Longitudinal evolution of rheumatoid factor-expressing lymphoma precursors in a patient with Sjögren's disease.

Even though immune checkpoint inhibitors (ICI) remain effective treatments for an increasing number of cancers, they are also liable to cause immune-related adverse events (irAE). Rheumatologic manifestations occur in 5-10 % of patients. The most common rheumatologic irAEs are immune checkpoint-induced inflammatory arthritis (ICI-IA) and immune checkpoint-induced polymyalgia rheumatica (ICI-PMR). While ICI-IA can mimic rheumatoid arthritis (RA), it is predominantly immuno-negative (absence of rheumatoid factor and anti-citrullinated peptide antibodies) and can persist subsequent to r ICI cessation. ICI-PMR is usually reversible. First-line treatments consist of corticosteroids at the lowest effective doses and are given for short periods. They are aimed at reducing symptoms such as joint swelling, with minimal (if any) disruption of ICI therapy. In patients with corticoid dependence at a dose > 10 mg/day, second-line treatments include methotrexate and biologic therapy: anti-IL6 and TNF inhibitors (TNFi). Management of these manifestations requires balancing the opposed perspectives of effective arthritis control and possible cancer progression. When possible, ICI cessation should be avoided, and immunomodulating therapies are to be applied cautiously. Co-management by patients, oncologists, and rheumatologists is of crucial importance when balancing the risks and benefits of treatment.

Biomarkers play acentral role in rheumatology for early detection, prognostic assessment, treatment stratification, and evaluation of the disease course, as early and targeted therapies are crucial for prognosis. In rheumatoid arthritis, rheumatoid factors and anti-citrullinated protein (CCP) antibodies are established diagnostic and prognostic biomarkers. For seronegative spondyloarthritis, HLA-B27 is the most important diagnostic marker, particularly in axial spondyloarthritis. In connective tissue diseases, antinuclear antibodies are essential for diagnosis, but their use for assessing activity is limited. Specific autoantibodies, complement factors, and urinary biomarkers are prognostically particularly relevant in systemic lupus erythematosus. In vasculitis diagnostics, anti-neutrophil cytoplasmic antibodies (ANCAs; anti-myeloperoxidase and anti-proteinase3) are essential for small-vessel vasculitis, while serological markers for large-vessel vasculitis are lacking.

Evidence suggests that Mycobacterium avium subspecies paratuberculosis (MAP) may contribute to autoimmune diseases such as rheumatoid arthritis (RA), partly through effector proteins—particularly the tyrosine phosphatases PtpA and PtpB—that modulate macrophage signaling and promote bacterial persistence. This study evaluated whether serum antibodies against these proteins serve as biomarkers of RA. Humoral responses to PtpA and PtpB were quantified in Mexican RA patients (n = 100) and healthy controls (n = 100) using in-house ELISAs. Associations with disease activity (DAS28), ROC performance, and logistic regression models were assessed. Results showed that anti-PtpB antibody levels were significantly higher in patients with RA than in healthy controls (median OD 0.185 vs. 0.080; p < 0.0001) and had moderate discriminative capacity (AUC = 0.762). Anti-PtpB reactivity increased with higher disease activity and showed a significant positive association with DAS28 (p < 0.05). In addition, there was a functional disability measured by HAQ (p < 0.001), as well as moderate correlations with erythrocyte sedimentation rate and rheumatoid factor. A combined logistic regression model integrating both antibodies markedly improved diagnostic accuracy (AUC = 0.934), achieving high sensitivity (90%) and specificity (89%). These findings suggest a potential association of MAP with RA immunopathogenesis and indicate that combined quantification of anti-PtpA and anti-PtpB antibodies captures complementary and non-redundant immunological information. This combined serological approach may enhance RA diagnosis and provide clinically relevant insights into disease activity and severity.

A 69-year-old woman with previously treated endometrial carcinoma developed progressive anemia, with hemoglobin declining to 4.2 g/dL and later stabilizing between 6-7 g/dL despite preserved leukocyte and platelet counts. Laboratory evaluation demonstrated elevated erythropoietin, lactate dehydrogenase (LDH), bilirubin, vitamin B12, and iron levels, prompting further investigation. The key diagnostic finding was the presence of neutrophil erythrocyte rosettes on peripheral smear-neutrophils encircled by antibody-coated red cells through Fc-mediated binding. This rare morphologic phenomenon, seldom described in autoimmune hemolytic anemia (AIHA), provided a crucial early clue, especially in the absence of spherocytes or red cell fragments. Reticulocytosis supported ongoing hemolysis, and monospecific direct antiglobulin test (DAT) later confirmed IgG-mediated AIHA. Elevated rheumatoid factor suggested an autoimmune predisposition. Recognition of neutrophil-erythrocyte rosettes in this case directly guided confirmatory testing and diagnosis, emphasizing their diagnostic significance.

