Pub Date : 2025-11-01DOI: 10.1016/j.jbspin.2025.106001
Marion Geoffroy , Myriam Beissat , L. Kanagaratnam , Stanley Ackah Miezan , Jean Hugues Salmon
Objectives
The primary objective of the study was to demonstrate the superiority of platelet-rich plasma injections in treating facet joint syndrome, compared to corticosteroid injections. Secondary objectives were to assess the efficacy of PRP compared to CTC on pain, functional impact, tolerance, and healthcare utilization following the initial infiltrative management.
Methods
Patients were randomized (1:1) to receive intra-articular injections into the painful facet joints with either PRP or CTC under radiographic guidance. The primary outcome measure was a 50% improvement in the NRS (from 0 to 10) for spontaneous lumbar pain at 6 months. Study design: Superiority, controlled, randomized (1:1), prospective, double-blind study.
Results
A total of 76 patients were included, at 6 months, 6 patients in the PRP group and 5 in the CTC group showed a 50% improvement in spontaneous NRS. No statistically significant differences were found in pain at 3, 6, or 12 months. Regarding functional evaluation, a statistically significant difference was observed in the PRP group at 3 months according to the ODI. No significant differences were found between groups in terms of satisfaction. Four patients experienced transient adverse effects, only 1 in the PRP group.
Conclusion
In patients with facet joint syndrome, PRP injections did not demonstrate superiority over CTC injections in terms of pain relief or clinically significant functional improvement at 6 months. These results do not support the use of PRP injections for facet joint syndrome.
{"title":"Platelet-rich plasma versus corticosteroids in facet joint syndrome: A controlled, randomized, double-blind study","authors":"Marion Geoffroy , Myriam Beissat , L. Kanagaratnam , Stanley Ackah Miezan , Jean Hugues Salmon","doi":"10.1016/j.jbspin.2025.106001","DOIUrl":"10.1016/j.jbspin.2025.106001","url":null,"abstract":"<div><h3>Objectives</h3><div>The primary objective of the study was to demonstrate the superiority of platelet-rich plasma injections in treating facet joint syndrome, compared to corticosteroid injections. Secondary objectives were to assess the efficacy of PRP compared to CTC on pain, functional impact, tolerance, and healthcare utilization following the initial infiltrative management.</div></div><div><h3>Methods</h3><div>Patients were randomized (1:1) to receive intra-articular injections into the painful facet joints with either PRP or CTC under radiographic guidance. The primary outcome measure was a 50% improvement in the NRS (from 0 to 10) for spontaneous lumbar pain at 6<!--> <!-->months. Study design: Superiority, controlled, randomized (1:1), prospective, double-blind study.</div></div><div><h3>Results</h3><div>A total of 76 patients were included, at 6<!--> <!-->months, 6 patients in the PRP group and 5 in the CTC group showed a 50% improvement in spontaneous NRS. No statistically significant differences were found in pain at 3, 6, or 12<!--> <!-->months. Regarding functional evaluation, a statistically significant difference was observed in the PRP group at 3<!--> <!-->months according to the ODI. No significant differences were found between groups in terms of satisfaction. Four patients experienced transient adverse effects, only 1 in the PRP group.</div></div><div><h3>Conclusion</h3><div>In patients with facet joint syndrome, PRP injections did not demonstrate superiority over CTC injections in terms of pain relief or clinically significant functional improvement at 6<!--> <!-->months. These results do not support the use of PRP injections for facet joint syndrome.</div></div>","PeriodicalId":54902,"journal":{"name":"Joint Bone Spine","volume":"93 3","pages":"Article 106001"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145440230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-22DOI: 10.1016/j.jbspin.2025.105994
Laëtitia Michou , Jacques P. Brown , Laurie Champagne , Maxime Vallée , Frédéric Fournier , Edith Gagnon , Arnaud Droit , Suzanne N. Morin
Objectives
We performed next generation sequencing in two affected-sibling pairs of atypical femur fractures (AFF) and in unrelated cases of AFF to identify genetic variants of bisphosphonates (BP)-associated AFF.
Methods
A whole exome sequencing (WES) was performed in two sisters with BP-associated AFF and their healthy brother naïve to BP treatment (family A). After bioinformatic filtering, the intrafamilial segregation was analysed. Then, we performed targeted sequencing of 62 genes, including 36 genes containing variants predicted to be damaging and segregating with the phenotype in both sisters of the family A, and 26 candidate genes for osteogenesis imperfecta (OI), hypophosphatasia and the mevalonate pathway. The targeted sequencing was performed on the family A, and on 47 unrelated participants and another affected sibling pair (family B) from the Quebec AFF Registry. 100 healthy controls recruited in same geographic area than patients were genotyped for rare variants.
