Y. Kashiwado, C. Kiyohara, Y. Kimoto, S. Nagano, T. Sawabe, K. Oryoji, S. Mizuki, H. Nishizaka, S. Yoshizawa, S. Yoshizawa, T. Tsuru, Y. Inoue, N. Ueda, Shun-ichiro Ota, Y. Suenaga, T. Miyamura, Y. Tada, H. Niiro, Koichiro Akashi, T. Horiuchi
{"title":"Clinical course of patients with rheumatoid arthritis who continue or discontinue biologic therapy after hospitalization for infection: a retrospective observational study","authors":"Y. Kashiwado, C. Kiyohara, Y. Kimoto, S. Nagano, T. Sawabe, K. Oryoji, S. Mizuki, H. Nishizaka, S. Yoshizawa, S. Yoshizawa, T. Tsuru, Y. Inoue, N. Ueda, Shun-ichiro Ota, Y. Suenaga, T. Miyamura, Y. Tada, H. Niiro, Koichiro Akashi, T. Horiuchi","doi":"10.1186/s13075-022-02820-y","DOIUrl":"https://doi.org/10.1186/s13075-022-02820-y","url":null,"abstract":"","PeriodicalId":51225,"journal":{"name":"Arthritis Research & Therapy","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2021-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43473228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tsuneyasu Yoshida, H. Yoshifuji, M. Shirakashi, A. Nakakura, K. Murakami, K. Kitagori, S. Akizuki, R. Nakashima, K. Ohmura, A. Morinobu
{"title":"Risk factors for the recurrence of relapsing polychondritis","authors":"Tsuneyasu Yoshida, H. Yoshifuji, M. Shirakashi, A. Nakakura, K. Murakami, K. Kitagori, S. Akizuki, R. Nakashima, K. Ohmura, A. Morinobu","doi":"10.1186/s13075-022-02810-0","DOIUrl":"https://doi.org/10.1186/s13075-022-02810-0","url":null,"abstract":"","PeriodicalId":51225,"journal":{"name":"Arthritis Research & Therapy","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2021-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48226812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hui-hui Li, Lintao Sai, Yuan Liu, Colman Freel, Kai Wang, Chi Zhou, Jing Zheng, Q. Shu, Ying-jie Zhao
{"title":"Systemic lupus erythematosus dysregulates the expression of long noncoding RNAs in placentas","authors":"Hui-hui Li, Lintao Sai, Yuan Liu, Colman Freel, Kai Wang, Chi Zhou, Jing Zheng, Q. Shu, Ying-jie Zhao","doi":"10.1186/s13075-022-02825-7","DOIUrl":"https://doi.org/10.1186/s13075-022-02825-7","url":null,"abstract":"","PeriodicalId":51225,"journal":{"name":"Arthritis Research & Therapy","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2021-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43902347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anne Gigout, Donata Harazin, Louise M Topping, Didier Merciris, Sven Lindemann, Christian Brenneis, Ahuva Nissim
{"title":"Early detection of osteoarthritis in the rat with an antibody specific to type II collagen modified by reactive oxygen species.","authors":"Anne Gigout, Donata Harazin, Louise M Topping, Didier Merciris, Sven Lindemann, Christian Brenneis, Ahuva Nissim","doi":"10.1186/s13075-021-02502-1","DOIUrl":"10.1186/s13075-021-02502-1","url":null,"abstract":"<p><strong>Background: </strong>Osteoarthritis (OA) is a disease of the whole joint, with articular cartilage breakdown as a major characteristic. Inflammatory mediators, proteases, and oxidants produced by chondrocytes are known to be responsible for driving cartilage degradation. Nevertheless, the early pathogenic events are still unclear. To investigate this, we employed an antibody that is specific to oxidative post-translationally modified collagen type II (anti-oxPTM-CII) to detect early cartilage pathogenic changes in two rat models of OA.</p><p><strong>Methods: </strong>The animals underwent surgery for destabilization of the medial meniscus (DMM) and were sacrificed after 3, 5, 7, 14, and 28 days. Alternatively, anterior cruciate ligament transection with partial meniscectomy (ACLT+pMx) was performed and animals were sacrificed after 1, 3, 5, 7, and 14 days. Joints were stained with toluidine blue and saffron du Gatinais for histological scoring, anti-oxPTM-CII, and anti-collagen type X antibodies (anti-CX).