This study aimed to assess the prevalence of comorbidities among patients with rheumatoid arthritis (RA) and identify factors associated with it. A cross-sectional study was conducted at 2 tertiary care hospitals among 653 patients with RA. Data on demographics, poor prognostic factors (high erythrocyte sedimentation rate [ESR], C-reactive protein [CRP], rheumatoid factor, anticyclic citrullinated peptide antibody titers, and Disease Activity Score in 28 joints [DAS28] > 5.1), and comorbidities were collected through a structured questionnaire and medical record review. Comorbidities were quantified by the Charlson Comorbidity Index (CCI). Logistic regression analyses were used to identify associated factors. A total of 646 (98.9%) patients had ≥ 1 comorbidity. The most prevalent were dyslipidemia (75.8%), obesity (58.7%), hypertension (42.7%), type 2 diabetes mellitus (30.3%), and osteoporosis (OP; 15.6%). Age ≥ 45 years was independently associated with coronary artery disease (odds ratio [OR] 9.71, 95% CI 1.91-178.00), OP (OR 19.60, 95% CI 5.96-121.00) and infectious diseases (OR 1.60, 95% CI 1.03-2.54). Female sex was associated with lower cardiovascular risk (OR 0.27, 95% CI 0.11-0.62), whereas female sex was associated with increased odds of OP (OR 3.55, 95% CI 1.71-8.37) and gastrointestinal (GI) disorders (OR 2.18, 95% CI 1.37-3.56). The use of targeted synthetic and biologic disease-modifying antirheumatic drugs increased the risk of infection (OR 14.80 and 4.11, respectively). High DAS28-CRP and ESR values were linked to GI comorbidities. The CCI survival index was significantly lower in older patients (≥ 45 years; mean 68.7 [SD 26.7]) than in younger patients (mean 93.3 [SD 6.7], P < 0.001). The prevalence of multimorbidity is high among patients with RA in Bangladesh, particularly early cardiovascular disease risk.

A substantial proportion of individuals with palindromic rheumatism develop rheumatoid arthritis (RA). This randomized, open-label, multicenter trial aimed to assess whether 2 years of treatment with abatacept (n = 34; 125 mg subcutaneous injections weekly during the first year and every 2 weeks during the second year) compared with oral hydroxychloroquine (n = 36; 5 mg kg-1 per day) could reduce the frequency of RA development in individuals with palindromic rheumatism positive for rheumatoid factor and/or anticitrullinated protein antibody. The primary outcome was the development of persistent arthritis that fulfilled the 2010 RA classification criteria of the American College of Rheumatology and the European Alliance of Associations for Rheumatology, as evaluated by the participant clinicians during the 24 months of follow-up. Secondary outcomes included the frequency, intensity and duration of joint attacks, the proportion of patients in remission and the frequency of adverse events. In the primary analysis, in the modified full analysis set with failure imputation, 7 (20.6%) of the 34 participants treated with abatacept and 18 (50.0%) of the 36 participants treated with hydroxychloroquine developed RA during the 24 months of follow-up (P = 0.010; risk difference 29.4%, 95% confidence interval 8.2 to 50.7), meeting the primary endpoint. Using the available-data-only approach, the corresponding figures were 3 (10.0%) of 30 individuals and 10 (35.7%) of 28 individuals, respectively (P = 0.019). Compared with participants treated with hydroxychloroquine, participants treated with abatacept had a significantly longer time to progression to RA (hazard ratio 0.27, 95% confidence interval 0.07 to 0.96; log-rank test P = 0.0299). Abatacept was also associated with a reduced intensity of joint attacks and a higher frequency of symptom remission; however, there were no differences in the frequency of attacks between the two study drugs. No relevant differences in the evolution of antimodified peptide and/or protein antibody titers were observed between the two treatment arms. Both drugs were well tolerated. In patients with seropositive palindromic rheumatism, compared with hydroxychloroquine, abatacept given for 2 years reduced the risk of progression to RA and improved symptoms. ClinicalTrials.gov identifier NCT03669367 and EudraCT no. 2017-004543-20.

