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dc.contributor.authorUpchurch, Katherine S.
dc.contributor.authorKay, Jonathan
dc.date2022-08-11T08:10:51.000
dc.date.accessioned2022-08-23T17:22:20Z
dc.date.available2022-08-23T17:22:20Z
dc.date.issued2012-12-01
dc.date.submitted2015-04-17
dc.identifier.citationRheumatology (Oxford). 2012 Dec;51 Suppl 6:vi28-36. doi: 10.1093/rheumatology/kes278. <a href="http://dx.doi.org/10.1093/rheumatology/kes278">Link to article on publisher's site</a>
dc.identifier.issn1462-0324 (Linking)
dc.identifier.doi10.1093/rheumatology/kes278
dc.identifier.pmid23221584
dc.identifier.urihttp://hdl.handle.net/20.500.14038/48724
dc.description.abstractTreatment for RA has changed profoundly over the past 25 years, evolving from a strategy of providing symptomatic relief, to implementation of therapeutic regimens that impact disease activity and ultimately have been shown to slow or arrest structural joint damage. Drug therapy for RA has evolved from salicylates, to NSAIDs, CSs, DMARDs, MTX, and finally to biologic response modifiers. MTX has become the initial drug of choice in most patients with RA, and some do well on MTX monotherapy without the addition of other agents. Combination regimens including MTX and other conventional DMARDs may be an effective early approach to treatment of RA. The biologic response modifiers (biologics) became available in the late 1990s, based on our understanding of the molecular mediators of synovial inflammation in RA. The first biologics inhibited TNF-alpha, a cytokine active in host defences against some infections and malignancies, but which also promotes inflammation and bone erosion. Inhibitors of TNF-alpha are mostly given with MTX, although some can be given as monotherapy. Studies consistently show that combination MTX + TNF-alpha inhibitor therapy leads to better outcomes than with either agent alone. Tight control strategies, employing objective measures, also lead to improved outcomes. When patients fail treatment with one or more TNF-alpha inhibitor + MTX, a number of other possible alternatives may be tried, including treatment with biologics having other mechanisms, such as antibodies to certain ILs, other cytokines and inflammatory mediators. Current therapy for RA is such that progression from symptom onset to significant disability is now no longer inevitable, and RA patients can anticipate comfortable and productive lives on medical therapy.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=23221584&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1093/rheumatology/kes278
dc.subjectAnti-Inflammatory Agents, Non-Steroidal
dc.subjectAntirheumatic Agents
dc.subjectArthritis, Rheumatoid
dc.subject*Biological Therapy
dc.subjectDisability Evaluation
dc.subjectDisease Progression
dc.subjectHumans
dc.subjectMethotrexate
dc.subjectTreatment Outcome
dc.subjectMusculoskeletal Diseases
dc.subjectRheumatology
dc.subjectSkin and Connective Tissue Diseases
dc.titleEvolution of treatment for rheumatoid arthritis
dc.typeJournal Article
dc.source.journaltitleRheumatology (Oxford, England)
dc.source.volume51 Suppl 6
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/rheumatology_pubs/122
dc.identifier.contextkey7002951
html.description.abstract<p>Treatment for RA has changed profoundly over the past 25 years, evolving from a strategy of providing symptomatic relief, to implementation of therapeutic regimens that impact disease activity and ultimately have been shown to slow or arrest structural joint damage. Drug therapy for RA has evolved from salicylates, to NSAIDs, CSs, DMARDs, MTX, and finally to biologic response modifiers. MTX has become the initial drug of choice in most patients with RA, and some do well on MTX monotherapy without the addition of other agents. Combination regimens including MTX and other conventional DMARDs may be an effective early approach to treatment of RA. The biologic response modifiers (biologics) became available in the late 1990s, based on our understanding of the molecular mediators of synovial inflammation in RA. The first biologics inhibited TNF-alpha, a cytokine active in host defences against some infections and malignancies, but which also promotes inflammation and bone erosion. Inhibitors of TNF-alpha are mostly given with MTX, although some can be given as monotherapy. Studies consistently show that combination MTX + TNF-alpha inhibitor therapy leads to better outcomes than with either agent alone. Tight control strategies, employing objective measures, also lead to improved outcomes. When patients fail treatment with one or more TNF-alpha inhibitor + MTX, a number of other possible alternatives may be tried, including treatment with biologics having other mechanisms, such as antibodies to certain ILs, other cytokines and inflammatory mediators. Current therapy for RA is such that progression from symptom onset to significant disability is now no longer inevitable, and RA patients can anticipate comfortable and productive lives on medical therapy.</p>
dc.identifier.submissionpathrheumatology_pubs/122
dc.contributor.departmentDepartment of Medicine, Division of Rheumatology
dc.source.pagesvi28-36


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