Clinical and experimental rheumatology最新文献

{"title":"Translation and validation in Italian of the methotrexate intolerance severity score for children and adults with arthritis.","authors":"Giusyda Tarantino, Rebecca Nicolai, Angela Aquilani, Andrea Tomasini, Antonella Celano, Aurora Pucacco, Silvia Magni-Manzoni, Fabrizio De Benedetti, Emiliano Marasco","doi":"10.55563/clinexprheumatol/656se0","DOIUrl":"10.55563/clinexprheumatol/656se0","url":null,"abstract":"<p><strong>Objectives: </strong>Methotrexate (MTX) is the most used drug to treat children and adults with arthritis and its use is burdened by adverse effects. The MTX intolerance severity score (MISS) was developed in English to identify patients who are intolerant to MTX. The aim of this study was to translate and validate the MISS in Italian.</p><p><strong>Methods: </strong>The Italian version of the MISS was developed following the \"guidelines for process of cross-cultural adaptation of self-reported measures\". The Italian version of the MISS was validated in 125 patients with juvenile idiopathic arthritis (JIA) followed at the Rheumatology Unit of Bambino Gesù Children Hospital. We assessed the construct validity and calculated the internal consistency of the Italian MISS. We performed ROC analysis to assess the overall performance of the Italian MISS.</p><p><strong>Results: </strong>We translated and adapted the MISS to the Italian language. The Italian MISS showed a very good internal consistency as shown by a Cronbach α of 0.87 (95% CI, 0.84-0.90) and a composite reliability of 0.89 (95% CI, 0.83-0.91).The Cohen's κ was 0.81 (95% CI, 0.71-0.91), suggesting a very good construct validity. The ROC analysis showed an area under the curve (AUC) of 0.97 (95% CI, 0.93-0.99). A threshold of 6 to define intolerant patients, showed a sensitivity of 98.3% and specificity of 81.2%.</p><p><strong>Conclusions: </strong>We developed the Italian version of the MISS and showed its validity and reliability to identify patients intolerant to MTX in clinical practice and in a research setting.</p>","PeriodicalId":10274,"journal":{"name":"Clinical and experimental rheumatology","volume":" ","pages":"2288-2294"},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141554243","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":"Clinical manifestations, treatment and prognosis of juvenile idiopathic arthritis with pulmonary involvement in China: a single centre study.","authors":"Fengqiao Gao, Junmei Zhang, Jianghong Deng, Weiying Kuang, Xiaohua Tan, Chao Li, Shipeng Li, Xuanyi Liu, Caifeng Li","doi":"10.55563/clinexprheumatol/udjbtq","DOIUrl":"10.55563/clinexprheumatol/udjbtq","url":null,"abstract":"<p><strong>Objectives: </strong>In recent years, the distinct clinical presentations and elevated mortality rates of various subtypes of juvenile idiopathic arthritis (JIA) with pulmonary involvement have garnered significant attention. This study aimed to elucidate the clinical characteristics of pulmonary involvement in patients with JIA to improve clinicians' knowledge.</p><p><strong>Methods: </strong>This single-centre retrospective study analysed the baseline data, treatment options, follow-up of sixty patients of JIA with pulmonary involvement in China. Patients with interstitial lung disease (ILD) were further classified in accordance with the 2013 American Thoracic Society/European Respiratory Society International multidisciplinary consensus on idiopathic interstitial pneumonia.</p><p><strong>Results: </strong>Sixty patients (5.03%) with JIA were complicated with pulmonary involvement. The highest subtype was systemic JIA (sJIA, 63.3%), followed by rheumatoid factor (RF)-positive polyarthritis (pJIA, 25.0%). The incidence of macrophage activation syndrome (MAS) was 21.6%. The most common diagnosis was ILD (90%). Respiratory symptoms/signs were initially experienced by 61.7% of the patients, and respiratory support was required by 21.7%. High-resolution CT classification of sJIA revealed non-specific interstitial pneumonia (NSIP) and organising pneumonia. High-resolution CT classification of pJIA was NSIP and usually interstitial pneumonia (UIP). Patients were treated with NSAIDs, along with glucocorticoids, DMARDs, and biological agents. The survival rates after 1 and 5 years were approximately 93.3% and 90.0%, respectively.