In rheumatoid arthritis (RA) mortality is higher than in the general population and is due to cardiovascular diseases (CVD) associated with traditional risk factors (TRFs) and autoimmune inflammation. An early predictor of CVD is arterial stiffness (AS), determined by pulse wave velocity (PWV) and the augmentation index (AIx). AS assessment can be used for cardiovascular risk stratification, complementing PWV and improving the accuracy of predicting cardiovascular events. The aim – to study the parameters of arterial stiffness in patients with rheumatoid arthritis, their relationship with clinical and immunological parameters and cardiovascular diseases traditional risk factors. Materials and methods . The study included 100 female patients with RA (90% of whom were seropositive for rheumatoid factor (RF)) with a median age of 43 [34; 51] years, disease duration of 5.3 [3.0; 12.0] years. High activity according to the DAS28 (Disease Activity Score 28) was predominantly present in 61% of RA patients. Extra-articular manifestations were detected in 37%, and complications – in 22%. The control group included 30 healthy women matched for age. All subjects underwent determination of TRFs and AS parameters – PWV and AIx. Results . RA patients, compared with controls, had higher PWV values: 7.1 [6.1; 8.0] m/s versus 6.2 [6.0; 7.0] m/s, respectively (p=0.004). No difference in AIx was observed. PWV and AIx correlated with age (r=0.655 and r=0.351), QRISK-3 (r=0.627 and r=0.504), intima-media thickness (r=0.463 and r=0.37), the presence of atherosclerosis (r=0.439 and r=0.295), and RA duration (r=0.271 and r=0.335) (p&lt;0.05). AIx was associated with anti-cyclic citrullinated peptide (anti-CCP; r=0.204; p=0.04). Elevated AS values were more common in patients with arterial hypertension, menopause, overweight, RF+/antiCCP+ patients, and with the development of complications (p&lt;0.05). Smoking and a history of cardiovascular disease did not significantly affect AR. We registered higher absolute values of PWV and AIx in hypertension (7.7 [7.0; 9.2] versus 6.8 [5.8; 7.8] m/s, 3.4 [0.9; 8.4] versus 0.4 [–0.7; 4.2]%, respectively) and in menopause (7.9 [7.1; 8.8] versus 6.6 [5.7; 7.7] m/s, 4.4 [1.2; 11.2] versus 0.3 [–0.8; 3.7]%, respectively; p&lt;0.05). In seropositive RA, AIx was higher compared to seronegative: 1.5 [–0.2; 5.0] versus –1.0 [–2.4; 3.6]% (p=0.002). Patients who developed RA complications had higher PWV and AIx values: 7.4 [6.8; 8.8] versus 7.0 [6.0; 7.9] m/s and 4.0 [1.2; 7.9] versus 0.7 [–0.5; 4.3]%, respectively (p&lt;0.05). In patients receiving glucocorticoids and disease-modifying antirheumatic drugs, PWV and AIx values were higher than in patients without therapy. Conclusion . The obtained results highlight the multifactorial mechanism of AS in RA. These data can serve as the basis for more accurate risk stratification and personalized therapy in patients with RA.

