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dc.contributor.authorLarreta Carrera, Enara
dc.contributor.authorIgartua Olaechea, Manuela ORCID
dc.contributor.authorHernández Martín, Rosa María ORCID
dc.contributor.authorSantos Vizcaíno, Edorta ORCID
dc.date.accessioned2025-02-07T16:03:22Z
dc.date.available2025-02-07T16:03:22Z
dc.date.issued2024
dc.identifier.citationEkaia 46 : 205-225 (2024)
dc.identifier.issn0214-9001
dc.identifier.urihttp://hdl.handle.net/10810/72394
dc.description.abstractRheumatoid arthritis (RA) is a chronic autoimmune disease that affects the synovial membrane. It causes the destruction of both cartilage and bone, leading to rigidity, inflammation, or loss of joint function, which results in a decrease in the patient’s quality of life, resulting in disability. Over the years, numerous research studies have been conducted on the treatment of RA, and currently, in addition to symptom relief, there have been advancements in modifying the progression of the disease through medications such as disease-modifying antirheumatic drugs (DMARDs). In this regard, adalimumab, a biologic DMARD, is a monoclonal antibody that targets tumor necrosis factor α (TNFα). As mentioned, promising results have been presented in controlling the development of this disease. In order to understand the reasons for this success, the characteristics of RA, the indication of adalimumab, its mechanism of action, and data regarding its bio-pharmaceutical parameters have been emphasized. However, it has been 20 years since adalimumab was introduced to the market, and therefore, collecting updated data is essential to evaluate its long-term effectiveness and safety. For this purpose, various studies conducted in recent years have been collected and the true potential of adalimumab has been examined. In conclusion, the research process is still ongoing to obtain a treatment that will achieve the recovery of RA. In the meantime, adalimumab has managed to somewhat control the disease and continue to improve the quality of life of patients.; Artritis erreumatoidea (rheumatoid arthritis, RA) mintz sinobialaren hantura kronikoa eragiten duen gaixotasun autoimmunea da. Kartilagoaren zein hezurraren suntsipena eragiten du; ondorioz, zurruntasuna, hantura edo artikulazioen funtzioaren galera gertatzen dira, eta horrek gaixoaren bizi-kalitatea murriztea dakar, ezgaitasuna eraginez. Urteetan zehar RAren tratamenduaren inguruko ikerketa ugari egin dira, eta egun, sintomak arintzeaz gain, gaixotasunaren bilakaera moteltzea ere lortu da gaixotasun erreumatikoaren garapena modulatzen duten farmakoei (disease modifying anti-rheumatic drugs, DMARD) esker. Ildo horretan, adalimumab DMARD biologikoa da, gaitasun immunomodulatzailea duen α tumorearen nekrosi-faktorearen (tumor necrosis factor a, TNFα) aurkako antigorputz monoklonala. Adalimumabekin emaitza itxaropentsuak lortu dira gaixotasun horren garapenaren kontrolean. Arrakasta horren zergatia ulertzeko asmoz, RAren ezaugarriak eta adalimumaben indikazioa, ekintza-mekanismoa eta bere parametro biofarmazeutikoen inguruko datuak aurkeztu dira. Hala ere, 20 urte igaro dira adalimumab merkaturatu zenetik, eta, beraz, datu eguneratuen bilketa egitea garrantzitsua da epe luzera erakutsi duen eraginkortasuna eta segurtasuna ebaluatzeko. Horretarako, azken urteotako saiakuntza eta ikerketa ezberdinak bildu dira, eta adalimumaben helmena benetan nolakoa den aztertu da. Amaitzeko, esan ikerketa-prozesu luzea geratzen dela RA sendatzea lortuko duen tratamendua eskuratzeko. Bitarte horretan, adalimumabek gaixotasuna nolabait kontrolpean izatea lortu du, eta gaixoen bizi-kalitatea hobetzen jarraituko du.
dc.language.isoeus
dc.publisherServicio Editorial de la Universidad del País Vasco/Euskal Herriko Unibertsitatearen Argitalpen Zerbitzua
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/
dc.titleAdalimumab artritis erreumatoidearen tratamendurako: Azken urteetako ikasketak
dc.typeinfo:eu-repo/semantics/article
dc.rights.holder© 2024 UPV/EHU Attribution-NonCommercial-ShareAlike 4.0 International
dc.identifier.doi10.1387/ekaia.24989


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© 2024 UPV/EHU Attribution-NonCommercial-ShareAlike 4.0 International
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