Advances in Rheumatology最新文献

{"title":"Integrated safety analysis of tofacitinib from Phase 2 and 3 trials of patients with ankylosing spondylitis.","authors":"Atul Deodhar, Servet Akar, Jeffrey R Curtis, Bassel El-Zorkany, Marina Magrey, Cunshan Wang, Joseph Wu, Solomon B Makgoeng, Ivana Vranic, Sujatha Menon, Dona L Fleishaker, Annette M Diehl, Lara Fallon, Arne Yndestad, Robert B M Landewé","doi":"10.1186/s42358-024-00402-x","DOIUrl":"https://doi.org/10.1186/s42358-024-00402-x","url":null,"abstract":"<p><strong>Objectives: </strong>Describe tofacitinib safety from an integrated analysis of randomized controlled trials (RCTs) in patients with ankylosing spondylitis (AS).</p><p><strong>Method: </strong>Pooled data from Phase 2 (NCT01786668; 04/2013-03/2015)/Phase 3 (NCT03502616; 06/2018-08/2020) RCTs in AS patients were analyzed (3 overlapping cohorts): 16-week placebo-controlled (tofacitinib 5 mg twice daily [BID] [n = 185]; placebo [n = 187]); 48-week only-tofacitinib 5 mg BID (n = 316); 48-week all-tofacitinib (≥ 1 dose of tofacitinib 2, 5, or 10 mg BID; n = 420). Baseline 10-year atherosclerotic cardiovascular disease (ASCVD) risk was determined in patients without history of ASCVD (48-week cohorts). Adverse events (AEs)/AEs of special interest were evaluated/compared with findings from other tofacitinib programs (16 Phase 2/Phase 3 rheumatoid arthritis [RA]; 2 Phase 3 psoriatic arthritis [PsA] RCTs) and a real-world cohort of AS patients initiating biologic disease-modifying antirheumatic drugs (US MarketScan).</p><p><strong>Results: </strong>Most patients (> 75%; 48-week cohorts) without history of ASCVD had low baseline 10-year ASCVD risk. One patient (tofacitinib 5 mg BID; in all 3 cohorts) had a serious infection (aseptic meningitis). Herpes zoster (non-serious) occurred in the 48-week only-tofacitinib 5 mg BID (n = 5 [1.6%]) and all-tofacitinib (n = 7 [1.7%]; one multi-dermatomal [tofacitinib 10 mg BID]) cohorts. No deaths, opportunistic infections, tuberculosis, malignancies, major adverse cardiovascular events, thromboembolic events, gastrointestinal perforations occurred.</p><p><strong>Limitations: </strong>short RCT durations/low patient numbers within cohorts.</p><p><strong>Conclusion: </strong>Tofacitinib 5 mg BID was well tolerated to 48 weeks in AS patients; safety profile was consistent with RA/PsA clinical programs and a cohort of AS patients from US routine clinical practice.</p><p><strong>Clinical trial registration numbers: </strong>NCT01786668 (2013-02-06); NCT03502616 (2018-04-11).</p>","PeriodicalId":48634,"journal":{"name":"Advances in Rheumatology","volume":"64 1","pages":"87"},"PeriodicalIF":2.0,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142856204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fibromyalgia comorbidity in Systemic Lupus Erythematosus patients: assessing impact on quality of life.","authors":"Jade A M Monteiro, Alexia L H Gama, Joao C S Oliveira, Matheus V Falcao, Ana Karla G Melo, Danielle C S Egypto, Alessandra S Braz","doi":"10.1186/s42358-024-00432-5","DOIUrl":"https://doi.org/10.1186/s42358-024-00432-5","url":null,"abstract":"<p><strong>Introduction: </strong>The prevalence of Fibromyalgia in patients with Systemic Lupus Erythematosus (SLE) is significantly higher compared to the general population. Despite this frequent association, Fibromyalgia remains underdiagnosed and consequently inadequately treated, negatively affecting the quality of life of these patients.</p><p><strong>Objective: </strong>This study aims to evaluate the occurrence of Fibromyalgia and its impact on the quality of life of Brazilian patients with SLE treated at a University Hospital in the state of Paraiba.</p><p><strong>Materials and methods: </strong>This descriptive, observational, and cross-sectional study included patients with SLE diagnosed according to the 2012 criteria of the Systemic Lupus Erythematosus International Collaborating Clinics (SLICC). The occurrence of Fibromyalgia was assessed using the American College of Rheumatology (ACR) criteria of 1990 and 2010/2011, revised in 2016. Quality of life was evaluated using the Short-Form 36 (SF-36) questionnaire for all patients, while the Fibromyalgia Impact Questionnaire (FIQ) was applied to those diagnosed with Fibromyalgia.