</p><p><strong>Results: </strong>We observed positive oxPTM-CII staining as early as 1 or 3 days after ACLT+pMx or DMM surgeries, respectively, before overt cartilage lesions were visible. oxPTM-CII was located mostly in the deep zone of the medial tibial cartilage, in the pericellular and territorial matrix of hypertrophic chondrocytes, and co-localized with CX staining. Staining was weak or absent for the lateral compartment or the contralateral knees except at later time points.</p><p><strong>Conclusion: </strong>The results demonstrate that oxidant production and chondrocyte hypertrophy occur very early in the onset of OA, possibly initiating the pathogenic events of OA. We propose to use anti-oxPTM-CII as an early biomarker for OA ahead of radiographic changes.</p>","PeriodicalId":51225,"journal":{"name":"Arthritis Research & Therapy","volume":"23 1","pages":"113"},"PeriodicalIF":4.9,"publicationDate":"2021-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8045329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25588913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Upregulated endonuclease Regnase-1 suppresses osteoarthritis by forming a negative feedback loop of catabolic signaling in chondrocytes.","authors":"Jeong-In Yang, Jang-Soo Chun","doi":"10.1186/s13075-021-02485-z","DOIUrl":"https://doi.org/10.1186/s13075-021-02485-z","url":null,"abstract":"<p><strong>Background: </strong>Ribonucleases (RNases) play central roles in the post-transcriptional regulation of mRNA stability. Our preliminary results revealed that the endonuclease Regnase-1 is specifically upregulated in osteoarthritic chondrocytes. We herein explored the possible functions and regulatory mechanisms of Regnase-1 in a mouse model of osteoarthritis (OA).</p><p><strong>Methods: </strong>The expression and target genes of Regnase-1 were identified by microarray analysis in primary-culture mouse articular chondrocytes. Experimental OA in mice was induced by destabilization of the medial meniscus (DMM). The function of Regnase-1 in DMM-induced post-traumatic OA mice was examined by adenovirus-mediated overexpression or knockdown in knee joint tissues, and also by using Regnase-1 heterozygous knockout mice (Zc3h12a<sup>+/-</sup>).</p><p><strong>Results: </strong>Among the RNases, Regnase-1 was exclusively upregulated in chondrocytes stimulated with OA-associated catabolic factors. Adenovirus-mediated overexpression or knockdown of Regnase-1 alone in joint tissues did not cause OA-like changes. However, overexpression of Regnase-1 in joint tissues significantly ameliorated DMM-induced post-traumatic OA cartilage destruction, whereas knockdown or genetic ablation of Regnase-1 exacerbated DMM-induced cartilage destruction. Mechanistic studies suggested that Regnase-1 suppresses cartilage destruction by modulating the expression of matrix-degrading enzymes in chondrocytes.</p><p><strong>Conclusion: </strong>Our results collectively suggest that upregulated Regnase-1 in OA chondrocytes may function as a chondro-protective effector molecule during OA pathogenesis by forming a negative feedback loop of catabolic signals, such as matrix-degrading enzyme expression, in OA chondrocytes.</p>","PeriodicalId":51225,"journal":{"name":"Arthritis Research & Therapy","volume":"23 1","pages":"114"},"PeriodicalIF":4.9,"publicationDate":"2021-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s13075-021-02485-z","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25588914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Johannes Knitza, Jacob Mohn, Christina Bergmann, Eleni Kampylafka, Melanie Hagen, Daniela Bohr, Harriet Morf, Elizabeth Araujo, Matthias Englbrecht, David Simon, Arnd Kleyer, Timo Meinderink, Wolfgang Vorbrüggen, Cay Benedikt von der Decken, Stefan Kleinert, Andreas Ramming, Jörg H W Distler, Nicolas Vuillerme, Achim Fricker, Peter Bartz-Bazzanella, Georg Schett, Axel J Hueber, Martin Welcker