CD161⁺ regulatory T cells (Tregs) are involved in rheumatoid arthritis (RA) pathogenesis. This study aimed to investigate the levels of circulating CD161⁺ Tregs in RA patients and to evaluate their associations with clinical features, laboratory indicators, and therapeutic responses. A total of 172 RA patients meeting the 2010 ACR/EULAR criteria and 110 age- and sex-matched healthy controls (HCs) were enrolled. The proportion of CD161⁺ Tregs in peripheral blood was quantified by flow cytometry. Correlations between CD161⁺ Treg levels and clinical manifestations, laboratory parameters, and disease activity scores (DAS28) were assessed. Twenty-four RA patients were longitudinally followed to assess post-treatment changes in CD161⁺ Tregs and disease activity. The proportions of CD161⁺ Tregs of the total Treg and CD4⁺ T cell populations were significantly elevated in RA patients compared to HCs (P < 0.001). Higher CD161⁺ Treg levels were associated with smoking history (P = 0.033) and inversely correlated with the presence of dry eye sicca (P = 0.030). These subsets showed positive correlations with IgA, IgM, rheumatoid factor (RF), RF-IgG, TNF-α+CD4+ T cell, Th17 and DAS28-ESR (P < 0.05), while exhibiting negative correlations with naïve Th cells and effector T (Teff) cells (P < 0.05). CD161⁺ Treg levels were higher in patients with long-standing RA (LRA) than in HCs (P < 0.05), and in patients with high disease activity (DAS28-ESR > 5.1) compared to those with moderate/low disease activity (P < 0.05). After treatment, decreased CD161⁺ Treg and disease activity scores were observed (P < 0.05), which were particularly pronounced in the group receiving csDMARDs combined with tocilizumab (an IL-6 inhibitor). However, csDMARDs alone or in combination with JAK inhibitors showed no or only partial efficacy. CD161⁺ Tregs are elevated in RA and associated with disease activity and immunologic indicators. CD161⁺ Tregs might serve as a biomarker for assessing RA disease activity. Key Points • The proportion of circulating CD161⁺ regulatory T cells is significantly increased in rheumatoid arthritis patients compared to healthy controls. • Higher CD161⁺ Treg levels correlate positively with disease activity scores (DAS28-ESR) and key serological markers (RF, IgA, IgM). • CD161⁺ Treg levels decreased significantly following effective therapy, paralleling reductions in disease activity,particularly in the group receiving csDMARDs combined with tocilizumab. • CD161⁺ Tregs show positive correlations with pro-inflammatory cells (TNF-α+CD4+T cell, Th17) and peripheral T follicular helper cells, underscoring their role in RA immunopathology.

Ethnopharmacological validation of Calotropis gigantea L. flower extract against rheumatoid arthritis: Anti-arthritic and immunomodulatory effects in a CFA-induced rat model.

When troponin results lie: A narrative review and practical approach to spurious hypertroponinemia.

To evaluate the anti-arthritic and disease-modifying potential of stigmasterol (STG), a plant-derived bioactive compound, in Freund's Complete Adjuvant (FCA)-induced polyarthritis in rats. Experimental arthritis was induced in albino Wistar rats using FCA. The anti-arthritic efficacy of STG was assessed through primary and secondary paw edema, arthritis index, and body-weight changes. Biochemical, haematological, and immunological parameters were evaluated, along with mRNA expression of key mediators using RT-PCR. Histopathological analysis of bone, kidney, and spleen tissues, as well as macroscopic and radiographic joint assessments, was performed. STG was administered orally at doses of 150 and 300mg/kg and compared with methotrexate (MTX). FCA induction produced severe arthritic manifestations, including marked paw swelling, an elevated arthritis index, increased rheumatoid factor and anti-cyclic citrullinated peptide levels, and upregulation of inflammatory mediators (TNF-α, NF-κB, IL-1β, IRAK, and IL-17), along with radiographic joint damage and histopathological abnormalities. STG treatment significantly reduced paw edema, improved arthritis severity, and normalized biochemical and haematological parameters in a dose-dependent manner. The higher dose (300mg/kg) showed efficacy comparable to MTX and significantly enhanced IL-10 expression, indicating restoration of immune balance. Stigmasterol exhibits potent anti-arthritic, disease-modifying, and organ-protective effects in FCA-induced arthritis, highlighting its therapeutic potential in arthritis management.

