PAPA, PASH and PAPASH Syndromes: Pathophysiology, Presentation and Treatment.

Pyoderma gangrenosum (PG) is a neutrophilic dermatosis usually manifesting as skin ulcers with undermined erythematous-violaceous borders. It may be isolated, associated with systemic conditions or occurring in the context of autoinflammatory syndromes such as PAPA (pyogenic arthritis, PG and acne),...

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Publicado en:American Journal of Clinical Dermatology Vol. 18; no. 4; pp. 555 - 563
Autores principales: Cugno, Massimo, Borghi, Alessandro, Marzano, Angelo
Formato: pictorial review tables/charts Journal Article
Publicado: Springer Nature Aug2017
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Aug2017
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      pub: Springer Nature
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        atl: PAPA, PASH and PAPASH Syndromes: Pathophysiology, Presentation and Treatment.
      aug:
        au:
          Cugno, Massimo
          Borghi, Alessandro
          Marzano, Angelo
        affil: Medicina Interna, Dipartimento di Fisiopatologia Medico-Chirurgica e dei Trapianti , Università degli Studi di Milano, Ospedale Maggiore Policlinico, Fondazione IRCCS Ca' Granda , Via Pace, 9 20122 Milan Italy
      sug:
        subj:
          Pyoderma Gangrenosum Diagnosis
          Pyoderma Gangrenosum Classification
          Pyoderma Gangrenosum Therapy
          Interleukins
          Immunologic Diseases
          Cytokines
          Diagnosis, Differential
          Treatment Outcomes Evaluation
          Pyoderma Gangrenosum Symptoms
      ab: Pyoderma gangrenosum (PG) is a neutrophilic dermatosis usually manifesting as skin ulcers with undermined erythematous-violaceous borders. It may be isolated, associated with systemic conditions or occurring in the context of autoinflammatory syndromes such as PAPA (pyogenic arthritis, PG and acne), PASH (PG, acne and suppurative hidradenitis) or PAPASH (pyogenic arthritis, acne, PG and suppurative hidradenitis). From a physiopathological point of view, all these conditions share common mechanisms consisting of over-activation of the innate immune system leading to increased production of the interleukin (IL)-1 family and 'sterile' neutrophil-rich cutaneous inflammation. From a genetic point of view, a number of mutations affecting the proteins of the inflammasome complex (the molecular platform responsible for triggering autoinflammation) or the proteins that regulate inflammasome function have been described in these disorders. As these debilitating entities are all associated with the over-expression of IL-1 and tumour necrosis factor (TNF)-α, biological drugs specifically targeting these cytokines are currently the most effective treatments but, given the emerging role of IL-17 in the pathogenesis of these syndromes, IL-17 antagonists may represent the future management of these conditions.
      pubtype: Academic Journal
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        pictorial
        review
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    language: English
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