</p><p><strong>Results: </strong>The sample comprised 107 SLE patients, with an average age of 54.1 years (SD:12.1), of whom 95.4% (102) were women. The prevalence of Fibromyalgia among SLE patients was 19.1% (21), all of whom were women with a mean age of 45.6 years (SD 9.6). The SF-36 scores of SLE patients with Fibromyalgia were consistently lower across all eight domains compared to those without Fibromyalgia, indicating a significant negative impact of this comorbidity.</p><p><strong>Conclusion: </strong>These findings are consistent with existing literature, highlighting the significant negative impact of Fibromyalgia on the quality of life of patients with SLE.</p><p><strong>Conclusion: </strong>These findings are consistent with existing literature, highlighting the significant negative impact of Fibromyalgia on the quality of life of patients with SLE.</p>","PeriodicalId":48634,"journal":{"name":"Advances in Rheumatology","volume":"64 1","pages":"90"},"PeriodicalIF":2.0,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142856246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hck promotes IL-1β-induced extracellular matrix degradation, inflammation, and apoptosis in osteoarthritis via activation of the JAK-STAT3 signaling pathway.","authors":"Zhenzhong Yan, Lin Ji","doi":"10.1186/s42358-024-00427-2","DOIUrl":"https://doi.org/10.1186/s42358-024-00427-2","url":null,"abstract":"<p><p>We investigated role of haematopoietic cell kinase (Hck) in osteoarthritis (OA) and to explore the underlying mechanisms driving its effects. An OA animal model was established and after OA induction, rats received intra-articular injections of lentivirus twice a week for four weeks. Rats were divided into four groups: control (healthy rats without OA), OA model (rats with induced OA), OA + Len-si-NC (OA rats treated with a non-targeting control lentivirus), and OA + Len-si-Hck (OA rats treated with lentivirus targeting Hck). Blood samples were collected, and serum cytokine levels were measured using ELISA. Afterward, the rats were sacrificed for histological analysis and TUNEL assay. In vitro, IL-1β-treated human chondrocytes were transfected with Hck, and the effects on cell viability, apoptosis, ECM degradation, and JAK-STAT3 signaling were assessed. Colivelin, a JAK-STAT3 agonist, was used to confirm the pathway's involvement. Results indicated increased Hck expression in the cartilage tissues of OA rats and in IL-1β-stimulated chondrocytes. Silencing Hck in vivo reduced IL-6 and TNF-α levels, apoptosis, and preserved cartilage structure. In vitro, Hck knockdown in IL-1β-treated chondrocytes resulted in enhanced cell viability, reduced apoptosis, and decreased ECM degradation. Notably, the expression of MMP3 and MMP13 was significantly lowered, while collagen II and aggrecan levels were restored. Additionally, Hck knockdown inhibited JAK-STAT3 activation, which was evident from reduced levels of phosphorylated JAK1 and STAT3. The addition of colivelin reversed these effects, confirming that Hck mediates its effects through the JAK-STAT3 pathway. Overall, our findings indicate that Hck is critical in OA progression by promoting inflammation, apoptosis, and ECM degradation through the JAK-STAT3 signaling pathway activation.</p>","PeriodicalId":48634,"journal":{"name":"Advances in Rheumatology","volume":"64 1","pages":"88"},"PeriodicalIF":2.0,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142856267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating the causal relationship between immune factors and ankylosing spondylitis: insights from a Mendelian Randomization study.","authors":"Ziming Geng, Yang Tong, Yang Chen, Jian Wang, Ziwen Liu, Jun Miao, Ruihua Li","doi":"10.1186/s42358-024-00428-1","DOIUrl":"https://doi.org/10.1186/s42358-024-00428-1","url":null,"abstract":"<p><strong>Background: </strong>Despite previous studies indicating a close relationship between immune system and ankylosing spondylitis (AS), the causal relationship between them remains unclear.</p><p><strong>Methods: </strong>Genome-wide association data were utilized to explore the causal link between 731 immune cells and AS using a bidirectional two-sample MR approach. The data included immune cell data from Orrù et al.'s study and AS data from the FinnGen consortium. Cochran's Q test and leave-one-out checked instrument variable (IV) heterogeneity. IVW was the primary method for causal analysis, with MR-Egger and MR-PRESSO addressing horizontal pleiotropy. FDR correction was applied to both analysis directions to rectify multiple testing errors.