Abstract Introduction With advances in CFTR modulator therapy and multidisciplinary care, adults with cystic fibrosis (CF) are living longer and increasingly developing non-CF-related comorbidities. Autoimmune interstitial lung disease (ILD), however, remains exceptionally rare and can be easily overlooked due to overlapping respiratory symptoms and imaging findings. We describe a case of diffuse cutaneous systemic sclerosis (SSc) associated ILD in a patient with long-standing CF, emphasizing the need for diagnostic vigilance when CF patients present with unexplained respiratory decompensation. Case A 67-year-old man with well-controlled cystic fibrosis (genotype W1282X/D1152H), maintained on elexacaftor/tezacaftor/ivacaftor (Trikafta), presented with progressive cough and dyspnea. He was initially treated for a presumed acute CF pulmonary exacerbation with intravenous tobramycin and Ceftazidime/avibactam without improvement. Given the lack of clinical response, his CFTR modulator therapy was subsequently switched to vanzacaftor/tezacaftor/deutivacaftor, yet his respiratory status continued to deteriorate with worsening exertional dyspnea and hypoxia. Repeat CT chest demonstrated progressive lower-lobe reticular changes and ground-glass opacities suggestive of nonspecific interstitial pneumonia with early fibrosis. Physical examination revealed skin tightening and Raynaud’s phenomenon. Serologic evaluation showed ANA 1:640 (speckled pattern), elevated Scl-70 antibody, and positive rheumatoid factor, prompting rheumatology referral and a diagnosis of systemic sclerosis-associated ILD. Right heart catheterization confirmed WHO Group 3 pulmonary hypertension. He did not tolerate mycophenolate or inhaled treprostinil and was subsequently initiated on tocilizumab. He declined antifibrotic therapy and lung transplantation, opting for a palliative approach. Discussion To our knowledge, this represents the first reported case of systemic sclerosis-associated ILD developing in a patient with CF. The coexistence of these two fibrosing lung diseases poses significant diagnostic and therapeutic challenges, as both can produce overlapping radiographic patterns and progressive functional decline. Management is further complicated by the need to balance immunosuppression against infection risk in a population already prone to recurrent airway colonization. While no evidence currently links CFTR modulators or chronic CF-related inflammation to the pathogenesis of systemic sclerosis, this case underscores a clinically meaningful intersection that expands the spectrum of pulmonary complications seen in the aging CF population Conclusion This case underscores the importance of maintaining a broad differential when evaluating respiratory decline in patients with cystic fibrosis, as non-CF etiologies may closely mimic pulmonary exacerbations. Early recognition of atypical comorbidities and engagement of a multidisciplinary care team are essential to ensure accurate diagnosis, guide complex management decisions, and optimize outcomes in the growing adult CF population. This abstract is funded by: None

The human microbiota is implicated in the development and progression of rheumatoid arthritis (RA). Given the increased RA burden in women and well-known correlations between the vaginal microbiota and local inflammation, we seek to understand the vaginal microenvironment in the context of RA pathology. Self-collected vaginal swabs and questionnaires on dietary, menstrual, and health information were obtained from 36 RA and 50 demographically-matched control women, 18-63 years of age. Medication regimen, along with disease activity and severity, was captured for the RA cohort. Vaginal swabs were subjected to long-read 16S rRNA gene sequencing, multiplex cytokine analyses, and quantification of rheumatoid factor, C-reactive protein, and anti-citrullinated protein antibodies (ACPAs). Vaginal microbial richness and Peptoniphilus and Prevotella, among other rare taxa, were elevated in RA versus control samples. Vaginal interleukin (IL)-18 and epidermeal growth factor (EGF) levels were increased in the RA group; IL-18 correlated with multiple microbial features, whereas EGF levels were not associated with bacterial composition or other host factors. When faceted by diet and menopausal status, several immune markers were increased in the RA vaginal environment. Vaginal ACPAs were higher in the RA group and positively correlated with Streptococcus and multiple vaginal inflammatory cytokines. We describe vaginal microbial and immunological differences in women with RA, particularly when accounting for diet and menopausal status, and disease activity and severity. This work opens a new avenue in the multidisciplinary approach to RA patient care.IMPORTANCERheumatoid arthritis (RA) is a debilitating autoimmune disease that disproportionately impacts women. Although it is widely recognized that microbial factors can trigger or aggravate RA symptoms and alter disease progression, it is unknown whether RA impacts the microbiota and immune responses within the vaginal tract. In this study, we compare the vaginal microbial communities and immune (cytokine) profiles in women with RA and healthy controls. Within RA patients, we also evaluate how these factors relate to clinical RA symptoms, RA biomarkers, and RA-related medications. Overall, we found that RA was associated with increased microbial diversity and multiple inflammatory markers, some of which were also associated with RA biomarkers and disease activity. These findings suggest that the vaginal tract may be an additional tissue impacted by RA disease, and further research is needed to understand mechanisms and potential for therapeutic intervention.

