Pyoderma gangrenosum
Pyoderma gangrenosum o se fa'ama'i e seasea ona tupu i le pa'u, lea e avea ai ma pustules tiga po'o nodule ma papala e faasolosolo ona tupu. Pyoderma gangrenosum e le fa'ama'i. O togafitiga e mafai ona aofia ai corticosteroids, cyclosporin, po'o monoclonal antibodies eseese. E ui lava e mafai ona aʻafia ai tagata o soʻo se matua, e tele lava le tagata e aʻafia i le 40‑ma‑50 tausaga.
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ReferencesPyoderma gangrenosum o se ma'i e seasea, maua e mafua ai le ma'i papala e mumu pe violè pito. O lo'o fa'avasegaina o se fa'ama'i fa'ama'i ma o se vaega o le neutrophilic dermatoses. O le mafua'aga o le pyoderma gangrenosum e lavelave; e a'afia ai fa'afitauli fa'atasi ma fa'alavelave fa'anatinati, ma fetuutuuna'i i tagata e fa'atupu le ma'i. Talu ai nei, na taula'i atu tagata su'esu'e i le follicule o lauulu e avea ma amataga o le ma'i.
Pyoderma gangrenosum is a rare inflammatory skin disease classified within the group of neutrophilic dermatoses and clinically characterized by painful, rapidly evolving cutaneous ulcers with undermined, irregular, erythematous-violaceous edges. Pyoderma gangrenosum pathogenesis is complex and involves a profound dysregulation of components of both innate and adaptive immunity in genetically predisposed individuals, with the follicular unit increasingly recognized as the putative initial target.
Pyoderma gangrenosum is a rare inflammatory skin disease classified within the group of neutrophilic dermatoses and clinically characterized by painful, rapidly evolving cutaneous ulcers with undermined, irregular, erythematous-violaceous edges. Pyoderma gangrenosum pathogenesis is complex and involves a profound dysregulation of components of both innate and adaptive immunity in genetically predisposed individuals, with the follicular unit increasingly recognized as the putative initial target.
Pyoderma gangrenosum o se ma'i e seasea maua i le pa'u e mafua ai le ma'i papala. E ui tatou te le malamalama atoatoa i lona mafua’aga, ae tatou te iloa o lo’o fa’ateleina gaioiga a nisi o sela puipuia. O le togafitia o le ma’i e le faigofie. E iai a matou vaila’au eseese e taofia ai le puipuiga o le tino po’o le suia o lona gaioiga. Faatasi ai ma nei mea, matou te taulai fo’i i le togafitia o manu’a ma le puleaina o tiga. Corticosteroids ma cyclosporine e masani lava o filifiliga muamua mo togafitiga, ae talu ai nei ua tele su’esu’e i le fa’aaogaina o togafitiga fa—apitoa e pei o TNF-α inhibitors. O nei meaola fa’aola ua fa’ateleina le fiafia, aemaise lava i tagata ma’i mamafa ma isi tulaga fa’ama’i, ma o lo’o fa’aaogaina muamua i le fa’agasologa o fa’ama’i.
Pyoderma gangrenosum is a rare neutrophilic dermatosis that leads to exceedingly painful ulcerations of the skin. Although the exact pathogenesis is not yet fully understood, various auto-inflammatory phenomena with increased neutrophil granulocyte activity have been demonstrated. Despite the limited understanding of the pathogenesis, it is no longer a diagnosis of exclusion, as it can now be made on the basis of validated scoring systems. However, therapy remains a major multidisciplinary challenge. Various immunosuppressive and immunomodulatory therapies are available for the treatment of affected patients. In addition, concomitant topical pharmacologic therapy, wound management and pain control should always be addressed. Corticosteroids and/or cyclosporine remain the systemic therapeutics of choice for most patients. However, in recent years, there has been an increasing number of studies on the positive effects of biologic therapies such as inhibitors of tumour necrosis factor-α; interleukin-1, interleukin-17, interleukin-23 or complement factor C5a. Biologics have now become the drug of choice in certain scenarios, particularly in patients with underlying inflammatory comorbidities, and are increasingly used at an early stage in the disease rather than in therapy refractory patients.
Pyoderma gangrenosum is a rare neutrophilic dermatosis that leads to exceedingly painful ulcerations of the skin. Although the exact pathogenesis is not yet fully understood, various auto-inflammatory phenomena with increased neutrophil granulocyte activity have been demonstrated. Despite the limited understanding of the pathogenesis, it is no longer a diagnosis of exclusion, as it can now be made on the basis of validated scoring systems. However, therapy remains a major multidisciplinary challenge. Various immunosuppressive and immunomodulatory therapies are available for the treatment of affected patients. In addition, concomitant topical pharmacologic therapy, wound management and pain control should always be addressed. Corticosteroids and/or cyclosporine remain the systemic therapeutics of choice for most patients. However, in recent years, there has been an increasing number of studies on the positive effects of biologic therapies such as inhibitors of tumour necrosis factor-α; interleukin-1, interleukin-17, interleukin-23 or complement factor C5a. Biologics have now become the drug of choice in certain scenarios, particularly in patients with underlying inflammatory comorbidities, and are increasingly used at an early stage in the disease rather than in therapy refractory patients.