</p><p><strong>Results: </strong>In our study, 22 immune phenotypes out of 731 were casually linked to AS. After excluding 5 less robust features, 17 immune factors remained, with 4 being protective and the rest posing risks. Through FDR correction, we found a significant causal relationship between HLA DR on CD14- CD16+ monocyte and AS (OR (95%CI) = 0.70(0.60 ~ 0.83), P = 2.06*10^-5). In the reverse analysis with AS as exposure, potential effects on 34 immune features were discovered. After correction, we confirmed significant causal relationships between AS and two immune features, namely CD20- B cell %lymphocyte (OR (95%CI) = 1.16(1.08-1.25), P = 1.91*10^-5) and CD20- B cell %B cell (OR (95%CI) = 1.17(1.09-1.26), P = 1.50*10^-5).</p><p><strong>Conclusions: </strong>Our study identified various features associated with AS in different types of immune cells. These findings provide important clues and a theoretical basis for further understanding the pathogenesis of AS, guiding clinical treatment, and drug design.</p>","PeriodicalId":48634,"journal":{"name":"Advances in Rheumatology","volume":"64 1","pages":"89"},"PeriodicalIF":2.0,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142856295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of type 2 ryanodine receptor stabilisation in autoimmune cell modulation.","authors":"Takashi Nawata, Takeshi Honda, Akihiko Sakamoto, Hitoshi Uchinoumi, Takeshi Suetomi, Yoshihide Nakamura, Shunya Tsuji, Hiroki Sakai, Shigeki Kobayashi, Takeshi Yamamoto, Masataka Asagiri, Motoaki Sano, Masafumi Yano","doi":"10.1186/s42358-024-00426-3","DOIUrl":"https://doi.org/10.1186/s42358-024-00426-3","url":null,"abstract":"","PeriodicalId":48634,"journal":{"name":"Advances in Rheumatology","volume":"64 1","pages":"86"},"PeriodicalIF":2.0,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142693774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Treatment with tofacitinib attenuates muscle loss through myogenin activation in the collagen-induced arthritis.","authors":"Thales Hein da Rosa, Bárbara Jonson Bartikoski, Rafaela Cavalheiro do Espírito Santo, Mirian Farinon, Jordana Miranda de Souza Silva, Renata Ternus Pedó, Maria Luísa Gasparini, Thais Karnopp, Leonardo Peterson Dos Santos, Gustavo Chapacais, Andressa di Domenico, Sofia Loch, Ricardo Machado Xavier","doi":"10.1186/s42358-024-00416-5","DOIUrl":"https://doi.org/10.1186/s42358-024-00416-5","url":null,"abstract":"<p><strong>Background: </strong>Sarcopenia is a muscle disease characterized by reduction of muscle strength and muscle mass. In RA, 25.9 to 43.3% of the patients present sarcopenia. The loss of muscle mass observed in RA patients occurs either by activation of catabolic pathways or by inhibition of anabolic pathways. Despite having a list of drugs capable of treating RA inflammation, their effect on muscle is unclear. Our objective was to evaluate the tofacitinib effect on the muscle mass of collagen-induced arthritis (CIA) mice.</p><p><strong>Methods: </strong>CIA was induced in male DBA/1J mice by subcutaneous injection of Type 2 Collagen plus Freund Adjuvant. Animals were randomized into 3 groups: CIA + tofacitinib; CIA + vehicle; and healthy controls. Treatment was administered twice a day, between days 18 and 45 after induction. Clinical score, edema, and body weight were evaluated during the experimental period. After euthanasia, tibiotarsal joints were collected for assessment of disease histopathological score, and tibialis anterior (TA) and gastrocnemius (GA) muscles were weighed to assess muscle mass. Muscle atrophy was evaluated by measurement of TA myofiber cross-sectional area (CSA). Protein expression was evaluated by western blot using GA homogenates. Serum inflammatory markers were evaluated by ELISA. Statistical analysis included ANOVA followed by Tukey's or with Kruskal-Wallis. The statistical difference was assumed for p < 0.05.</p><p><strong>Results: </strong>Tofacitinib treatment decreased arthritis severity by reducing clinical score, and hind paw edema in comparison with the vehicle group. Tofacitinib showed weight gain, higher TA and GA weights, and increased CSA compared to the vehicle group. On day 45, Tofacitinib presented increased muscle strength compared to the vehicle group, however, no difference was found in muscle fatigue. Pax7 expression was unchanged, while MyoD expression showed an increasing trend, and myogenin expression was significantly increased in Tofacitinib compared to vehicle and control groups. The treatment didn't modify Murf-1 expression. Tofacitinib mice showed decreased serum levels of TNF and increased IL-6 serum levels.