To investigate longitudinal trends in the proportion of seronegative rheumatoid arthritis (RA) and to compare clinical outcomes between seronegative and seropositive patients in a Japanese single-centre cohort. We included 4,354 RA patients with a disease duration < 4years from the Institute of Rheumatology, Rheumatoid Arthritis cohort. Seronegativity was defined as the absence of both rheumatoid factor (RF) and anti-citrullinated peptide (CCP) antibody. We assessed the association between enrolment period and seronegativity using multivariable logistic regression. A mixed-effects model was used to compare 3-year trends in Disease Activity Score in 28 joints using erythrocyte sedimentation rate (DAS28-ESR), clinical disease activity index (CDAI), and the Japanese version of the Health Assessment Questionnaire (J-HAQ) scores between serostatus groups. The proportion of seronegative RA increased from 14.4% in 2000-2010 to 17.9% in 2011-2021. The later period was associated with seronegativity (adjusted odds ratio [95% confidence interval]: 1.32 [1.08-1.61]), negative RF (1.23 [1.05-1.45]), and negative anti-CCP antibody (1.31 [1.11-1.56]). At 3years, seronegative patients had better mean (95% confidence interval) CDAI (4.50 [3.48-5.53] vs. 5.57 [4.66-6.48]), DAS28-ESR (2.13 [1.93-2.32] vs. 2.54 [2.37-2.71]), and J-HAQ (0.43 [0.33-0.54] vs. 0.52 [0.42-0.61]) compared with seropositive patients. The proportions of patients achieving J-HAQ remission were comparable between the groups. The proportion of seronegative RA has increased significantly over time. Seronegative patients demonstrate a favourable disease course with a higher rate of remission compared with seropositive patients, thus identifying them as a distinct RA subgroup. Key Points • The proportion of seronegative rheumatoid arthritis increased over time in a large Japanese cohort. • Patients with seronegative rheumatoid arthritis had significantly higher rates of clinical remission over 3years. • The increasing proportion and distinct prognosis of seronegative rheumatoid arthritis may require specific management strategies.

Background: Sjögren’s disease (SjD) is a chronic autoimmune rheumatic disorder primarily affecting exocrine glands, leading to dryness and systemic involvement. B-cell hyperactivity and autoantibody production drive its pathogenesis and contribute to increased lymphoma risk. Although several long-term studies exist, we present a review of a closely monitored cohort assessed over 40 years. Methods: Retrospective observational study at University College London Hospital included patients fulfilling the 2016 ACR/EULAR criteria for SjD between 1986–2025. Patients with associated SjD were excluded. Associations between serological markers and clinical features were analysed using chi-square or Fisher’s exact tests (p < 0.05). Differences between ethnic groups were also assessed. Results: 283 patients were included, 93.3% female, with mean age at diagnosis of 50.1 ± 15.2 years and mean follow-up of 12.5 ± 8.6 years. Common manifestations were fatigue (61.5%), parotid swelling (30.5%), arthritis (25.8%), and Raynaud’s phenomenon (27.6%). Anti-Ro and anti-La antibodies were present in 75.7% and 45.2%, respectively; rheumatoid factor in 57.3%. Lymphoma developed in 9.9% (mostly non-Hodgkin MALT) and was associated with hypergammaglobulinemia (p = 0.03; RR = 2.56) and parotid swelling (p < 0.001; RR = 5.53). Serological markers correlated with systemic features including lymphadenopathy, vasculitis, and pulmonary involvement. Caucasian patients showed higher mortality (p < 0.001; RR = 3.89) and peripheral nervous system involvement (p = 0.02; RR = 2.18), and less ANA positivity (p = 0.004; RR = 0.88), anti-Ro (p = <0.001; RR = 0.77) and RF (p = 0.04; RR = 0.81) and hypergammaglobulinemia (p = <0.001; RR = 0.63) when compared with non-Caucasian patients. Conclusions: This long-term cohort confirms the strong association between B-cell activation markers and adverse outcomes in Sjögren’s disease. Hypergammaglobulinemia and parotid swelling emerged as key predictors of lymphoma, supporting their role in risk stratification. These findings reinforce the importance of long-term monitoring and may help guide personalized clinical management and surveillance strategies.

