Abstract
BACKGROUND: Rheumatoid arthritis is a phenotypically diverse disease. AIM: To analyze the role of some triggers of rheumatoid arthritis and joint symptoms in individuals at risk of the disease at preclinical stages and their link with clinical and laboratory indices. MATERIAL AND METHODS: In groups of patients with early rheumatoid arthritis (n=461), their relatives (n=247) and 299 healthy individuals, information on a possible trigger was analyzed, namely, past infections,, anxiety level, number of childbirths, age of menopause onset, body mass index. The impact of these triggers on clinical and laboratory indices, namely with complex activity indices, morning stiffness duration, joint functional disability using Health Assessment Questionnaire, erythrocyte sedimentation rate, levels of C-reactive protein, antibodies to cyclic citrullinated peptides, rheumatoid factor was analyzed, using Mann–Whitney, Spearman Rank Order Correlation, Multiple regression analysis. RESULTS: The most frequently identified triggers for the development of the disease and preclinical joint symptoms were the onset of menopause (17.6% and 11.7%), infections (13.4%, 15.8%), and mental stress (15.2%, 18.2%). Preclinical joint symptoms were also provoked by intense physical activity (19.8%). When the disease was provoked by an infection or the onset of menopause, an increase in the number/duration of infections (p=0.000) and body mass index (p=0.019 and p=0.024) was found compared to the control. When preclinical joint symptoms were provoked by infections or physical activity, the number/duration of annual infections exceeded those in the control (p=0,000, p=0,000 respectively). When preclinical joint symptoms was were provoked by infection (p=0.010) or by menopause onset (p=0.033), or physical activity (p=0.020), a higher Westergren's erythrocyte sedimentation rate (ESR) value was observed than that in the cases provoked by mental stress. The arthralgia score was highest in cases developed with onset of menopause compared to cases provoked by infections (p=0.053), childbirth (p=0.012). When preclinical joint symptoms were provoked by mental stress, this indicator was higher than that in cases provoked by physical exertion (p=0.002). In the preclinical group, erythrocyte sedimentation rate and C-reactive protein values depended on the body mass index (p=0.005 and p=0.028). In early rheumatoid arthritis with a high level of personal anxiety, the concentrations of antibodies to cyclic citrullinated peptides (p=0.044) and rheumatoid factor (p=0.009) were lower than that in the cases with an intermediate level of personal anxiety. CONCLUSION: Thus, the triggers studied have imprinted on the phenotypes of rheumatoid arthritis and preclinical joint symptoms.
Published Version
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