</p><p><strong>Conclusion: </strong>Tofacitinib attenuated muscle loss in arthritic mice, increased muscle weight and muscle CSA. Activation of satellite cell regeneration, based on the increased expression of myogenin, is a potential mechanism involved in tofacitinib action against muscle loss.</p>","PeriodicalId":48634,"journal":{"name":"Advances in Rheumatology","volume":"64 1","pages":"85"},"PeriodicalIF":2.0,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142630682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Takayasu's arteritis associated with tuberculosis: a retrospective study.","authors":"Ana Luisa Souza Pedreira, Maria de Lourdes Castro de Oliveira Figueiroa, Mariana Oliveira Miranda, Alisson Regis de Santana, Victor Pereira Mattos, Adriane Sousa da Paz, Camila Cendon Duran, Mittermayer Barreto Santiago","doi":"10.1186/s42358-024-00424-5","DOIUrl":"https://doi.org/10.1186/s42358-024-00424-5","url":null,"abstract":"<p><strong>Background: </strong>Takayasu arteritis (TA) and tuberculosis (TB) share similar histopathological and immunological characteristics. Studies comparing patients with TA with or without active or latent TB infection (LTBI) have revealed some differences in clinical and angiographic profiles. Patient with TA and history of TB exhibited more constitutional symptoms and structural damage to the aorta. This study compared the clinical and radiological features of patients with TA with and without active TB or LTBI.</p><p><strong>Methods: </strong>We retrospectively analyzed the data of patients with TA at a public tertiary referral outpatient clinic in northeast Brazil from January 2017 to June 2022. Comparisons of clinical features were made according to the presence of TB.</p><p><strong>Results: </strong>Fifty patients met the eligibility criteria, and a association with TB was identified in 20 (40%) patients (active TB in six and LTBI in 14). There was a predominance of females, and the average age of patients was 40 years. Weight loss was more common in patients with TA and TB (p = 0.005). No significant intergroup differences were noted in terms of comorbidities, medications, erythrocyte sedimentation rates, or C-reactive protein levels. Significant differences were found in abdominal aortic involvement (25% of patients with TA and TB vs. 11.4% in subjects with TA without TB; p = 0.013). Dilations and aneurysms were significantly more common in patients with TA and TB (p = 0.009 and p = 0.027, respectively).</p><p><strong>Conclusion: </strong>Patients with TA and TB have a higher prevalence of dilatation and aneurysms, most commonly in the abdominal aorta.</p>","PeriodicalId":48634,"journal":{"name":"Advances in Rheumatology","volume":"64 1","pages":"84"},"PeriodicalIF":2.0,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142630662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of the causal relationship between immune cells and rheumatoid arthritis from the perspective of genetic variation: a bidirectional two-sample Mendelian randomization study.","authors":"Feng Cheng, YingJia Zhu, XiaoQian Liu, RuiKun Zhang, Fei Xia, LinPu Ge","doi":"10.1186/s42358-024-00425-4","DOIUrl":"https://doi.org/10.1186/s42358-024-00425-4","url":null,"abstract":"<p><strong>Background: </strong>Immune factors are crucial in the pathogenesis of rheumatoid arthritis (RA), and immune cells play a key role in the development of RA. However, there is still disagreement regarding the specific roles of each type of immune cell in the pathological process of RA.</p><p><strong>Methods: </strong>This study used bidirectional two-sample Mendelian randomization (MR) analysis to determine the causal relationship between immune cell characteristics and RA. Utilizing publicly available genetic data, we initially treated immune cell characteristics as exposures to investigate their causal effects on the risk of RA. Subsequently, we performed reverse two-sample MR using the positively selected cells from the initial analysis as outcomes, aiming to identify the core immune cells involved. Finally, a comprehensive sensitivity analysis was conducted to validate the robustness, heterogeneity, and horizontal pleiotropy of the results.</p><p><strong>Results: </strong>Using data from 731 immune cells as exposures and cell SNPs as instruments, we independently conducted two-sample MR analysis for each patient with RA. The main analytical method used was the IVW method, with a significance level set at P < 0.05 for inclusion. In total, we identified 42 immune cell phenotypes that were causally associated with the onset of RA. For the reverse MR analysis, we used RA as the exposure factor and focused on 42 immune cell phenotypes as outcomes. Our analysis revealed causal relationships between the onset of RA and 7 immune cell phenotypes. Among these, 6 showed positive causal relationships, while 1 exhibited a negative causal relationship.