Pyoderma gangrenosum
Is galar annamh, athlastach craicinn é Pyoderma gangrenosum ina n-éiríonn ulcras nó nodules pianmhar a fhásann de réir a chéile. Níl pyoderma gangrenosum tógálach. Féadfar corticosteroids, ciclosporin, nó antasubstaintí monaclónacha éagsúla a áireamh i gcóireálacha. Cé gur féidir leis dul i bhfeidhm ar dhaoine d'aois ar bith, is mó a théann i bhfeidhm ar dhaoine ina 40í agus 50idí.
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Ar cos duine a bhfuil colitis ulcerative air.
References
Is riocht annamh craiceann é Pyoderma gangrenosum a fhágann othrais phianmhar le himill dhearga nó chorcra. Tá sé rangaithe mar ghalar athlastach agus tá sé mar chuid de ghrúpa ar a dtugtar deirmitín neodrófaileacha. Is cúis chasta í an chúis pyoderma gangrenosum , agus baineann fadhbanna le himdhíonacht dhúchasach agus oiriúnaitheach i ndaoine atá seans maith go géiniteach. Le déanaí, dhírigh taighdeoirí ar an follicule gruaige mar phointe tosaigh féideartha an ghalair.
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.
Is riocht annamh é Pyoderma gangrenosum ar an gcraiceann agus othrais thar a bheith pianmhar. Cé nach dtuigimid go hiomlán a chúis, tá a fhios againn go bhfuil gníomhaíocht mhéadaithe cealla imdhíonachta áirithe i gceist leis. Níl sé fós éasca an galar a chóireáil. Tá drugaí éagsúla againn a shochtann an córas imdhíonachta nó a athraíonn a ghníomhaíocht. In éineacht leo seo, dírímid freisin ar na créachta a chóireáil agus pian a bhainistiú. Is minic gurb iad corticosteroids agus cyclosporine an chéad rogha le haghaidh cóireála, ach le déanaí, rinneadh níos mó taighde ar úsáid a bhaint as teiripí bitheolaíocha cosúil le coscairí TNF-α. Is fearr na bitheolaíochta seo níos mó, go háirithe in othair a bhfuil riochtaí athlastacha eile orthu, agus tá siad á n-úsáid níos luaithe i bpróiseas an ghalair.
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.
