Pyoderma gangrenosum
Pyoderma gangrenosum er sjaldgæfur, bólgusjúkdómur í húð þar sem sársaukafullir graftar eða hnúðar verða að sárum sem vaxa smám saman. Pyoderma gangrenosum er ekki smitandi. Meðferðir geta falið í sér barkstera, ciclosporin eða ýmis einstofna mótefni. Þó það geti haft áhrif á fólk á hvaða aldri sem er, hefur það aðallega áhrif á fólk á fertugs- og fimmtugsaldri.
☆ Í niðurstöðum Stiftung Warentest 2022 frá Þýskalandi var ánægja neytenda með ModelDerm aðeins minni en með greiddum fjarlækningaráðgjöfum.
Á fæti einstaklings með sáraristilbólgu.
References
Pyoderma gangrenosum er sjaldgæfur húðsjúkdómur sem veldur sársaukafullum sárum með rauðum eða fjólubláum brúnum. Það er flokkað sem bólgusjúkdómur og er hluti af hópi sem kallast daufkyrningahúðsjúkdómar. Orsök pyoderma gangrenosum er flókin og felur í sér vandamál með bæði meðfædda og aðlögunarhæfni ónæmis hjá fólki sem er erfðafræðilega viðkvæmt. Nýlega hafa vísindamenn einbeitt sér að hársekkjum sem hugsanlegan upphafspunkt sjúkdómsins.
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 er sjaldgæfur húðsjúkdómur sem veldur mjög sársaukafullum sárum. Þó að við skiljum ekki að fullu orsök þess, vitum við að það felur í sér aukna virkni ákveðinna ónæmisfrumna. Að meðhöndla sjúkdóminn er ekki enn auðvelt. Við höfum ýmis lyf sem bæla ónæmiskerfið eða breyta virkni þess. Samhliða þessu leggjum við áherslu á að meðhöndla sárin og meðhöndla sársauka. Barksterar og cíklósporín eru oft fyrsti kosturinn við meðferð, en undanfarið hafa verið fleiri rannsóknir á notkun líffræðilegra meðferða eins og TNF-α hemla. Þessi líffræðilegu lyf eru æ æskilegri, sérstaklega hjá sjúklingum með aðra bólgusjúkdóma, og þau eru notuð fyrr í sjúkdómsferlinu.
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.