</p><p><strong>Conclusions: </strong>Patients with JIA with pulmonary involvement present with early onset, high mortality rate. JIA patients should undergo physical examination thoroughly and high-resolution CT scans, lung function tests for evaluating and monitoring the occurrence and development of pulmonary involvement in early stages to improve prognosis.</p>","PeriodicalId":10274,"journal":{"name":"Clinical and experimental rheumatology","volume":" ","pages":"2303-2311"},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142281250","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":"Oxidised low-density lipoprotein and antibodies against oxidised low-density lipoprotein in patients with antiphospholipid syndrome.","authors":"Yongjing Luo, Lei Zhu, Xiaoyan Xing, Yunshan Zhou, Yuzhou Gan, Chun Li","doi":"10.55563/clinexprheumatol/ntj6n5","DOIUrl":"10.55563/clinexprheumatol/ntj6n5","url":null,"abstract":"<p><strong>Objectives: </strong>Recurrent thrombosis is one of the main clinical features of antiphospholipid syndrome (APS), and recent studies revealed that APS shares similar pathophysiological mechanisms with atherosclerosis. Oxidised low-density lipoprotein (OxLDL) and antibodies against OxLDL (anti-OxLDL) are involved in the development of atherosclerosis. This study aims to investigate the clinical significance of OxLDL and anti-OxLDL in APS patients.</p><p><strong>Methods: </strong>One hundred and seventy APS patients and 39 healthy controls (HC) were enrolled. Clinical and laboratory data were collected from Clinical Data Center of Peking University People's Hospital. OxLDL and anti-OxLDL were detected using enzyme-linked immunosorbent assay.</p><p><strong>Results: </strong>Among the 170 APS patients, 106 had isolated thrombotic APS. Compared with HC, APS patients exhibited higher titres of OxLDL [413.86 (220.11-853.67) ng/mL vs. 45.54 (0-105.98) ng/mL, p<0.001] and anti-OxLDL [107.62 (75.68-174.18) U/L vs. 44.13 (18.44-79.76) U/L, p<0.001]. Also, APS patients exhibited a higher positivity rate for OxLDL (88.2% vs. 5.1%, p<0.001) and anti-OxLDL (84.1% vs. 36.5%, p<0.001) compared to HC. APS patients with elevated levels of OxLDL had a higher rate of LAC positivity (68.0% vs. 45.0%, p=0.042). Furthermore, APS patients with positive anti-OxLDL demonstrated a higher occurrence of venous thrombosis (46.2% vs. 18.5%, p=0.008) and a lower rate of Coomb's test positivity (52.6% vs. 76.2%, p=0.049). Multivariate logistic regression revealed that anti-OxLDL positivity (OR 12.424, 95%CI 1.108-139.330, p=0.041) were risk factors for venous thrombotic APS.</p><p><strong>Conclusions: </strong>This study indicates that the presence of anti-OxLDL may serve as potential markers for venous thrombosis in APS patients. OxLDL and anti-OxLDL may function as valuable biomarkers for monitoring APS.</p>","PeriodicalId":10274,"journal":{"name":"Clinical and experimental rheumatology","volume":" ","pages":"2229-2237"},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104900","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":"Understanding mechanisms of JAK1 inhibition on synovial fibroblasts using combinatorial approaches of bulk and single cell RNAseq analyses.","authors":"Yuna Son, Daniel Korenfeld, Abel Suarez-Fueyo, Melanie Ruzek, Jing Wang, Bohdan Harvey","doi":"10.55563/clinexprheumatol/s705qn","DOIUrl":"10.55563/clinexprheumatol/s705qn","url":null,"abstract":"<p><strong>Objectives: </strong>The aim of these studies was to characterise the molecular effects of a tool JAK1 inhibitor on cultured primary fibroblast-like synoviocytes (FLS) from patients with rheumatoid arthritis (RA) through both total and individual cell analysis.</p><p><strong>Methods: </strong>RA-FLS cultures from 6 (Bulk RNA-seq) or 4 (ScRNA-seq) donors were pre-treated with various concentrations (100 nM and 1μM) of ABT-317 with/without exposure to 25% SEB-conditioned PBMC medium to mimic the RA inflammatory milieu. Cells were subjected to both bulk RNA-seq (36 libraries) and single cell RNA-seq (scRNA-seq; 24 libraries) to identify biological processes impacted by CM and ABT-317 treatments.