Results
Sixty-three rare and deleterious variants were detected by the WES and shared by the two affected sisters of the family A. Among those variants, a rare likely pathogenic variant (p.Leu3fs) of the WNT1 gene, already linked to OI and early onset osteoporosis, was also shared by a third individual, an unrelated case with BP-associated AFF. The pair of siblings of family B carried a novel variant (p.Glu1323fs) in the COL1A2 gene, linked to OI. One unrelated case had a novel variant in the FDFT1 gene, involved in the mevalonate pathway. These rare variants were not found in 100 healthy controls.
Conclusion
Some BP-associated AFFs may occur in the setting of clinically undiagnosed underlying genetic disorders predisposing to osteoporosis and fractures, such as OI.
{"title":"Identification of rare genetic variants in familial forms and unrelated cases of bisphosphonates-associated atypical femur fracture","authors":"Laëtitia Michou , Jacques P. Brown , Laurie Champagne , Maxime Vallée , Frédéric Fournier , Edith Gagnon , Arnaud Droit , Suzanne N. Morin","doi":"10.1016/j.jbspin.2025.105994","DOIUrl":"10.1016/j.jbspin.2025.105994","url":null,"abstract":"<div><h3>Objectives</h3><div>We performed next generation sequencing in two affected-sibling pairs of atypical femur fractures (AFF) and in unrelated cases of AFF to identify genetic variants of bisphosphonates (BP)-associated AFF.</div></div><div><h3>Methods</h3><div>A whole exome sequencing (WES) was performed in two sisters with BP-associated AFF and their healthy brother naïve to BP treatment (family A). After bioinformatic filtering, the intrafamilial segregation was analysed. Then, we performed targeted sequencing of 62 genes, including 36 genes containing variants predicted to be damaging and segregating with the phenotype in both sisters of the family A, and 26 candidate genes for osteogenesis imperfecta (OI), hypophosphatasia and the mevalonate pathway. The targeted sequencing was performed on the family A, and on 47 unrelated participants and another affected sibling pair (family B) from the Quebec AFF Registry. 100 healthy controls recruited in same geographic area than patients were genotyped for rare variants.</div></div><div><h3>Results</h3><div>Sixty-three rare and deleterious variants were detected by the WES and shared by the two affected sisters of the family A. Among those variants, a rare likely pathogenic variant (p.Leu3fs) of the <em>WNT1</em> gene, already linked to OI and early onset osteoporosis, was also shared by a third individual, an unrelated case with BP-associated AFF. The pair of siblings of family B carried a novel variant (p.Glu1323fs) in the <em>COL1A2</em> gene, linked to OI. One unrelated case had a novel variant in the <em>FDFT1</em> gene, involved in the mevalonate pathway. These rare variants were not found in 100 healthy controls.</div></div><div><h3>Conclusion</h3><div>Some BP-associated AFFs may occur in the setting of clinically undiagnosed underlying genetic disorders predisposing to osteoporosis and fractures, such as OI.</div></div>","PeriodicalId":54902,"journal":{"name":"Joint Bone Spine","volume":"93 2","pages":"Article 105994"},"PeriodicalIF":4.3,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145369367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gout, one of the most prevalent inflammatory arthropathies, arises from hyperuricemia and is increasingly recognized as a condition extending beyond the joints. Hyperuricemia, the core risk factor for gout, is also an independent risk factor for cardiovascular disease (CVD), complications, and mortality. Multiple conditions that predispose to gout and hyperuricemia, including obesity, metabolic syndrome, type 2 diabetes, hypertension, and chronic kidney disease (CKD), also elevate the risk of atherosclerosis, the central contributor to CVD and the leading cause of mortality in Western societies. The association between gout and atherosclerosis highlights the need for deeper understanding of causal links between these conditions. Because evidence remains insufficient to support urate-lowering therapies for improving cardiovascular outcomes, attention has shifted to other mechanisms connecting gout and atherosclerosis. Given the lack of convincing data for clinically significant monosodium urate crystal (MSUc) deposition in atherosclerotic plaques, this review focuses on the hypothesis that expansion of local articular to systemic inflammation, driven by macrophage activation by MSUc, is the primary mechanism accelerating atherosclerosis in gout. Mechanistically, we explore how epigenetic regulators normally restrain MSU-induced local inflammation, thereby protecting against atherosclerosis. We further discuss how aging-related somatic mutations in genes involved in clonal hematopoiesis of indeterminate potential (CHIP) disrupt this protection, resulting in heightened systemic inflammation and atherosclerosis in patients with gout.
