Longitudinal monitor of Jun N-terminal kinase pathway associated phosphatase reflects clinical efficacy to triple conventional disease-modifying anti-rheumatic drugs treatment in rheumatoid arthritis patients

INFLAMMOPHARMACOLOGY(2021)

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摘要
Objective This study aimed to investigate the correlation of Jun N-terminal kinase pathway associated phosphatase (JKAP) with inflammation, disease activity, and clinical efficacy to triple conventional disease-modifying anti-rheumatic drugs (cDMARDs) in rheumatoid arthritis (RA) patients. Methods A total of 119 active RA patients about to receive triple cDMARDs treatment were enrolled. Serum JKAP was detected by enzyme-linked immunosorbent assay at week0, week6, week12, and week24 (W24). According to clinical response status or remission status at W24, RA patients were classified as response patients and non-response patients, or remission patients and non-remission patients, respectively. Results JKAP was negatively correlated with erythrocyte sedimentation rate (ESR), C-reactive protein, and 28-joints disease activity score based on ESR (DAS28 score (ESR)), while JKAP was not correlated with disease duration, tender joint count, swollen joint count, health assessment questionnaire for rheumatoid arthritis or treatment history. Furthermore, during 24-week triple cDMARDs treatment, JKAP was increased overtime. Subgroup analyses showed that JKAP displayed a rising trend in response patients, remission patients, non-remission patients but not non-response patients, meanwhile its increment was more obvious in remission patients versus non-remission patients. Additionally, JKAP at W24 was higher in response patients compared with non-response patients, and JKAP at W12 and W24 was higher in remission patients compared with non-remission patients. Conclusion Longitudinal monitor of JKAP might reflect clinical efficacy to the treatment of triple cDMARDs, which could improve outcomes in RA patients.
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关键词
Rheumatoid arthritis, Jun N-terminal kinase pathway associated phosphatase, Conventional disease-modifying anti-rheumatic drugs, Clinical response, Clinical remission
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