</p><p><strong>Results: </strong>In our bulk RNA-seq analysis, a total of 2,605 differentially expressed genes (DEGs) were identified between CM-stimulation and unstimulated groups, while 1,122 DEGs were found between ABT-317 1μM and DMSO in CM-stimulated groups using thresholds of log2 (fold change) ≥ |0.58| and FDR ≤ 10%. Both bulk and single cell mRNA analysis of RA-FLS treated with a combination of CM and ABT-317 demonstrated the expected changes in inflammatory pathways such as interferon and IL-6 signalling. However, other non-inflammation associated pathways were also altered by ABT-317. In addition, the single cell analysis highlighted that FLS segregate into distinctive clusters upon combination CM and ABT-317 treatment, suggesting JAK inhibition can drive RA-FLS into multiple heterogenous cell populations. Interestingly, one of the unique RA-FLS clusters that emerged from the CM and ABT-317 treatment showed matrix metalloproteinase-3 (MMP3)high expression as well as several gene signatures that are not found in any other ABT-317 derived clusters.</p><p><strong>Conclusions: </strong>JAK inhibition with ABT-317 is effective at globally inhibiting CM-induced pro- and non-inflammatory pathways in FLS cultures, but also results in several distinct fibroblast populations with unique gene-associated pathways. This study advances the molecular understanding of JAK1 inhibitor effects on fibroblasts that may contribute to clinical efficacy.</p>","PeriodicalId":10274,"journal":{"name":"Clinical and experimental rheumatology","volume":" ","pages":"2194-2205"},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141442186","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":"Autoimmune inner ear disease associated with antiphospholipid antibodies.","authors":"Antonio Bustos-Merlo, Alberto Ortiz-Parra, Antonio Rosales-Castillo, Juan Manuel Espinosa-Sanchez, Nuria Navarrete-Navarrete","doi":"10.55563/clinexprheumatol/gu70rz","DOIUrl":"10.55563/clinexprheumatol/gu70rz","url":null,"abstract":"<p><strong>Objectives: </strong>The percentage of autoimmune diseases in Western countries is approximately 8% of the total population. Despite numerous studies indicating an increase in prevalence and incidence over the past two decades, autoimmune vestibular disorders seem to be underdiagnosed, primarily due to the lack of a definitive test capable of identifying the specific antigen of the inner ear. Autoimmune inner ear disease (AIED) is defined as a rapidly progressive and often fluctuating bilateral neurosensorial hearing loss that develops over a period of weeks or months. AIED can affect only the inner ear or be part of systemic diseases such as granulomatosis with polyangiitis, Cogan's syndrome, systemic lupus erythematosus, polyarteritis nodosa, or relapsing polychondritis, among others. Our main objective was to conduct a study on the presence of antiphospholipid antibodies (aPL) in patients with AIED seen in a specialised clinic.</p><p><strong>Methods: </strong>We designed an observational retrospective study in which we selected patients from a total group of 55 with AIED referred to the Autoimmune Diseases Clinic, those with confirmed positivity for antiphospholipid antibodies, and described their clinical, analytical, and epidemiological characteristics.</p><p><strong>Results: </strong>We found a prevalence of 29% positivity for antiphospholipid antibodies, with lupus anticoagulant (LA) being the most frequently detected, followed by anticardiolipin (aCL) and anti-beta2 glycoprotein (anti-B2GP). Double positivity was observed in 25% of patients. The main clinical manifestations were bilateral hearing loss, vestibular symptoms, and tinnitus. Only 25% of patients experienced audiometric improvement during the course of the disease.</p><p><strong>Conclusions: </strong>We emphasise the importance of identifying the presence of aPL in AIED, enabling the establishment of appropriate and specific therapeutic management to prevent audiometric deterioration.