Laura C Coates1, Oliver FitzGerald2, Philip S Helliwell3, Carle Paul4. 1. Faculty of Medicine and Health, Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, 2nd Floor, Chapel Allerton Hospital, Harehills Lane, Leeds LS7 4SA, UK. 2. Department of Rheumatology, St Vincent's University Hospital and Conway Institute, University College, Dublin, Ireland. 3. Faculty of Medicine and Health, Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, 2nd Floor, Chapel Allerton Hospital, Harehills Lane, Leeds LS7 4SA, UK. Electronic address: P.Helliwell@leeds.ac.uk. 4. Larrey Hospital, Paul Sabatier University, Toulouse, France.
Abstract
OBJECTIVES: To review the pathophysiology, co-morbidities, and therapeutic options for psoriasis, psoriatic arthritis and rheumatoid arthritis in order to further understand the similarities and differences in treatment paradigms in the management of each disease. New targets for individualized therapeutic decisions are also identified with the aim of improving therapeutic outcome and reducing toxicity. SEARCH STRATEGY: Using the PubMed database, we searched literature published from 2000 to 2015 using combinations of the key words "psoriasis," "psoriatic arthritis," "rheumatoid arthritis," "pathogenesis," "immunomodulation," and "treatment." INCLUSION AND EXCLUSION CRITERIA: This was a non-systematic review and there were no formal inclusion and exclusion criteria. DATA EXTRACTION: Abstracts identified in the search were screened for relevance and articles considered appropriate evaluated further. References within these selected articles were also screened. Information was extracted from 198 articles for inclusion in this report. DATA SYNTHESIS: There was no formal data synthesis. Articles were reviewed and summarized according to disease area (psoriasis, psoriatic arthritis, and rheumatoid arthritis). HEADLINE RESULTS: The pathophysiology of psoriasis, psoriatic arthritis, and rheumatoid arthritis involves chronic inflammation mediated by pro-inflammatory cytokines. Dysfunction in integrated signaling pathways affecting different constituents of the immune system result in varying clinical features in the three diseases. Co-morbidities, including cardiovascular disease, malignancies, and non-alcoholic fatty liver disease are increased. Increased understanding of the immunopathogenesis allowed development of targeted treatments; however, despite a variety of potentially predictive genetic, protein and cellular biomarkers, there is still significant unmet need in these three inflammatory disorders.
OBJECTIVES: To review the pathophysiology, co-morbidities, and therapeutic options for psoriasis, psoriatic arthritis and rheumatoid arthritis in order to further understand the similarities and differences in treatment paradigms in the management of each disease. New targets for individualized therapeutic decisions are also identified with the aim of improving therapeutic outcome and reducing toxicity. SEARCH STRATEGY: Using the PubMed database, we searched literature published from 2000 to 2015 using combinations of the key words "psoriasis," "psoriatic arthritis," "rheumatoid arthritis," "pathogenesis," "immunomodulation," and "treatment." INCLUSION AND EXCLUSION CRITERIA: This was a non-systematic review and there were no formal inclusion and exclusion criteria. DATA EXTRACTION: Abstracts identified in the search were screened for relevance and articles considered appropriate evaluated further. References within these selected articles were also screened. Information was extracted from 198 articles for inclusion in this report. DATA SYNTHESIS: There was no formal data synthesis. Articles were reviewed and summarized according to disease area (psoriasis, psoriatic arthritis, and rheumatoid arthritis). HEADLINE RESULTS: The pathophysiology of psoriasis, psoriatic arthritis, and rheumatoid arthritis involves chronic inflammation mediated by pro-inflammatory cytokines. Dysfunction in integrated signaling pathways affecting different constituents of the immune system result in varying clinical features in the three diseases. Co-morbidities, including cardiovascular disease, malignancies, and non-alcoholic fatty liver disease are increased. Increased understanding of the immunopathogenesis allowed development of targeted treatments; however, despite a variety of potentially predictive genetic, protein and cellular biomarkers, there is still significant unmet need in these three inflammatory disorders.
Authors: Alexis Ogdie; Neilia Kay McGill; Daniel B Shin; Junko Takeshita; Thorvardur Jon Love; Megan H Noe; Zelma C Chiesa Fuxench; Hyon K Choi; Nehal N Mehta; Joel M Gelfand Journal: Eur Heart J Date: 2018-10-14 Impact factor: 29.983
Authors: Alexis Ogdie; Sungat K Grewal; Megan H Noe; Daniel B Shin; Junko Takeshita; Zelma C Chiesa Fuxench; Rotonya M Carr; Joel M Gelfand Journal: J Invest Dermatol Date: 2017-11-02 Impact factor: 8.551