Εμφάνιση απλής εγγραφής

dc.creatorDaoussis D., Bogdanos D.P., Dimitroulas T., Sakkas L., Andonopoulos A.P.en
dc.date.accessioned2023-01-31T07:50:26Z
dc.date.available2023-01-31T07:50:26Z
dc.date.issued2020
dc.identifier10.1007/s00296-020-04659-5
dc.identifier.issn01728172
dc.identifier.urihttp://hdl.handle.net/11615/73069
dc.description.abstractTreatment of acute gout consists of non-steroidal anti-inflammatory drugs (NSAIDs), colchicine and steroids. However, the typical patient with gout has multiple comorbidities such as cardiovascular disease, hypertension, renal dysfunction or diabetes/metabolic syndrome that represent contraindications to these therapeutic options. The aim of this study is to review the available evidence regarding the use of ACTH as an alternative therapeutic option for acute gout and explore potential mechanisms of action. We performed an electronic search (MEDLINE, Scopus and Web of Science) using the keywords ACTH or adrenocorticotropic hormone combined with gout or crystal-induced arthritis. ACTH appears suitable for patients with many comorbidities due to its good safety profile. Clinical evidence shows that ACTH is at least as effective as classic agents. The mechanism of action of ACTH in gout is not entirely known. Robust experimental evidence points to the direction that ACTH does not act solely by triggering the release of endogenous steroids but also appears to downregulate inflammatory responses by activating melanocortin receptors on innate immune cells, such as macrophages. Moreover, indirect evidence indicates that ACTH may have an IL-1 antagonistic effect. We propose that ACTH may be an alternative therapeutic option for gout in patients with multiple comorbidities. Large-scale studies assessing the efficacy and safety of ACTH compared to classic therapeutic options are needed. © 2020, Springer-Verlag GmbH Germany, part of Springer Nature.en
dc.language.isoenen
dc.sourceRheumatology Internationalen
dc.source.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85088640995&doi=10.1007%2fs00296-020-04659-5&partnerID=40&md5=245b829721c1af5b3ef4aa09337f1d62
dc.subjectcorticotropinen
dc.subjectinterleukin 1en
dc.subjectmelanocortinen
dc.subjectmelanocortin receptoren
dc.subjectcorticotropinen
dc.subjecthormoneen
dc.subjectinterleukin 1en
dc.subjectantagonistic effecten
dc.subjectbiological therapyen
dc.subjectclinical studyen
dc.subjectcomorbidityen
dc.subjectdown regulationen
dc.subjectdrug efficacyen
dc.subjectdrug mechanismen
dc.subjectdrug safetyen
dc.subjectevidence based medicineen
dc.subjectgouten
dc.subjecthumanen
dc.subjectimmunocompetent cellen
dc.subjectmacrophageen
dc.subjectMedlineen
dc.subjectnonhumanen
dc.subjectpriority journalen
dc.subjectReviewen
dc.subjectScopusen
dc.subjectsignal transductionen
dc.subjectsystematic reviewen
dc.subjectWeb of Scienceen
dc.subjectanimalen
dc.subjectbiological therapyen
dc.subjectdrug effecten
dc.subjectgouten
dc.subjectmouseen
dc.subjectproceduresen
dc.subjectAdrenocorticotropic Hormoneen
dc.subjectAnimalsen
dc.subjectArthritis, Goutyen
dc.subjectBiological Therapyen
dc.subjectHormonesen
dc.subjectHumansen
dc.subjectInterleukin-1en
dc.subjectMacrophagesen
dc.subjectMiceen
dc.subjectSpringer Science and Business Media Deutschland GmbHen
dc.titleAdrenocorticotropic hormone: an effective “natural” biologic therapy for acute gout?en
dc.typeotheren


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