Pyoderma gangrenosum
Pyoderma gangrenosum bụ ọrịa akpụkpọ anụ na-adịghị ahụkebe ebe ọnya na-egbu mgbu ma ọ bụ nodules na-aghọ ọnya na-eto nwayọọ nwayọọ. Pyoderma gangrenosum anaghị efe efe. Ọgwụgwọ nwere ike ịgụnye corticosteroids, cyclosporin, ma ọ bụ ọgwụ mgbochi monoclonal dị iche iche. Ọ bụ ezie na ọ nwere ike imetụta mmadụ n'afọ ọ bụla, ọ na-emetụkarị ndị dị n'afọ iri anọ ruo iri ise.
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N'ụkwụ onye nwere ulcerative colitis.
relevance score : -100.0%
ReferencesPyoderma gangrenosum bụ ọrịa akpụkpọ ahụ na-adịghị ahụkebe nke na-ebute ọnya na-egbu mgbu, nwere akụkụ uhie ma ọ bụ purplish. A na-ekewa ya dị ka ọrịa mkpali, ma ọ bụ akụkụ nke otu a na-akpọ neutrophilic dermatosis. Ihe kpatara pyoderma gangrenosum dị mgbagwoju anya, gụnyere nsogbu na usoro mgbochi ọrịa na mgbanwe ndị metụtara mkpụrụ ndụ ihe nketa. N'oge na-adịbeghị anya, ndị nchọpụta lekwasịrị anya na ntutu isi dị ka ebe nwere ike ịmalite ọrịa ahụ.
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 bụ ọrịa akpụkpọ ahụ na-adịghị ahụkebe nke na-akpata ọnya na-emerụ ahụ. Ọ bụ ezie na anyị ka na-amaghị kpọmkwem ihe kpatara ya, anyị maara na ọ metụtara mmụba ụfọdụ mkpụrụ ndụ na-alụso ọrịa ọgụ. Ịgwọ ọrịa a adịghị mfe. Anyị nwere ọgwụ dị iche iche nke na-egbochi usoro mgbalị ahụ ma ọ bụ na-agbanwe ọrụ ya. N'akụkụ ndị a, anyị na-elekwasị anya n'ịgwọ ọnya na ịchịkwa mgbu. Corticosteroids na cyclosporine bụ nhọrọ mbụ maka ọgwụgwọ, mana n'oge na-adịbeghị anya, enweela nyocha ndị ọzọ maka iji ọgwụ ndị na-egbochi TNF-α. Enwekwara mmasị na ọgwụ ndị dị ndụ, karịsịa n’ụlọ ndị nwere ọrịa mgbagwoju anya, a na-ejikarị ha mee ihe n’oge mbụ nke ọrịa.
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.