{"title":"Accuracy, patient-perceived usability, and acceptance of two symptom checkers (Ada and Rheport) in rheumatology: interim results from a randomized controlled crossover trial.","authors":"Johannes Knitza, Jacob Mohn, Christina Bergmann, Eleni Kampylafka, Melanie Hagen, Daniela Bohr, Harriet Morf, Elizabeth Araujo, Matthias Englbrecht, David Simon, Arnd Kleyer, Timo Meinderink, Wolfgang Vorbrüggen, Cay Benedikt von der Decken, Stefan Kleinert, Andreas Ramming, Jörg H W Distler, Nicolas Vuillerme, Achim Fricker, Peter Bartz-Bazzanella, Georg Schett, Axel J Hueber, Martin Welcker","doi":"10.1186/s13075-021-02498-8","DOIUrl":"10.1186/s13075-021-02498-8","url":null,"abstract":"<p><strong>Background: </strong>Timely diagnosis and treatment are essential in the effective management of inflammatory rheumatic diseases (IRDs). Symptom checkers (SCs) promise to accelerate diagnosis, reduce misdiagnoses, and guide patients more effectively through the health care system. Although SCs are increasingly used, there exists little supporting evidence.</p><p><strong>Objective: </strong>To assess the diagnostic accuracy, patient-perceived usability, and acceptance of two SCs: (1) Ada and (2) Rheport.</p><p><strong>Methods: </strong>Patients newly presenting to a German secondary rheumatology outpatient clinic were randomly assigned in a 1:1 ratio to complete Ada or Rheport and consecutively the respective other SCs in a prospective non-blinded controlled randomized crossover trial. The primary outcome was the accuracy of the SCs regarding the diagnosis of an IRD compared to the physicians' diagnosis as the gold standard. The secondary outcomes were patient-perceived usability, acceptance, and time to complete the SC.</p><p><strong>Results: </strong>In this interim analysis, the first 164 patients who completed the study were analyzed. 32.9% (54/164) of the study subjects were diagnosed with an IRD. Rheport showed a sensitivity of 53.7% and a specificity of 51.8% for IRDs. Ada's top 1 (D1) and top 5 disease suggestions (D5) showed a sensitivity of 42.6% and 53.7% and a specificity of 63.6% and 54.5% concerning IRDs, respectively. The correct diagnosis of the IRD patients was within the Ada D1 and D5 suggestions in 16.7% (9/54) and 25.9% (14/54), respectively. The median System Usability Scale (SUS) score of Ada and Rheport was 75.0/100 and 77.5/100, respectively. The median completion time for both Ada and Rheport was 7.0 and 8.5 min, respectively. Sixty-four percent and 67.1% would recommend using Ada and Rheport to friends and other patients, respectively.</p><p><strong>Conclusions: </strong>While SCs are well accepted among patients, their diagnostic accuracy is limited to date.</p><p><strong>Trial registration: </strong>DRKS.de, DRKS00017642 . Registered on 23 July 2019.</p>","PeriodicalId":51225,"journal":{"name":"Arthritis Research & Therapy","volume":"23 1","pages":"112"},"PeriodicalIF":4.9,"publicationDate":"2021-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8042673/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25605304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Javier Rueda-Gotor, Raquel López-Mejías, Sara Remuzgo-Martínez, Verónica Pulito-Cueto, Alfonso Corrales, Leticia Lera-Gómez, Virginia Portilla, Íñigo González-Mazón, Ricardo Blanco, Rosa Expósito, Cristina Mata, Javier Llorca, Vanesa Hernández-Hernández, Carlos Rodríguez-Lozano, Nuria Barbarroja, Rafaela Ortega Castro, Esther Vicente, Cristina Fernández-Carballido, María Paz Martínez-Vidal, David Castro-Corredor, Joaquín Anino-Fernández, Diana Peiteado, Chamaida Plasencia-Rodríguez, Eva Galíndez-Agirregoikoa, María Luz García-Vivar, Oreste Gualillo, Juan Carlos Quevedo-Abeledo, Santos Castañeda, Iván Ferraz-Amaro, Miguel Á González-Gay, Fernanda Genre