</p><p><strong>Conclusions: </strong>Our study emphasized the causal relationship between immune cells and RA through bidirectional two-sample MR analysis, identifying the immune cells causally associated with RA.</p>","PeriodicalId":48634,"journal":{"name":"Advances in Rheumatology","volume":"64 1","pages":"83"},"PeriodicalIF":2.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142564918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: II Brazilian Society of Rheumatology consensus for lupus nephritis diagnosis and treatment.","authors":"Edgard Torres Dos Reis-Neto, Luciana Parente Costa Seguro, Emília Inoue Sato, Eduardo Ferreira Borba, Evandro Mendes Klumb, Lilian Tereza Lavras Costallat, Marta Maria das Chagas Medeiros, Eloisa Bonfá, Nafice Costa Araújo, Simone Appenzeller, Ana Carolina de Oliveira E Silva Montandon, Emily Figueiredo Neves Yuki, Roberto Cordeiro de Andrade Teixeira, Rosa Weiss Telles, Danielle Christinne Soares do Egypto, Francinne Machado Ribeiro, Andrese Aline Gasparin, Antonio Silaide de Araujo Junior, Cláudia Lopes Santoro Neiva, Debora Cerqueira Calderaro, Odirlei Andre Monticielo","doi":"10.1186/s42358-024-00423-6","DOIUrl":"https://doi.org/10.1186/s42358-024-00423-6","url":null,"abstract":"","PeriodicalId":48634,"journal":{"name":"Advances in Rheumatology","volume":"64 1","pages":"82"},"PeriodicalIF":2.0,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142548384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A functional exercise program improves pain and health related quality of life in patients with fibromyalgia: a randomized controlled trial.","authors":"Giovana Fernandes, Michele Nery, Sandra Mara Meireles, Rebeka Santos, Jamil Natour, Fabio Jennings","doi":"10.1186/s42358-024-00422-7","DOIUrl":"10.1186/s42358-024-00422-7","url":null,"abstract":"<p><strong>Background/objective: </strong>Fibromyalgia is a non-inflammatory syndrome characterized by generalized muscle pain, with other symptoms. Numerous forms of physical training for this population have been studied through high-quality randomized clinical trials involving strength, flexibility, aerobic conditioning and multicomponent exercise interventions. This research evaluated the effectiveness of a functional exercise program at reducing pain, improving functional capacity, increasing muscle strength as well as improving flexibility, balance and quality of life in individuals with fibromyalgia.</p><p><strong>Methods: </strong>Eighty-two women with fibromyalgia were randomized into two groups. The functional exercise group performed functional exercises in 45-minute sessions twice per week for 14 weeks. The stretching exercise group performed flexibility exercises with the same duration and frequency. Outcome measures were: visual analog scale for widespread pain; Fibromyalgia Impact Questionnaire for health-related quality of life; Timed Up and Go test for functional performance; one-repetition maximum for muscle strength, Sit and Reach test on Wells bench for flexibility; Berg Balance Scale for balance; SF-36 for general quality of life.</p><p><strong>Results: </strong>After the intervention, the functional exercise group had a statistically significant reduction in pain (interaction p = 0.002), and improvement in health-related quality of life measured by the Fibromyalgia Impact Questionnaire (interaction p < 0.001) and in general health state domain of SF-36 (interaction p = 0.043) compared to the stretching exercise group. No significant differences between groups were found regarding improvements in functional capacity, muscle strength, flexibility or balance.</p><p><strong>Conclusion: </strong>Functional exercise training was effective at reducing pain and improving quality of life in patients with fibromyalgia compared to stretching exercises.</p><p><strong>Trial registration: </strong>ClinicalTrials.gov Identifier: NCT03682588 First prospectively registered in March 2018.</p>","PeriodicalId":48634,"journal":{"name":"Advances in Rheumatology","volume":"64 1","pages":"81"},"PeriodicalIF":4.6,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142510984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}