Pyoderma gangrenosum
Mae Pyoderma gangrenosum yn glefyd croen prin, llidiol lle mae llinorod neu nodwlau poenus yn troi'n wlserau sy'n tyfu'n raddol. nid yw pyoderma gangrenosum yn heintus. Gall triniaethau gynnwys corticosteroidau, ciclosporin, neu wrthgyrff monoclonaidd amrywiol. Er y gall effeithio ar bobl o unrhyw oedran, mae'n effeithio'n bennaf ar bobl yn eu 40au a'u 50au.
☆ Yng nghanlyniadau Stiftung Warentest 2022 o’r Almaen, roedd boddhad defnyddwyr â ModelDerm ond ychydig yn is nag ymgynghoriadau telefeddygaeth taledig.
Ar goes person â colitis briwiol.
References
Mae Pyoderma gangrenosum yn gyflwr croen prin sy'n achosi wlserau poenus gydag ymylon coch neu borffor. Mae'n cael ei ddosbarthu fel clefyd llidiol ac mae'n rhan o grŵp o'r enw dermatoses niwtroffilig. Mae achos pyoderma gangrenosum yn gymhleth, gan gynnwys problemau gydag imiwnedd cynhenid ac ymaddasol mewn pobl sy'n dueddol o fod yn enetig. Yn ddiweddar, mae ymchwilwyr wedi canolbwyntio ar y ffoligl gwallt fel man cychwyn posibl y clefyd.
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.
Mae Pyoderma gangrenosum yn gyflwr croen prin sy'n achosi wlserau poenus iawn. Er nad ydym yn deall ei achos yn llawn, rydym yn gwybod ei fod yn cynnwys mwy o weithgaredd rhai celloedd imiwn. Nid yw trin y clefyd yn hawdd o hyd. Mae gennym wahanol gyffuriau sy'n atal y system imiwnedd neu'n addasu ei gweithgaredd. Ochr yn ochr â'r rhain, rydym hefyd yn canolbwyntio ar drin y clwyfau a rheoli poen. Yn aml, corticosteroidau a cyclosporine yw'r dewis cyntaf ar gyfer triniaeth, ond yn ddiweddar, bu mwy o ymchwil ar ddefnyddio therapïau biolegol fel atalyddion TNF-α. Mae'r biolegau hyn yn cael eu ffafrio fwyfwy, yn enwedig mewn cleifion â chyflyrau llidiol eraill, ac maen nhw'n cael eu defnyddio'n gynharach yn y broses afiechyd.
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.
