Pyoderma gangrenosum
Pyoderma gangrenosum ose fa'ama'i e seasea ona tupu i le pa'u, lea e avea ai pustules tiga po'o nodule ma papala e faasolosolo ona tupu. Pyoderma gangrenosum e le fa'afua. Togafitiga e mafai ona aofia ai corticosteroids, ciclosporin, poʻo monoclonal antibodies eseese. E ui lava e mafai ona afaina tagata i soʻo se tausaga, e tele lava ina aʻafia ai tagata i le 40 ma le 50s o latou tausaga.
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ReferencesPyoderma gangrenosum o se maʻi o le paʻu e seasea, i le which painful pustules (pustula e tiga) po o nodules (nodula) e tupu i ulusā e fa‘ateleina i le taimi. E le o se maʻi fa‘afefe. O filifiliga o le togafitiga e mafai ona aofia ai corticosteroids, ciclosporin, po’o le tele o le monoclonal antibodies. E ui e mafai ona tupu i soʻo se vaitau, e masani ona afaina tagata i le vaitau 40‑50.
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 ose maʻi e seasea maua ile paʻu e mafua ai le maʻi papala. E ui tatou te le malamalama atoatoa i lona mafuaʻaga, ae tatou te iloa e aofia ai le faʻateleina o gaioiga a nisi o sela puipuia. O le togafitia o le maʻi e leʻo faigofie. E iai a matou vailaʻau eseese e taofia ai le puipuiga o le tino poʻo le suia o lana gaioiga. Faatasi ai ma nei mea, matou te taulai atu foi i le togafitia o manuʻa ma le puleaina o tiga. Corticosteroids ma ciclosporin (cyclosporine) e masani lava o le filifiliga muamua mo togafitiga, ae talu ai nei, ua tele suʻesuʻega i le faʻaaogaina o togafitiga faʻapitoa e pei o le TNF-α inhibitors. O nei meaola faʻaola ua faʻaeteleina le fiafia, aemaise lava i tagata maʻi ma isi tulaga faʻamaʻi, ma o loʻo faʻaogaina muamua i le faʻagasologa o faʻamaʻi.
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.
