Open AccessPsoriasis and inflammatory bowel diseases: pathogenetic pathways and the choice of biologic therapy (a literature review)
Author(s) -
Л. С. Круглова,
Andrey Lvov,
A Kagramanova,
О. В. Князев
Publication year - 2019
Publication title -
alʹmanah kliničeskoj mediciny
Language(s) - English
Resource type - Journals
eISSN - 2587-9294
pISSN - 2072-0505
DOI - 10.18786/2072-0505-2019-47-062
Subject(s) - medicine , psoriasis , ustekinumab , adalimumab , secukinumab , ulcerative colitis , psoriatic arthritis , infliximab , inflammatory bowel disease , etanercept , immunology , disease , arthritis , crohn's disease , tumor necrosis factor alpha
Psoriasis and inflammatory bowel disease (IBD) are multifactorial chronic immuno-inflammatory potentially disabling disorders with similar genetic factors and immunological pathways, in particular, genetic polymorphisms of IL-23R, which determines the signal IL-12/23-mediated pathway of immunopathogenesis. The emergence of genetically engineered biological agents has changed the prognosis for both psoriasis and IBD. The intersection of the therapeutic spectrum in psoriasis and IBD is a very important point when choosing the management strategy for these patients. Infliximab and adalimumab are effective in the treatment of psoriasis, psoriatic arthritis, Crohn's disease, ulcerative colitis (evidence level 1A). Ustekinumab demonstrates effectiveness in the treatment of psoriasis, psoriatic arthritis (evidence level 1A) and Crohn's disease (evidence level 1B). Etanercept and secukinumab have been shown to be effective against psoriasis, psoriatic arthritis (evidence level 1A) and ineffective and even associated with exacerbation risk in Crohn's disease and ulcerative colitis. Inhibition of regulatory cytokines IL-12/23 also has a number of advantages compared to the blockade of effector cytokines (TNF-α, IL-17) due to potentially long-term and stable treatment results and less frequent administration.