</p>","PeriodicalId":10274,"journal":{"name":"Clinical and experimental rheumatology","volume":" ","pages":"2268-2271"},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141757471","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":"Description of self-efficacy for managing symptoms and emotions in a large rheumatology clinic population.","authors":"Rachel Dayno, Michael D George, Marissa Blum, Kimberly DeQuattro, Sharon Kolasinksi, Dana DiRenzo","doi":"10.55563/clinexprheumatol/2dohgg","DOIUrl":"10.55563/clinexprheumatol/2dohgg","url":null,"abstract":"<p><strong>Objectives: </strong>Self-efficacy is the inner confidence in one's ability to manage specific goals or tasks. The purpose of this study was to describe self-efficacy for people living with various rheumatologic disease and explore its associations with health-related quality of life (HRQoL).</p><p><strong>Methods: </strong>This study was a retrospective, cross-sectional analysis of patients in a large rheumatology division who had office visits and completed questionnaires from May 2022 to January 2023. Questionnaires included the Patient Reported Outcome Measurement Information System (PROMIS)-29 v2.1 and Self-Efficacy for Managing Symptoms (SE Symptoms) and Emotions (SE Emotions) Computer Adaptive Tests, among others. Rheumatologic diagnosis was confirmed by the rheumatologist at the time of the encounter and additional comorbidities were identified via chart review. Mean PROMIS T-scores were compared across demographics and rheumatologic diagnosis and multivariable linear regression models (MLR) were constructed to explore determinants of self-efficacy.</p><p><strong>Results: </strong>There were 1,114 patients who completed office visits during the study timeframe; 401 patients (36%) had complete data. Compared to those with high SE symptoms and SE emotions those with low SE symptoms and SE emotions had significantly worse HRQoL in all PROMIS domains by 5-10 mean T-score units (p<0.001). Fatigue, depression, and pain interference were strong determinants of SE symptoms and fatigue, anxiety, and depression were strong determinants of SE emotions in MLR.</p><p><strong>Conclusions: </strong>Self-efficacy can be easily measured as part of routine clinical care using highly precise and reliable PROMIS measures. Self-efficacy is low amongst patients with rheumatologic diseases followed in a large academic centre for routine care and is highly associated with HRQoL.</p>","PeriodicalId":10274,"journal":{"name":"Clinical and experimental rheumatology","volume":" ","pages":"2175-2182"},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364608","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":"Monogenic interferon-mediated diseases: novel phenotype and genotype characteristics from a Saudi population.","authors":"AlHanouf Al-Saleem, Shahad Alansari, Mohammed Almuhaizea, Sulaiman M Al-Mayouf","doi":"10.55563/clinexprheumatol/aa6drm","DOIUrl":"10.55563/clinexprheumatol/aa6drm","url":null,"abstract":"<p><strong>Objectives: </strong>IFN-mediated diseases are mendelian innate immunodysregulatory disorders that present early in life with fevers, sterile organ inflammation, and a high type-I IFN-response gene signature in peripheral blood cells. To date, monumental discoveries of novel genetic variants with various phenotypic features have been recognised. We aimed to describe the genotype and phenotype findings in Saudi children diagnosed with autoinflammatory interferonopathy and to report novel findings.</p><p><strong>Methods: </strong>This is a descriptive retrospective cohort study of children with genetically confirmed type I interferonopathies. Medical records were reviewed for demographic, family history, clinical and laboratory data. All patients underwent genetic testing.</p><p><strong>Results: </strong>A total of 20 patients (11 females) were included in the study. Sixteen patients (80%) presented within the first 2 years. The median age of disease onset was 0.87 years (IQR: 0.5-2) and the median age of diagnosis was 4.5 years (IQR: 2-7.5). The rates of consanguinity and family history of affected members were high (88% and 47%, respectively). Among the cohort of patients, whole exome sequencing was conducted for 15 patients. Three patients underwent targeted gene tests, and 2 patients had a leukoencephalopathy genetic panel. Eight patients were diagnosed with Aicardi-Goutières syndrome, attributed to variants in the RNASEH2A, RNASEH2C, and IFIH1 genes. Additionally, 2 patients were identified with STING-associated vasculopathy with onset in infancy linked to the TMEM173 variant. One patient exhibited chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperature due to PSMB8, and another