{"title":"Vaspin in atherosclerotic disease and cardiovascular risk in axial spondyloarthritis: a genetic and serological study.","authors":"Javier Rueda-Gotor, Raquel López-Mejías, Sara Remuzgo-Martínez, Verónica Pulito-Cueto, Alfonso Corrales, Leticia Lera-Gómez, Virginia Portilla, Íñigo González-Mazón, Ricardo Blanco, Rosa Expósito, Cristina Mata, Javier Llorca, Vanesa Hernández-Hernández, Carlos Rodríguez-Lozano, Nuria Barbarroja, Rafaela Ortega Castro, Esther Vicente, Cristina Fernández-Carballido, María Paz Martínez-Vidal, David Castro-Corredor, Joaquín Anino-Fernández, Diana Peiteado, Chamaida Plasencia-Rodríguez, Eva Galíndez-Agirregoikoa, María Luz García-Vivar, Oreste Gualillo, Juan Carlos Quevedo-Abeledo, Santos Castañeda, Iván Ferraz-Amaro, Miguel Á González-Gay, Fernanda Genre","doi":"10.1186/s13075-021-02499-7","DOIUrl":"https://doi.org/10.1186/s13075-021-02499-7","url":null,"abstract":"<p><strong>Background: </strong>Vaspin is a novel anti-inflammatory adipokine associated with cardiovascular (CV) disease and inflammation in chronic inflammatory conditions different from axial spondyloarthritis (axSpA). Given the high incidence of CV disease (mainly due to accelerated atherosclerosis) exhibited by axSpA patients, we wondered if vaspin could also be a key molecule in this process. However, data on the role of vaspin regarding atherosclerotic disease in the context of axSpA is scarce. For this reason, we aimed to evaluate the implication of vaspin, at the genetic and serological level, in subclinical atherosclerosis and CV risk in axSpA.</p><p><strong>Methods: </strong>This study included 510 patients diagnosed with axSpA. Carotid ultrasound (US) was performed to evaluate the presence of subclinical atherosclerosis. Three vaspin gene variants (rs2236242, rs7159023, and rs35262691) were genotyped by TaqMan probes. Serum vaspin levels were assessed by enzyme-linked immunosorbent assay. Statistical analysis was performed using STATA® v.11.1.</p><p><strong>Results: </strong>Serum vaspin levels were significantly higher in female patients than in males and also in obese patients when compared to those with normal weight (p < 0.05). At the genetic level, we disclosed that the minor allele of rs2236242 (A) was associated with lower serum vaspin levels in axSpA, while the rs7159023 minor allele (A) was linked to higher serum levels (p < 0.05). When the three polymorphisms assessed were combined conforming haplotypes, we disclosed that the TGC haplotype related to high serum levels of vaspin (p = 0.01). However, no statistically significant association was observed between vaspin and markers of subclinical atherosclerosis, both at the genetic and serological level.</p><p><strong>Conclusions: </strong>Our results revealed that vaspin is linked to CV risk factors that may influence on the atherosclerotic process in axSpA. Additionally, we disclosed that serum vaspin concentration is genetically modulated in a large cohort of patients with axSpA.</p>","PeriodicalId":51225,"journal":{"name":"Arthritis Research & Therapy","volume":"23 1","pages":"111"},"PeriodicalIF":4.9,"publicationDate":"2021-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s13075-021-02499-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25586684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiaobo Zhu, Chien-Wei Lee, Hongtao Xu, Yu-Fan Wang, Patrick S H Yung, Yangzi Jiang, Oscar K Lee
{"title":"Phenotypic alteration of macrophages during osteoarthritis: a systematic review.","authors":"Xiaobo Zhu, Chien-Wei Lee, Hongtao Xu, Yu-Fan Wang, Patrick S H Yung, Yangzi Jiang, Oscar K Lee","doi":"10.1186/s13075-021-02457-3","DOIUrl":"https://doi.org/10.1186/s13075-021-02457-3","url":null,"abstract":"<p><strong>Objective: </strong>Osteoarthritis (OA) has long been regarded as a disease of cartilage degeneration, whereas mounting evidence implies that low-grade inflammation contributes to OA. Among inflammatory cells involved, macrophages play a crucial role and are mediated by the local microenvironment to exhibit different phenotypes and polarization states. Therefore, we conducted a systematic review to uncover the phenotypic alterations of macrophages during OA and summarized the potential therapeutic interventions via modulating macrophages.