{"title":"Connecting the dots: Gouty arthritis, clonal haematopoiesis and myeloid activation, in a unified inflammation model for atherosclerosis progression","authors":"Faith Inkum , Xiaoxiao Geng , Robert Terkeltaub , Isidoro Cobo","doi":"10.1016/j.jbspin.2025.105993","DOIUrl":"10.1016/j.jbspin.2025.105993","url":null,"abstract":"<div><div>Gout, one of the most prevalent inflammatory arthropathies, arises from hyperuricemia and is increasingly recognized as a condition extending beyond the joints. Hyperuricemia, the core risk factor for gout, is also an independent risk factor for cardiovascular disease (CVD), complications, and mortality. Multiple conditions that predispose to gout and hyperuricemia, including obesity, metabolic syndrome, type 2 diabetes, hypertension, and chronic kidney disease (CKD), also elevate the risk of atherosclerosis, the central contributor to CVD and the leading cause of mortality in Western societies. The association between gout and atherosclerosis highlights the need for deeper understanding of causal links between these conditions. Because evidence remains insufficient to support urate-lowering therapies for improving cardiovascular outcomes, attention has shifted to other mechanisms connecting gout and atherosclerosis. Given the lack of convincing data for clinically significant monosodium urate crystal (MSUc) deposition in atherosclerotic plaques, this review focuses on the hypothesis that expansion of local articular to systemic inflammation, driven by macrophage activation by MSUc, is the primary mechanism accelerating atherosclerosis in gout. Mechanistically, we explore how epigenetic regulators normally restrain MSU-induced local inflammation, thereby protecting against atherosclerosis. We further discuss how aging-related somatic mutations in genes involved in clonal hematopoiesis of indeterminate potential (CHIP) disrupt this protection, resulting in heightened systemic inflammation and atherosclerosis in patients with gout.</div></div>","PeriodicalId":54902,"journal":{"name":"Joint Bone Spine","volume":"93 3","pages":"Article 105993"},"PeriodicalIF":4.3,"publicationDate":"2025-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145356823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-21DOI: 10.1016/j.jbspin.2025.105992
Martin Krusche, Phillip Kremer, Isabell Haase
{"title":"Social media and its impact on mental health in rheumatic diseases.","authors":"Martin Krusche, Phillip Kremer, Isabell Haase","doi":"10.1016/j.jbspin.2025.105992","DOIUrl":"https://doi.org/10.1016/j.jbspin.2025.105992","url":null,"abstract":"","PeriodicalId":54902,"journal":{"name":"Joint Bone Spine","volume":" ","pages":"105992"},"PeriodicalIF":4.3,"publicationDate":"2025-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145356897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
To describe the baseline characteristics of patients enrolled in the TRANSLATE2 cohort (NCT04227535), a national, multicenter, prospective case-control study designed to investigate the genetic and non-genetic determinants of interstitial lung disease (ILD) in rheumatoid arthritis (RA).
Methods
Cases with RA-ILD and RA controls without ILD were consecutively included in TRANSLATE2 with a 5-year prospective follow-up. All participants fulfilled the ACR/EULAR 2010 classification criteria for RA. ILD presence or absence was confirmed for every participant by chest high-resolution computed tomography (HRCT). Baseline demographic and clinical data were collected. Blood samples were collected at enrollment for centralized biobanking of DNA, RNA, and serum to support future genetic and biomarker studies. For ILD cases, chest HRCT scans were centrally reviewed to determine HRCT pattern. For the current study, associations with ILD were tested using univariable and multivariable logistic regression models.
Results
Among the 506 patients included (275 RA-ILD, 231 RA-noILD), RA-ILD cases were more frequently male (48.4% vs. 29.9%), older at enrollment (66.6 [9.9] vs. 58.5 [13.2] years) and older at RA onset (52.2 [14.7] vs. 45.8 [14.3] years). ILD was independently associated with male sex (OR 1.82; 95% CI 1.06, 3.14) and older age at RA onset (OR per 10 years 1.28; 95% CI 1.10,1.50). For ILD cases, the most frequent HRCT patterns were definite for usual interstitial pneumonia (39.3%) and non-specific interstitial pneumonia (17.8%). At enrollment, respiratory symptoms were observed in 67.3% with a mean forced vital capacity % predicted of 87.6% (21.7) and a mean diffusing capacity of the lung for carbon monoxide % predicted of 58.4% (18.8).
