastos/patologia , Líquen Plano/patologiaRESUMO
The transforming growth factor-beta 1 (TGFß1) promotes fibrosis, differentiating epithelial cells and quiescent fibroblasts into myofibroblasts and increasing expression of extracellular matrix. Recent investigations have shown that PPAR (peroxisome proliferator-activated receptor*) is a negative regulator of fibrotic events induced by TGFß1. Dehydroepiandrosterone (DHEA) is an immunomodulatory hormone essential for PPAR functions, and is reduced in some processes characterized by fibrosis. Although scarring alopecia characteristically develops in the female biological period in which occurs decreased production of DHEA, there are no data in the literature relating its reduction to fibrogenic process of this condition. This article aims to review the fibrogenic activity of TGFß1, its control by PPAR and its relation with DHEA in the frontal fibrosing alopecia.
Assuntos
Alopecia/patologia , Alopecia/fisiopatologia , Desidroepiandrosterona/fisiologia , Alopecia/etiologia , Alopecia/terapia , Feminino , Fibroblastos/patologia , Fibroblastos/fisiologia , Fibrose , Humanos , Líquen Plano/patologia , PPAR gama/fisiologia , Fator de Crescimento Transformador beta1/fisiologiaRESUMO
During infectious diseases, neuroendocrine and immune networks act in concert, facilitating host response. It is known that infections cause profound immune changes, but the impact upon immunoendocrine circuits has been less studied. Disorders in the hypothalamic-pituitary-adrenal (HPA) axis were frequently observed associated with infections, and these changes often occur in parallel to alterations in the systemic cytokine network. Explanations for the infection-associated immunoendocrine disturbances include several and not mutually exclusive possibilities. Changes in cytokine levels can enhance or suppress the HPA axis, by acting at the hypothalamus-pituitary unit and/or at the adrenal glands. In situ inflammatory reactions or structural changes like vascular alterations or an enhanced extracellular matrix deposition in the endocrine microenvironment may also lead to a transient HPA dysfunction. Lastly, a microbe-related effect by means of pathogen infiltration or exploitation of the host's hormonal microenvironment may be involved as well. A better understanding of the relevance of immunoendocrine communication during infectious diseases, and how disturbances in the flux of information lead to neuroendocrine immune-related disorders will provide important insights into mechanisms underlying the disease pathology.
Assuntos
Doenças Transmissíveis/fisiopatologia , Citocinas/fisiologia , Hormônios/fisiologia , Sistema Hipotálamo-Hipofisário/fisiopatologia , Sistema Hipófise-Suprarrenal/fisiopatologia , Animais , Bovinos , Desidroepiandrosterona/fisiologia , Proteínas da Matriz Extracelular/fisiologia , Feminino , Glucocorticoides/fisiologia , Interações Hospedeiro-Parasita/imunologia , Interações Hospedeiro-Parasita/fisiologia , Interações Hospedeiro-Patógeno/fisiologia , Humanos , Inflamação/imunologia , Inflamação/fisiopatologia , Masculino , Camundongos , Modelos Imunológicos , Papio , Doenças Parasitárias em Animais/imunologia , Doenças Parasitárias em Animais/fisiopatologia , Estresse Fisiológico/imunologia , Estresse Fisiológico/fisiologia , Células Th1/imunologia , Células Th2/imunologiaRESUMO
This paper reviews recent work suggesting that human immunosenescence may be closely related to both chronic stress and stress hormones. The age-related immunological changes are also similarly found during chronic stress or glucocorticoid exposure. These data further suggest that endogenous glucocorticoids could be associated with immunosenescence. When compared with young subjects, healthy elders are emotionally distressed in parallel to increased cortisol/dehydroepiandrosterone ratio. Furthermore, chronically stressed elderly subjects may be particularly at risk of stress-related pathology because of further alterations in glucocorticoid-immune signaling. Age-related increase in cortisol/dehydroepiandrosterone ratio could be understood as a major determinant of immunological changes observed during aging. Strictly healthy elders are somewhat protected from chronic stress exposure and show normal cortisol levels and increased T cell function. This information adds a new key dimension to the biology of aging and stress.
Assuntos
Envelhecimento/imunologia , Estresse Psicológico/imunologia , Idoso , Idoso de 80 Anos ou mais , Envelhecimento/fisiologia , Envelhecimento/psicologia , Senilidade Prematura/etiologia , Cuidadores/psicologia , Doença Crônica , Ritmo Circadiano , Citocinas/fisiologia , Desidroepiandrosterona/metabolismo , Desidroepiandrosterona/fisiologia , Sulfato de Desidroepiandrosterona/sangue , Feminino , Glucocorticoides/sangue , Glucocorticoides/fisiologia , Humanos , Hidrocortisona/sangue , Hidrocortisona/metabolismo , Sistema Imunitário/crescimento & desenvolvimento , Inflamação/imunologia , Inflamação/fisiopatologia , Masculino , Pessoa de Meia-Idade , Modelos Biológicos , Taxa SecretóriaRESUMO
UNLABELLED: We studied the effects of chronic renal failure on the pituitary-cortisol axis and adrenal androgen function in 26 patients (16 male and 10 female), aged 6.5 to 22.5 years (mean 14.5). Ten patients were prepubertal, 8 pubertal, and 8 post-pubertal. All of them were on chronic hemodialysis. Pubic hair development was delayed in 56% of the patients. Serum cortisol was increased in 15 out of the 26 patients. Serum delta 4-androstenedione was high in 11 out of 15 patients in Tanner's stage I or II and in 1 out of 11 patients in Tanner's stage III, IV or V (p less than 0.01). Serum cortisol was elevated in 10 out of 12 patients with high serum delta 4-androstenedione and in only 5 out of 14 with normal delta 4-androstenedione (p less than 0.02). Serum dehydroepiandrosterone sulphate was normal in 22 patients and elevated in 4 males. There was a significant inverse correlation between bone age and serum cortisol (r: -0.59; p less than 0.005) and a significant positive correlation between bone age and serum dehydroepiandrosterone sulphate (r: 0.45 p less than 0.01). Serum ACTH was normal. A reduction by 50% in cortisol and 78% in dehydroepiandrosterone sulphate was found after dexamethasone suppression, but delta 4-androstenedione did not suppress after dexamethasone. After ACTH stimulation test cortisol increased by 50% and delta 4-androstenedione by 80%. CONCLUSIONS: The increased levels of cortisol and delta 4-androstenedione with partial resistance to dexamethasone suggest that these patients have a hypothalamic-pituitary dysfunction similar to that found in Cushing's disease or in chronic stress. The difference in the responses of delta 4-androstenedione and dehydroepiandrosterone sulphate observed is consistent with the existence of different mechanisms of control for these two steroids.