</p><p><strong>Methods: </strong>A systematic review of multiple databases (PubMed, Web of Science, ScienceDirect, Medline) was performed up to February 29, 2020. Included articles were discussed and evaluated by two independent reviewers. Relevant information was analyzed with a standardized and well-designed template.</p><p><strong>Results: </strong>A total of 28 studies were included. Results were subcategorized into two sections depending on sources from human tissue/cell-based studies (12 studies) and animal experiments (16 studies). The overall observation indicated that M1 macrophages elevated in both synovium and circulation during OA development, along with lower numbers of M2 macrophages. The detailed alterations of macrophages in both synovium and circulation were listed and analyzed. Furthermore, interventions against OA via regulating macrophages in animal models were highlighted.</p><p><strong>Conclusion: </strong>This study emphasized the importance of the phenotypic alterations of macrophages in OA development. The classical phenotypic subcategory of M1 and M2 macrophages was questionable due to controversial and conflicting results. Therefore, further efforts are needed to categorize macrophages in an exhaustive manner and to use advanced technologies to identify the individual roles of each subtype of macrophages in OA.</p>","PeriodicalId":51225,"journal":{"name":"Arthritis Research & Therapy","volume":"23 1","pages":"110"},"PeriodicalIF":4.9,"publicationDate":"2021-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s13075-021-02457-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25578672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jingjing Zhu, Zheng Niu, Lars Alfredsson, Lars Klareskog, Leonid Padyukov, Xia Jiang
{"title":"Age at menarche, age at natural menopause, and risk of rheumatoid arthritis - a Mendelian randomization study.","authors":"Jingjing Zhu, Zheng Niu, Lars Alfredsson, Lars Klareskog, Leonid Padyukov, Xia Jiang","doi":"10.1186/s13075-021-02495-x","DOIUrl":"https://doi.org/10.1186/s13075-021-02495-x","url":null,"abstract":"<p><strong>Background: </strong>Hormonal reproductive factors have been suggested to play an important role in the etiology of rheumatoid arthritis (RA), an autoimmune inflammatory disorder affecting primarily women. We conducted a two-sample Mendelian randomization (MR) study examining three relevant exposures, age at menarche (AAM), age at natural menopause (ANM), and age at first birth (AFB) with the risk of RA.</p><p><strong>Methods: </strong>We collected summary statistics from the hitherto largest GWAS conducted in AAM (N = 329,345), ANM (N = 69,360), AFB (N = 251,151), and RA (N<sub>case</sub> = 14,361, N<sub>control</sub> = 43,923), all of European ancestry. We constructed strong instruments using hundreds of exposure-associated genetic variants and estimated causal relationship through different MR approaches including an inverse-variance weighted method, an MR-Egger regression and a weighted median method. We conducted a multivariable MR to control for pleiotropic effect acting in particular through obesity and socioeconomic status. We also performed important sensitivity analyses to verify model assumptions.</p><p><strong>Results: </strong>We did not find any evidence in support for a causal association between genetically predicted reproductive factors and risk of RA (OR<sub>per-SD increment in AAM</sub> = 1.06 [0.98-1.15]; OR<sub>per-SD increment in ANM</sub> = 1.05 [0.98-1.11], OR <sub>per-SD increment in AFB</sub> = 0.85 [0.65-1.10]). Results remained consistent after removing palindromic SNPs (OR<sub>per-SD increment in AAM</sub> = 1.06 [0.97-1.15], OR<sub>per-SD increment in ANM</sub> = 1.05 [0.98-1.13], OR<sub>per-SD increment in AFB</sub> = 0.81 [0.61-1.07]) or excluding SNPs associated with potential confounding traits (OR<sub>per-SD increment in AAM</sub> = 1.03 [0.94-1.12], OR<sub>per-SD increment in ANM</sub> = 1.04 [0.95-1.14]). No outlying instrument was identified through the leave-one-out analysis.