Pyoderma gangrenosum
Ko te Pyoderma gangrenosum he mate kiri onge, mumura ka puta nga pustules mamae me nga nodules hei whewhe ka tipu haere. Pyoderma gangrenosum ehara i te hopuhopu. Ko nga maimoatanga ka uru ki nga corticosteroids, cyclosporin, etahi momo paturopi monoclonal ranei. Ahakoa ka pa ki nga taangata ahakoa te pakeke, ko te nuinga ka pa ki nga taangata 40 me te 50 tau.
☆ I te 2022 Stiftung Warentest hua mai i Tiamana, he iti noa iho te pai o nga kaihoko ki a ModelDerm i nga korero mo te waea rongoa utu.
I runga i te waewae o te tangata he ulcerative colitis.
References
Ko te Pyoderma gangrenosum he mate kiri onge e puta ai nga whewhe mamae me nga tapa whero, papura ranei. Kua whakarōpūtia hei mate mumura, he wahanga o te roopu e kiia nei ko te neutrophilic dermatoses. He uaua te take o te pyoderma gangrenosum , he raruraru kei roto i te mate o roto me te urutau ki roto i nga tangata e pa ana ki te ira. I tata nei, kua aro nga kairangahau ki te makawe makawe hei timatanga o te mate.
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.
Ko te Pyoderma gangrenosum he mate kiri onge e puta ai nga whewhe tino mamae. Ahakoa kaore matou i te tino marama ki tona take, e mohio ana matou he nui ake nga mahi a etahi o nga pūtau mate. Ko te rongoa i te mate kaore i te ngawari. He maha nga raau taero e pehi ana i te punaha raupatu, hei whakarereke ranei i tana mahi. I te taha o enei, ka aro ano matou ki te rongoa i nga patunga me te whakahaere mamae. Ko nga corticosteroids me te cyclosporine te nuinga o nga wa ko te whiriwhiri tuatahi mo te maimoatanga, engari i enei ra, kua nui ake nga rangahau mo te whakamahi rongoa koiora penei i te aukati TNF-α. Ko enei koiora kei te pai ake, ina koa i nga turoro me etahi atu mate mumura, a kei te whakamahia i mua atu i te tukanga mate.
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.
