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Depression in Rheumatoid Arthritis and an Estimation of the Bi-directional Association of Depression and Disease Burden: A DissertationDepression is a common comorbidity in rheumatoid arthritis (RA), yet it may not be adequately recognized during routine clinical care. RA symptoms may confer a risk for depression, and vice versa; depression may affect RA disease activity and response to treatment. The study aims were to compare patient- and physician-reported depression measures, evaluate the temporal bi-directional association between RA disease activity and depressive symptomology, and assess depression as a moderator of RA treatment. Patients were identified using a national RA registry sample (Consortium of Rheumatology Researchers of North America; CORRONA). Depression prevalence and incidence rates were estimated, and concordance and disagreement using measures reported separately by patients and physicians, as well as baseline cross-sectional associations between RA disease and a history of depression. A survival analysis was conducted to temporally predict the incident onset of self-reported depressive symptoms using the different metrics of RA disease activity. Also, mixed effects models were used to assess prospective changes in RA disease activity by prevalent and incident depressive symptom status. Lastly, logistic regression models compared the likelihood of clinical response to RA treatment during follow-up in those with and without depression when starting biologic disease modifying anti-rheumatic drug (DMARD) therapy. Patient-reported depression rates were much higher and significantly different from physician based comorbidity estimates. Patient and physician RA disease activity measures were associated with an increased risk for depression onset, but not laboratory-reported serum biomarkers. Similarly, depression was temporally associated with significantly slower rates of decline regarding every patient-reported disease activity measure, some physician-reported metrics, but not acute phase reactants. Moreover, there was a significantly lower probability of achieving clinical remission among those with depression on a biologic DMARD after 6 months and an analogous effect at 12-months that was slightly lower in magnitude, which did not reach statistical significance. Rheumatologists under-reported the occurrence of prevalent and incident depressive symptoms, and thus are likely unaware of its presence in their RA patients. Further, the results suggest the bi-directional effects between these conditions are related to the cognitive and behavioral aspects of depression and their interactions with disease activity, rather than shared immunological mechanisms in the context of cell-mediated immunity. When also considering the impact on clinical response to biologic DMARDS, the findings collectively imply that rheumatologists must address any challenges due to depression to provide the best care to their patients.
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Descriptive Comparisons of the Impact of Apremilast and Methotrexate Monotherapy in Oligoarticular Psoriatic Arthritis: the Corrona Psoriatic Arthritis/Spondyloarthritis Registry ResultsOBJECTIVE: Therapeutic response was evaluated among new apremilast, methotrexate, or biologic disease-modifying anti-rheumatic drug (bDMARD) initiators with oligoarticular psoriatic arthritis (PsA). METHODS: Patients with oligoarticular PsA in the Corrona PsA/Spondyloarthritis Registry initiating treatment with apremilast, methotrexate, or bDMARD and completing 6-month follow-up were included. RESULTS: In total, 150 patients initiated monotherapy (apremilast: n=34; methotrexate: n=15; bDMARD: n=101). Apremilast initiators had higher baseline disease activity than methotrexate initiators. At follow-up, apremilast initiators experienced numerically greater disease activity improvements than methotrexate initiators and similar improvements to bDMARD initiators. CONCLUSION: Findings suggest apremilast monotherapy is an effective option for patients with oligoarticular PsA.
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Osteopontin: a bridge between bone and the immune systemThe molecular mechanisms underlying the putative role of osteopontin in the chronic inflammatory disease rheumatoid arthritis are unclear. A study in a murine model of arthritis now demonstrates that a specific antibody directed against the exposed osteopontin epitope SLAYGLR is capable of preventing inflammatory cell infiltration in arthritic joints.