patient had DNase II. Moreover, 8 patients presented with rare interferonopathy conditions, including three with ISG15, 3 with ZNFX1, 1 with the SOCS1 variant, and 1 the STAT1 variant. Of 12 variants, six (50%) found to have novel genetic variants. The most frequent features were fever (75%), neurology (70%), mucocutaneous (60%), gastrointestinal (50%), and pulmonary (50%). Hypogammaglobinaemia and recurrent infections were seen in (45%) and (20%), respectively. Fifteen patients (75%) had elevated inflammatory markers. The majority of patients received intensive treatment, including corticosteroids, JAK inhibitors, IVIG, and various immunosuppressive agents. Despite these interventions, a partial response to treatment was observed, and cumulative disease damage primarily manifested as growth failure and developmental delay.</p><p><strong>Conclusions: </strong>Our findings support the previous reports; early-onset fever, neurology, and respiratory features should raise the suspicion of interferonopathies. However, there is eminent evidence of phenotypic variability. Our data also expanded the spectrum of clinical findings in relation to novel genetic variants.</p>","PeriodicalId":10274,"journal":{"name":"Clinical and experimental rheumatology","volume":" ","pages":"2295-2302"},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141554292","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":"RAGE signalling contributes to oxidative stress and inflammation in knee osteoarthritis patients with metabolic syndrome.","authors":"Uzma N Awan, Rizwana S Waraich, Ruqaya Nangrejo, Syed Shahid Noor, Iftikhar A Siddiqui, Kashif Ikram","doi":"10.55563/clinexprheumatol/t3mejo","DOIUrl":"10.55563/clinexprheumatol/t3mejo","url":null,"abstract":"<p><strong>Objectives: </strong>Metabolic factors play significant role in the natural history of knee osteoarthritis (KO). There is a limited understanding of molecular and cellular events that give rise to the disease in patients. This study explored the possible cellular mechanisms by which metabolic syndrome leads to KO.</p><p><strong>Methods: </strong>This cross-sectional study enrolled 80 subjects with KO who fulfilled the ACR diagnostic criteria and were undergoing total knee replacement surgery. The patients were divided into two groups: KO patients without metabolic syndrome and KO patients with metabolic syndrome.</p><p><strong>Results: </strong>We hypothesised that metabolic syndrome may accelerate pathogenesis of OA by enhanced RAGE axis in articular cartilage and Infrapatellar fat pad of the knee joint. We have found enhanced protein expression of receptor for advanced glycation end products (RAGE) and its ligands AGEs and HMGB-1 in knee joint tissue of KO patients with metabolic syndrome as compared to KO patients without metabolic syndrome. Further downstream, the gene expression of oxidative stress regulators such as NADPH and inflammation, NFĸB were upregulated in KO patients with MetS as compared to KO patients alone. Higher levels of advanced oxidation products and inflammatory marker IL-17 were exhibited in synovial fluid of KO patients with metabolic syndrome. The enhanced levels of these oxidative stress and inflammatory markers were reflected in the serum of KO patients with metabolic syndrome as well.</p><p><strong>Conclusions: </strong>We conclude that enhanced function of RAGE axis could be one of the mechanisms by which metabolic syndrome leads to KO.</p>","PeriodicalId":10274,"journal":{"name":"Clinical and experimental rheumatology","volume":" ","pages":"2258-2264"},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141615971","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":"Comparison of SARS-COV-2 humoral response between rheumatoid arthritis, psoriatic arthritis and spondyloarthritis patients and controls in two unvaccinated cohorts.","authors":"Adeline Ruyssen-Witrand, Chloé Dimeglio, Erika Nogue, Nicolas Molinary, Thao Pham, Cécile Gaujoux-Viala, Corinne Miceli-Richard, Olivier Fogel, Fabrice Herin, Guillaume Martin-Blondel, Francis Berenbaum, Véronique Breuil, Isabelle Chary-Valckenaere, Cyrille Confavreux, Valérie Devauchelle-Pensec, Bruno Fautrel, René-Marc Flipo, Denis Mulleman, Christophe Richez, Anne Tournadre, Olivier Vittecoq, Arnaud Constantin, Jacques Izopet, Jacques Morel","doi":"10.55563/clinexprheumatol/48440j","DOIUrl":"10.55563/clinexprheumatol/48440j","url":null,"abstract":"<p><strong>Objectives: </strong>To compare the humoral response after a SARS-CoV-2 infection in an inflammatory rheumatic disease population with a healthy control population in a case-control study.