Conclusion
The TRANSLATE2 cohort provides a comprehensive and deeply phenotyped dataset that offers a unique opportunity to investigate the genetic architecture, risk factors, and natural history of RA-ILD.
目的：描述TRANSLATE2队列（NCT04227535）患者的基线特征，TRANSLATE2队列是一项全国性、多中心、前瞻性病例对照研究，旨在研究类风湿关节炎（RA）中间质性肺疾病（ILD）的遗传和非遗传决定因素。方法：TRANSLATE2连续纳入RA-ILD病例和无ILD的RA对照，并进行5年前瞻性随访。所有参与者均符合ACR/EULAR 2010 RA分类标准。通过胸部高分辨率计算机断层扫描（HRCT）确认每位参与者是否存在ILD。收集基线人口统计学和临床数据。在入组时采集血样，用于DNA、RNA和血清的集中生物银行，以支持未来的遗传和生物标志物研究。对于ILD病例，集中复查胸部HRCT扫描以确定HRCT模式。在目前的研究中，使用单变量和多变量逻辑回归模型检验了与ILD的关系。结果：在纳入的506例患者中（275例RA- ild， 231例RA- noild）， RA- ild患者多为男性（48.4%对29.9%），入组时年龄较大（66.6[9.9]对58.5[13.2]岁），RA发病时年龄较大（52.2[14.7]对45.8[14.3]岁）。ILD与男性（OR 1.82; 95% CI 1.06, 3.14）和RA发病年龄较大（OR每10年1.28;95% CI 1.10,1.50）独立相关。对于ILD病例，最常见的HRCT表现为常规间质性肺炎（39.3%）和非特异性间质性肺炎（17.8%）。入组时，67.3%的患者出现呼吸系统症状，预计平均强迫肺活量为87.6%(21.7%)，预计平均一氧化碳肺弥散量为58.4%（18.8%）。结论：TRANSLATE2队列提供了一个全面而深入的表型数据集，为研究RA-ILD的遗传结构、风险因素和自然史提供了独特的机会。287/300单词。
{"title":"Baseline characteristics of the TRANSLATE2 cohort: A prospective study on rheumatoid arthritis-associated interstitial lung disease","authors":"Pierre-Antoine Juge , Marie-Pierre Debray , Valérie Devauchelle Pensec , Christophe Richez , Jérôme Avouac , Lidwine Wemeau-Stervinou , René-Marc Flipo , Hilario Nunes , Nathalie Saidenberg-Kermanac’h , Jacques-Eric Gottenberg , Stéphane Jouneau , Arnaud Constantin , Vincent Cottin , Hubert Marotte , Martin Soubrier , Bruno Fautrel , Gaëtane Nocturne , Pascal Richette , Francis Berenbaum , Hagit Zylberman-Yona , Philippe Dieudé","doi":"10.1016/j.jbspin.2025.105991","DOIUrl":"10.1016/j.jbspin.2025.105991","url":null,"abstract":"<div><h3>Objectives</h3><div>To describe the baseline characteristics of patients enrolled in the TRANSLATE2 cohort (<span><span>NCT04227535</span><svg><path></path></svg></span>), a national, multicenter, prospective case-control study designed to investigate the genetic and non-genetic determinants of interstitial lung disease (ILD) in rheumatoid arthritis (RA).</div></div><div><h3>Methods</h3><div>Cases with RA-ILD and RA controls without ILD were consecutively included in TRANSLATE2 with a 5-year prospective follow-up. All participants fulfilled the ACR/EULAR 2010 classification criteria for RA. ILD presence or absence was confirmed for every participant by chest high-resolution computed tomography (HRCT). Baseline demographic and clinical data were collected. Blood samples were collected at enrollment for centralized biobanking of DNA, RNA, and serum to support future genetic and biomarker studies. For ILD cases, chest HRCT scans were centrally reviewed to determine HRCT pattern. For the current study, associations with ILD were tested using univariable and multivariable logistic regression models.</div></div><div><h3>Results</h3><div>Among the 506 patients included (275 RA-ILD, 231 RA-noILD), RA-ILD cases were more frequently male (48.4% vs. 29.9%), older at enrollment (66.6 [9.9] vs. 58.5 [13.2] years) and older at RA onset (52.2 [14.7] vs. 45.8 [14.3] years). ILD was independently associated with male sex (OR 1.82; 95% CI 1.06, 3.14) and older age at RA onset (OR per 10 years 1.28; 95% CI 1.10,1.50). For ILD cases, the most frequent HRCT patterns were definite for usual interstitial pneumonia (39.3%) and non-specific interstitial pneumonia (17.8%). At enrollment, respiratory symptoms were observed in 67.3% with a mean forced vital capacity % predicted of 87.6% (21.7) and a mean diffusing capacity of the lung for carbon monoxide % predicted of 58.4% (18.8).</div></div><div><h3>Conclusion</h3><div>The TRANSLATE2 cohort provides a comprehensive and deeply phenotyped dataset that offers a unique opportunity to investigate the genetic architecture, risk factors, and natural history of RA-ILD.</div></div>","PeriodicalId":54902,"journal":{"name":"Joint Bone Spine","volume":"93 2","pages":"Article 105991"},"PeriodicalIF":4.3,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145330803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Janus kinase (JAK) inhibitors are effective treatments for autoimmune rheumatic diseases (AIRDs). However, concomitant use of JAK inhibitors with CYP enzyme inhibitors or OAT3 inhibitors can lead to drug-drug interactions. This study aimed to evaluate the impact of the concomitant use of CYP and OAT3 inhibitors on discontinuation of treatment and infectious complications in patients treated with JAK inhibitors.
