Pyoderma gangrenosum - Ipyoderma Gangrenosum
Ipyoderma Gangrenosum (Pyoderma gangrenosum) sisifo solusu esinqabileyo, sokudumba, apho amaqhuqhuva abuhlungu okanye amaqhuqhuva abe zizilonda ezikhula ngokuqhubekayo. Ipyoderma gangrenosum (pyoderma gangrenosum) ayosuleli. Unyango lunokubandakanya i-corticosteroids, i-ciclosporin, okanye ii-antibodies ezahlukeneyo ze-monoclonal. Nangona inokuchaphazela abantu nayiphi na iminyaka, ichaphazela kakhulu abantu abaphakathi kweminyaka ye-40 ne-50.
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ReferencesPyoderma gangrenosum yimeko yolusu engqabileyo ebangela izilonda ezibuhlungu ezinemiphetho ebomvu okanye emifusa. Ihlelwe njengesifo sokukrala kwaye iyinxalenye yeqela elibizwa ngokuba yi-neutrophilic dermatoses. Unobangela we pyoderma gangrenosum awucacanga, ubandakanya iingxaki zokugonywa kwemvelo kunye nokuguquka kubantu abathambekele kwimfuzo. Kwangoku, abaphandi bagxile kwi-follicle yeenwele njengendawo enokubakho ukuqala kwesi sifo.
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 yimeko yolusu enqabileyo ebangela izilonda ezibuhlungu kakhulu. Ngelixa singawuqondi ngokupheleleyo unobangela wayo, siyazi ukuba ibandakanya umsebenzi owandisiweyo weeseli ezithile zomzimba. Ukunyanga esi sifo akukabi lula. Sineziyobisi ezahlukeneyo ezichaphazela inkqubo yokuzikhusela yomzimba okanye eziguqula indlela esebenza ngayo. Kule meko, sigxile ekunyangeni amanxeba nokulawula iintlungu. I‑Corticosteroids kunye ne‑cyclosporine zihlala zisetyenziswa njengokhetho lokuqala lonyango, kodwa kutshanje kukho uphando oluninzi malunga nokusetyenziswa kwezonyango zebhayoloji ezifana ne‑TNF‑α inhibitors. Ezi zonyango ze‑bhayoloji zikhethwa ngakumbi kwizigulana abaneminye imiba yokuvuvukala, kwaye zisetyenziswa ngokukhawuleza kwinkqubo yokunyanga.
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.
