Search

Objective: Treatment guidelines for rheumatoid arthritis (RA) recommend targeting low disease activity or remission and switching therapies for patients not reaching those targets. We evaluated real‐world use of disease activity measures, treatment discontinuation, and switching patterns among patients with RA initiating a first‐line tumor necrosis factor inhibitor (TNFi). Methods: Data from adult patients with RA initiating a first‐line TNFi were collected from the American Rheumatology Network (January 2014–August 2021). The proportion of patients with recorded disease activity scores (Clinical Disease Activity Index [CDAI] or Routine Assessment of Patient Index Data 3 [RAPID3]) at TNFi initiation was assessed. Among patients with moderate or severe RA at TNFi initiation, reasons for discontinuation and subsequent advanced therapy were evaluated. Results: Among TNFi initiators (n = 15,182), 44.8% recorded a CDAI/RAPID3 score at treatment initiation; of those who did not, 47.0% had recorded a tender and/or swollen joint count or pain score. Among patients with moderate or severe RA (n = 1,651), 52% discontinued their initial TNFi during follow‐up, of which 15%, 46%, 28%, and 12% initiated the same TNFi, another TNFi, a non‐TNFi biologic, or a Janus kinase inhibitor, respectively. The proportion of patients restarting the same TNFi or initiating another TNFi varied according to TNFi discontinuation reason. Conclusion: In clinical practice, over half of patients with RA initiating a first‐line TNFi did not have baseline disease activity assessments. Many patients cycled through TNFi despite citing lack of efficacy as the most common reason for discontinuation. Consistent, objective monitoring of treatment response and timely switch to effective therapy is needed in patients with RA. [ABSTRACT FROM AUTHOR]

BACKGROUND: Biosimilars, highly similar versions of biologic agents, can offer patients equivalent efficacy at reduced costs, which could help expand medication access to more patients. Market uptake and adoption of biosimilars in the United States have been relatively slow, however. This summary aims to explore the challenges and opportunities in healthcare systemwide adoption of biosimilars based on a roundtable discussion including multistakeholder healthcare providers. OBJECTIVES: To identify barriers that contribute to slow market uptake and adoption of biosimilars in the United States and suggest strategies to mitigate such barriers. DISCUSSION: The article systematically examines factors affecting biosimilar adoption and offers insights into potential solutions and system-based strategies to facilitate the adoption and implementation of biosimilar agents in healthcare systems. Misinformation and knowledge gaps among providers and patients continue to hinder the adoption of biosimilars. External barriers related to payers' incentives, patent litigation, and Medicare policy were also identified as obstacles to the adoption of biosimilars. Strategies can be designed and implemented to overcome many of these barriers and realize the economic and societal benefits of biosimilar drugs. CONCLUSION: Overcoming key barriers to biosimilar adoption may be possible by implementing actionable system-level strategies that enable the dissemination of accurate and timely information to key stakeholders and improve organizational readiness for institutions considering biosimilar implementation. The resulting benefits would help to achieve the goals of reducing cost and thereby improving patient access while simultaneously reducing the historical barriers to broad biosimilar adoption. [ABSTRACT FROM AUTHOR]

Abstract: Elements of the innate and adaptive immune response have been implicated in the development of tissue damage after ischemic reperfusion (I/R). Here we demonstrate that T cells infiltrate the intestine of C57BL/6 mice subjected to intestinal I/R during the first hour of reperfusion. The intensity of the T cell infiltration was higher in B6.MRL/lpr mice subjected to intestinal I/R and reflected more severe tissue damage than that observed in control mice. Depletion of T cells limited I/R damage in B6.MRL/lpr mice, whereas repletion of B6.MRL/lpr lymph node-derived T cells into the I/R-resistant Rag-1−/− mouse reconstituted tissue injury. The tissue-infiltrating T cells were found to produce IL-17. Finally, IL-23 deficient mice, which are known not to produce IL-17, displayed significantly less intestinal damage when subjected to I/R. Our data assign T cells a major role in intestinal I/R damage by virtue of producing the pro-inflammatory cytokine IL-17. [Copyright &y& Elsevier]

Examines a case of an elderly woman with a mechanical mitral valve experiencing fever and chest pain. Medical history; Description of endocarditis; Types of prosthetic heart valve failure.