Pyoderma gangrenosum
https://en.wikipedia.org/wiki/Pyoderma_gangrenosum
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Haavandilise koliidiga inimese jalal.
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References
Pyoderma Gangrenosum: An Updated Literature Review on Established and Emerging Pharmacological Treatments 35606650 NIH
Pyoderma gangrenosum on haruldane nahahaigus, mis põhjustab punaste või lillakate servadega valulikke haavandeid. See on klassifitseeritud põletikuliseks haiguseks ja kuulub neutrofiilsete dermatooside rühma. Pyoderma gangrenosum põhjus on keeruline, hõlmates probleeme nii kaasasündinud kui ka adaptiivse immuunsusega inimestel, kes on geneetiliselt altid. Viimasel ajal on teadlased keskendunud juuksefolliikulile kui haiguse potentsiaalsele lähtepunktile.
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: Treatment Options 37610614 NIH
Pyoderma gangrenosum on haruldane nahahaigus, mis põhjustab äärmiselt valusaid haavandeid. Kuigi me ei mõista selle põhjust täielikult, teame, et see hõlmab teatud immuunrakkude suurenenud aktiivsust. Haiguse ravimine pole endiselt lihtne. Meil on erinevaid ravimeid, mis pärsivad immuunsüsteemi või muudavad selle aktiivsust. Lisaks sellele keskendume ka haavade ravile ja valu leevendamisele. Kortikosteroidid ja tsüklosporiin on sageli ravi esimene valik, kuid viimasel ajal on rohkem uuritud bioloogiliste ravimeetodite, näiteks TNF-α inhibiitorite kasutamist. Neid bioloogilisi ravimeid eelistatakse üha enam, eriti muude põletikuliste seisunditega patsientidel, ja neid kasutatakse haigusprotsessis varem.
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.