Abstract
Rheumatoid arthritis (RA) is the most common inflammatory arthropathy worldwide. Possible manifestations of RA can be represented by a wide variability of symptoms, clinical forms, and course options. This multifactorial disease is triggered by a genetic predisposition and environmental factors. Both clinical and genealogical studies have demonstrated disease case accumulation in families. Revealing the impact of candidate gene missense variants on the disease course elucidates understanding of RA molecular pathogenesis. A multivariate genomewide association study (GWAS) based analysis identified the genes and signalling pathways involved in the pathogenesis of the disease. However, these identified RA candidate gene variants only explain 30% of familial disease cases. The genetic causes for a significant proportion of familial RA have not been determined until now. Therefore, it is important to identify RA risk groups in different populations, as well as the possible prognostic value of some genetic variants for disease development, progression, and treatment. Our review has two purposes. First, to summarise the data on RA candidate genes and the increased disease risk associated with these alleles in various populations. Second, to describe how the genetic variants can be used in the selection of drugs for the treatment of RA.
Highlights
Rheumatoid arthritis (RA) is a chronic autoinflammatory disease affecting connective tissue, characterised by progressive joint damage and specific systemic disorders
In the absence of unfavourable prognosis factors, another csDMARD is added to methotrexate
Up to 40% of patients remain resistant to this therapy, as estimated by various authors, it has been shown to date that some of them may respond to anti-IL6 receptor (IL6R) therapy
Summary
Rheumatoid arthritis (RA) is a chronic autoinflammatory disease affecting connective tissue, characterised by progressive joint damage and specific systemic disorders. RA is considered to be a multifactorial disease triggered by a genetic predisposition and environmental factors. Both clinical and genealogical studies have shown that the disease can accumulate in families. This relationship has been confirmed by modern molecular genetics. The opportunity to identify RA risk groups in different populations, as well as the possible prognostic value of some genetic variants for disease development, progression, and treatment, including a personalised antirheumatic therapy response, has promoted new studies of germline genetic variants in RA patients [1,2]. A total of 125 sources were selected, of which 96 are mentioned in this review
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