</p><p><strong>Conclusions: </strong>Our MR study does not convincingly support a casual effect of reproductive factors, as reflected by age at menarche, age at menopause, and age at first birth, on the development of RA. Despite the largely augmented set of instruments we used, these instruments only explained a modest proportion of phenotypic variance of exposures. Our knowledge regarding this topic is still insufficient and future studies with larger sample size should be designed to replicate or dispute our findings.</p>","PeriodicalId":51225,"journal":{"name":"Arthritis Research & Therapy","volume":"23 1","pages":"108"},"PeriodicalIF":4.9,"publicationDate":"2021-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s13075-021-02495-x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25586542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ni Zeng, Xin-Yuan Chen, Zhi-Peng Yan, Jie-Ting Li, Tao Liao, Guo-Xin Ni
{"title":"Efficacy and safety of sprifermin injection for knee osteoarthritis treatment: a meta-analysis.","authors":"Ni Zeng, Xin-Yuan Chen, Zhi-Peng Yan, Jie-Ting Li, Tao Liao, Guo-Xin Ni","doi":"10.1186/s13075-021-02488-w","DOIUrl":"https://doi.org/10.1186/s13075-021-02488-w","url":null,"abstract":"<p><strong>Objective: </strong>To perform a meta-analysis comparing the structural progression and clinical symptom outcomes as well as adverse events experienced from intra-articular injections of sprifermin compared to a placebo treatment for patients with knee osteoarthritis (KOA).</p><p><strong>Method: </strong>We systematically searched the literature for studies that compared long-term outcomes between sprifermin and placebo injections for KOA treatment. Meta-analysis was performed with RevMan5.3 using an inverse variance approach with fixed or random effects models. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated.</p><p><strong>Results: </strong>Eight studies were included. Overall, there was significantly less improvement of WOMAC total scores in patients receiving sprifermin, compared with the placebo (mean difference (MD) = 3.23, 95% CI 0.76-5.69; I<sup>2</sup> = 0%; P = 0.01). Further, sprifermin injection patients gained more, and lost less, cartilage thickness and volume in total femorotibial joint (cartilage thickness: standardized mean differences (SMD) = 0.55, 95% CI 0.26-0.84; I<sup>2</sup> = 78%; P = 0.0002; cartilage volume: SMD = 0.39, 95% CI 0.20-0.58; I<sup>2</sup> = 49%; P < 0.0001). Changes in the cartilage surface morphology of the medial tibio-femoral joint (MD = -0.30, 95% CI -0.44 to -0.16; I<sup>2</sup> = 0%; P < 0.0001) and patello-femoral joint (MD = -0.22; 95% CI -0.37 to -0.07; I<sup>2</sup> = 0%; P = 0.004) showed a significant difference between the sprifermin and placebo injections. Moreover, there were no significant differences between sprifermin and the placebo in the risk of treatment-emergent adverse events (OR = 1.05; 95% CI 0.52-2.14; I<sup>2</sup> = 48%; P = 0.89).</p><p><strong>Conclusion: </strong>The data from the included studies provide strong evidence to determine the effect of intra-articular sprifermin on joint structure in individuals with KOA and show no specific adverse effects. Nevertheless, intra-articular sprifermin did not likely have any positive effect on symptom alleviation.</p>","PeriodicalId":51225,"journal":{"name":"Arthritis Research & Therapy","volume":"23 1","pages":"107"},"PeriodicalIF":4.9,"publicationDate":"2021-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s13075-021-02488-w","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25586543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}