Pyoderma gangrenosum
Pyoderma gangrenosum cuta ce da ba kasafai ba, mai kumburin fata inda ƙwanƙwasawa ko nodules masu raɗaɗi suka zama gyambon da ke girma a hankali. Pyoderma gangrenosum ba cuta bane. Jiyya na iya haɗawa da corticosteroids, cyclosporin, ko ƙwayoyin rigakafi na monoclonal daban-daban. Ko da yake yana iya shafar mutane na kowane zamani, galibi yana shafar mutane masu shekaru 40 zuwa 50.
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A kafar mutumin da ke fama da ciwon ciki.
References
Pyoderma gangrenosum cuta ce da ba kasafai ake samun fata ba wanda ke haifar da gyambo mai raɗaɗi tare da ja ko gefuna masu launin shuɗi. An rarraba shi azaman cutar kumburi kuma wani ɓangare ne na ƙungiyar da ake kira neutrophilic dermatosis. Dalilin pyoderma gangrenosum yana da rikitarwa, yana tattare da matsaloli tare da rigakafi na asali da kuma daidaitawa a cikin mutanen da ke da alaƙa da kwayoyin halitta. Kwanan nan, masu bincike sun mayar da hankali kan gashin gashi a matsayin yiwuwar farawa da cutar.
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 cuta ce da ba kasafai ake samun fata ba tana haifar da ciwon ulcer mai tsananin zafi. Duk da yake ba mu fahimci dalilinsa ba, mun san yana tattare da ƙarin ayyuka na wasu ƙwayoyin rigakafi. Magance cutar ba ta da sauƙi. Muna da magunguna daban-daban waɗanda ke danne tsarin rigakafi ko canza ayyukan sa. Tare da waɗannan, muna kuma mai da hankali kan magance raunuka da sarrafa ciwo. Corticosteroids da cyclosporine galibi sune zaɓi na farko don magani, amma kwanan nan, an sami ƙarin bincike akan amfani da hanyoyin ilimin halitta kamar masu hana TNF-α. Ana ƙara fi son waɗannan ƙwayoyin halitta, musamman a cikin marasa lafiya da wasu yanayi masu kumburi, kuma ana amfani da su a baya a cikin tsarin cutar.
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.