Methods
Using the National Health Insurance Research Database, this retrospective cohort study included patients with rheumatoid arthritis, psoriatic arthritis and atopic dermatitis treated with JAK inhibitors in 2021–2023. The risks of discontinuation of treatment and infectious complications were evaluated using Cox proportional hazards models, adjusted for age, gender, other infectious and concomitant use of steroids or methotrexate.
Results
Among 7591 patients, concomitant use of strong CYP3A4, or CYP2C19 inhibitors increased the risk of treatment discontinuation for tofacitinib and baricitinib from 41% to 144%. The risk of overall infectious complications also increased when tofacitinib was used concomitantly with strong CYP2C19 inhibitors. The risk of pneumonia was further increased by concomitant use of strong CYP2C19 inhibitors with all JAK inhibitors and CYP3A4 inhibitors with tofacitinib. The risk of urinary tract infection was increased by concomitant use of strong CYP2C19 inhibitors when used with tofacitinib, or baricitinib.
Conclusions
Concomitant use of strong CYP3A4, and CYP2C19 inhibitors with JAK inhibitors significantly increases the risk of discontinuation of treatment and infectious complications in patients with AIRDs. Careful consideration of drug-drug interactions is necessary when prescribing JAK inhibitors to optimize treatment persistence and minimize adverse events.
{"title":"Impact of drug-drug interaction of JAK inhibitors, CYP enzyme inhibitors and OAT3 inhibitors on persistence and infection rates in patients with autoimmune rheumatic diseases","authors":"Yu-Hsuan Joni Shao , Tzu-Tung Kuo , Yi-Ju Liao , Yi-Ting Chen , I.-Chieh Chen , Chung-Mao Kao , Yen-Ju Chen , Yi-Ming Chen","doi":"10.1016/j.jbspin.2025.105990","DOIUrl":"10.1016/j.jbspin.2025.105990","url":null,"abstract":"<div><h3>Objectives</h3><div>Janus kinase (JAK) inhibitors are effective treatments for autoimmune rheumatic diseases (AIRDs). However, concomitant use of JAK inhibitors with CYP enzyme inhibitors or OAT3 inhibitors can lead to drug-drug interactions. This study aimed to evaluate the impact of the concomitant use of CYP and OAT3 inhibitors on discontinuation of treatment and infectious complications in patients treated with JAK inhibitors.</div></div><div><h3>Methods</h3><div>Using the National Health Insurance Research Database, this retrospective cohort study included patients with rheumatoid arthritis, psoriatic arthritis and atopic dermatitis treated with JAK inhibitors in 2021–2023. The risks of discontinuation of treatment and infectious complications were evaluated using Cox proportional hazards models, adjusted for age, gender, other infectious and concomitant use of steroids or methotrexate.</div></div><div><h3>Results</h3><div>Among 7591 patients, concomitant use of strong CYP3A4, or CYP2C19 inhibitors increased the risk of treatment discontinuation for tofacitinib and baricitinib from 41% to 144%. The risk of overall infectious complications also increased when tofacitinib was used concomitantly with strong CYP2C19 inhibitors. The risk of pneumonia was further increased by concomitant use of strong CYP2C19 inhibitors with all JAK inhibitors and CYP3A4 inhibitors with tofacitinib. The risk of urinary tract infection was increased by concomitant use of strong CYP2C19 inhibitors when used with tofacitinib, or baricitinib.</div></div><div><h3>Conclusions</h3><div>Concomitant use of strong CYP3A4, and CYP2C19 inhibitors with JAK inhibitors significantly increases the risk of discontinuation of treatment and infectious complications in patients with AIRDs. Careful consideration of drug-drug interactions is necessary when prescribing JAK inhibitors to optimize treatment persistence and minimize adverse events.