Abstract
The range of causal combinations of various types of intestinal lesions and spondyloarthritis (SpA) is extremely wide: from subclinical pathology to manifest manifestations of Crohn’s disease and ulcerative colitis. In studies of the last decade it is assumed that not only inflammatory bowel diseases (IBD), psoriasis, but also SpA are diseases with activated innate immunity, which provides an early non-specific response mediated by the barrier function of the epithelium. Modern data on the cellular and molecular mechanisms of SpA pathogenesis allow rheumatologists to hypothesize the concept of a “barrier organ disease” as the preclinical stage of development of diseases belonging to the SpA group, which is based on impaired immune tolerance to autologous synanthropic microflora in genetically predisposed individuals.Key words: microbiome; spondyloarthritis; inflammatory bowel disease, pathogenesis
Highlights
which provides an early non-specific response mediated by the barrier function of the epithelium
molecular mechanisms of SpA pathogenesis allow rheumatologists to hypothesize the concept of a “barrier organ disease
as the preclinical stage of development of diseases belonging to the SpA group
Summary
Появились новые доказательства в поддержку теории, что измененная синантропная микрофлора является фактором инициации и поддержания хронического воспаления при спондилоартритах (СпА) [2,4,5], к которым в настоящее время относят: анкилозирующий спондилит (АС), псориатический артрит (ПсА), реактивные артриты (РеА), энтеропатические артропатии (артриты при воспалительных заболеваниях кишечника (ВЗК)) и недифференцированные спондилоартриты [6]. Поскольку клинический опыт ведения пациентов с ВЗК и с псориазом уже давно показал, что эти диагнозы могут быть сопутствующими, а эпидемиологические исследования продемонстрировали значительное увеличение частоты встречаемости как псориаза при ВЗК, так и ВЗК при псориазе, по сравнению с популяцией [16].
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