</p><p><strong>Methods: </strong>Cases: between March and September 2021, all consecutive unvaccinated patients followed for rheumatoid arthritis (RA), spondyloarthritis (SpA) or psoriatic arthritis (PsA) in 16 hospitals in France were systematically screened with a SARS-CoV-2 serological test. Patients with a positive test were included in the COVID-RIC-2 cohort.</p><p><strong>Controls: </strong>between June and July 2020, healthcare professionals working in the Toulouse University Hospital were screened with a SARS-CoV-2 serological test. Those with a positive test were included in the COVID-BIOTOUL cohort and matched to those from COVID-RIC-2 by age, sex and time-sampling on infection date.</p><p><strong>Analyses: </strong>total SARS-CoV-2 antibody titres were centrally measured and compared.</p><p><strong>Results: </strong>95 patients from COVID-RIC-2 (mean age 49 years, 76% females, median delay of COVID infection: 149 days) including 48 RA, 33 SpA and 14 PsA were compared to 95 matched controls. Globally, there was no significant difference of SARS-CoV-2 antibody titres between both populations: 155 Binding Antibody Units (BAU) (IQR:7-376) in COVID-RIC-2 vs. 120 BAU (IQR:35-320) in COVID-BIOTOUL. There was a trend towards higher antibody titres in patients from COVID-RIC-2 with severe COVID-19 symptoms. In COVID-RIC-2, there was no impact of age, sex, time-sampling or underlying disease on antibody titres and patients taking glucocorticoids, abatacept or rituximab trended toward having lower antibody titres after COVID-19 infection.</p><p><strong>Conclusions: </strong>This study provides reassuring data on humoral response after COVID-19 infection in patients treated with disease-modifying anti-rheumatic drugs.</p>","PeriodicalId":10274,"journal":{"name":"Clinical and experimental rheumatology","volume":" ","pages":"2141-2149"},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142496176","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":"The epigenetic effects of glucocorticoids, sex hormones and vitamin D as steroidal hormones in rheumatic musculoskeletal diseases.","authors":"Emanuele Gotelli, Rosanna Campitiello, Elvis Hysa, Stefano Soldano, Andrea Casabella, Carmen Pizzorni, Sabrina Paolino, Alberto Sulli, Vanessa Smith, Maurizio Cutolo","doi":"10.55563/clinexprheumatol/t03g31","DOIUrl":"10.55563/clinexprheumatol/t03g31","url":null,"abstract":"<p><p>Chronic rheumatological diseases are multifactorial conditions in which both the neuroendocrine hormone pathway, including cortisol, sex hormones and active vitamin D3 (calcitriol), all deriving from cholesterol, and the epigenetic modifications that they cause play an important role. In fact, epigenetics modulates the function of the DNA of immune cells, through three main mechanisms: DNA methylation, modifications to the histones that make up chromatin and production of non-coding RNAs (microRNA - miRNA). In this narrative review, the main data regarding the epigenetic modifications induced by cortisol, 17β-oestradiol, progesterone, testosterone and calcitriol on immune cells were collected, discussing how these can interfere in the predisposition and course of chronic rheumatological diseases (i.e. rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis). An ever-increasing number of miRNAs have been identified, which are produced by neuroendocrine hormones and can influence the inflammatory-fibrotic response at various levels. Concerning the involvements of the neuro-endocrine-immunology within the pathophysiology of rheumatic diseases, the epigenetic effects induced by steroid hormones must be taken into consideration to evaluate their impact on the progression of the single condition and even inside the single patient.</p>","PeriodicalId":10274,"journal":{"name":"Clinical and experimental rheumatology","volume":" ","pages":"2131-2140"},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104905","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}