</div></div>","PeriodicalId":54902,"journal":{"name":"Joint Bone Spine","volume":"93 2","pages":"Article 105990"},"PeriodicalIF":4.3,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145330868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The skeleton is able to secrete hormones and mediate endocrine functions. Particularly, the fibroblast growth factor 23 (FGF23) has received considerable attention for its unique phosphaturic properties, raising the bone to the status of an essential endocrine regulator. Excess in circulating levels of FGF23, not so surprisingly, then associated to mineral imbalance, in hereditary/acquired mineral and skeletal disorders. A key player, FGF23 excess precedes mineral and skeletal disturbances. However, unexpected effects have been described in the recent years. Various demonstrations have been made that FGF23 is directly regulated by non-mineral stress, including: inflammation, iron deficiency, and glycolysis. In turn, an emerging body of research shows association and causality between FGF23 and the cardiovascular system at large, from the iron metabolism to erythropoiesis, and to the cardiac muscle. This review summarizes canonical and novel effects of FGF23. FGF23 cleavage generates C-terminal peptides that also mediate biological functions. In aggregate, FGF23 measurements should be considered for larger application, as its excess can precede hypophosphatemia, explain hypophosphatemia or resistance to phosphate loading, and possibly predict cardiovascular progression in a wide range of uremic and non-uremic conditions.
{"title":"FGF23: A player not only in bone diseases","authors":"Amélie Cifuentes , Zacharie Laskar-Marchesseau , Guillaume Courbon","doi":"10.1016/j.jbspin.2025.105988","DOIUrl":"10.1016/j.jbspin.2025.105988","url":null,"abstract":"<div><div>The skeleton is able to secrete hormones and mediate endocrine functions. Particularly, the fibroblast growth factor 23 (FGF23) has received considerable attention for its unique phosphaturic properties, raising the bone to the status of an essential endocrine regulator. Excess in circulating levels of FGF23, not so surprisingly, then associated to mineral imbalance, in hereditary/acquired mineral and skeletal disorders. A key player, FGF23 excess precedes mineral and skeletal disturbances. However, unexpected effects have been described in the recent years. Various demonstrations have been made that FGF23 is directly regulated by non-mineral stress, including: inflammation, iron deficiency, and glycolysis. In turn, an emerging body of research shows association and causality between FGF23 and the cardiovascular system at large, from the iron metabolism to erythropoiesis, and to the cardiac muscle. This review summarizes canonical and novel effects of FGF23. FGF23 cleavage generates C-terminal peptides that also mediate biological functions. In aggregate, FGF23 measurements should be considered for larger application, as its excess can precede hypophosphatemia, explain hypophosphatemia or resistance to phosphate loading, and possibly predict cardiovascular progression in a wide range of uremic and non-uremic conditions.</div></div>","PeriodicalId":54902,"journal":{"name":"Joint Bone Spine","volume":"93 2","pages":"Article 105988"},"PeriodicalIF":4.3,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145253818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-06DOI: 10.1016/j.jbspin.2025.105986
Xiaochun Cui , Qi Wang , Jun Li
{"title":"Ischiofemoral impingement syndrome","authors":"Xiaochun Cui , Qi Wang , Jun Li","doi":"10.1016/j.jbspin.2025.105986","DOIUrl":"10.1016/j.jbspin.2025.105986","url":null,"abstract":"","PeriodicalId":54902,"journal":{"name":"Joint Bone Spine","volume":"93 1","pages":"Article 105986"},"PeriodicalIF":4.3,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145253864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号