The clinical and immunologic significance of rheumatoid factors (RF) in psoriatic arthritis (PsA) remains unclear. We aimed to determine the frequency and impact of RF positivity on clinical outcomes and biologic (b) disease-modifying anti-rheumatic drug (DMARD) discontinuation in PsA. Patients enrolled after 1996 from a large PsA cohort were included for this study. RF was tested annually and was defined as ever positive or newly positive (excluding those positive at enrolment). Associations of RF with clinical outcomes, including achievement of minimal disease activity (MDA), components of MDA, and bDMARD discontinuation, were assessed using univariable (UV) and multivariable (MV) generalized estimating equations. Among 1074 patients, RF positivity was observed in 173 (16.1%) overall, including 55 (5.1%) who were positive at baseline. RF positivity was significantly associated with reduced odds for achievement of MDA (MV, OR 0.53, 95% CI 0.37-0.77), driven by worse patient pain, patient global, and physical function, particularly in the bDMARD subgroup. These associations persisted in the bDMARDs subgroup when analyses were restricted to new RF positivity. Additionally, ever and new RF positivity was associated with increased odds for bDMARD discontinuation (MV, OR 2.65, 95% CI 1.34-5.24 and 2.78, 95% CI 1.57-4.92, respectively) independent of joint and skin disease activity. RF was observed in 16.1% of the cohort, with 5.1% being positive at baseline. RF positivity was associated with lower odds for achievement of MDA and with bDMARD discontinuation.

To compare the clinical characteristics and outcomes between patients with rheumatoid factor (RF)-positive and RF-negative polyarticular juvenile idiopathic arthritis (pJIA). A retrospective analysis was conducted on clinical data of 131 children diagnosed with pJIA at the Children's Hospital, Zhejiang University School of Medicine from January 2019 to January 2025. Patients were divided into an RF-positive group (n=59) and an RF-negative group (n=72) based on serum RF status. Disease activity was assessed using the Juvenile Arthritis Disease Activity Score-27 (JADAS-27). All patients were followed for at least 6 months, with a maximum follow-up duration of 6 years. Clinical features, laboratory findings, and outcomes were compared between the two groups. Among the 131 pJIA patients, 122 (93.1%) had high disease activity at baseline. Compared with the RF-negative group, the RF-positive group had a higher proportion of females (58.3% vs. 84.7%, P<0.01), an older age at onset (7.14±3.98 years vs. 8.86±4.02 years, P<0.05), and a higher prevalence of interstitial lung disease (4.2% vs. 23.7%, P<0.01). The most frequently affected joints were the wrist in the RF-positive group, and the knee joints in the RF-negative group. At baseline, serum levels of IL-2, IL-6, IL-10, and tumor necrosis factor-α were significantly higher in the RF-positive group than those in the RF-negative group (all P<0.05). A total of 101 patients (77.1%) received biologic-targeted therapies, 46 (78.0%) in RF-positive group, and 55 (76.4%) in RF-negative group. Among them, 23 RF-positive patients (50.0%) and 12 RF-negative patients (21.8%) required two or more biologic-targeted drugs. RF positivity was identified as an independent risk factor for the use of two or more biologic-targeted drugs (OR=3.232, 95%CI: 1.109-9.421, P<0.05). Both groups showed significant reductions in JADAS-27 scores at 3, 6, 12, 24, 36, 48, 60, 72 months after treatment initiation compared with baseline (all P<0.01), with no significant differences in JADAS-27 scores or remission rates between the two groups at any follow-up time point (all P>0.05). The median time to achieve first clinical remission after treatment was 24 months in both groups (P>0.05). No significant differences were observed in remission rates or the proportion of patients requiring two or more biologic-targeted drugs among different types of biologic-targeted drugs (all P>0.05). Children with RF-positive pJIA showed higher baseline inflammatory status and a higher incidence of pulmonary involvement, yet they achieved comparable remission rates to those with RF-negative pJIA. Biologic-targeted therapies may contribute to improved remission rates and outcomes, but RF-positive patients may require switching or combination therapy with different targets to achieve clinical remission.

Polymyalgia rheumatica (PMR) is a chronic disease affecting the musculoskeletal system in patients over 50 years of age and is characterized by bilateral restriction of movement in the shoulder and hip joints, as well as prolonged morning stiffness. This disease is characterized by an increase in the erythrocyte sedimentation rate and the concentration of C-reactive protein in the blood. A clinical case of PMR in a 67-year-old patient with postmenopausal osteoporosis, which complicates treatment with glucocorticoids, is described. In addition to the mandatory diagnostic criteria, additional signs were identified, the total of which amounted to 6 points: morning stiffness lasting more than 45 minutes (2 points), pain in the hip joints and limited mobility of those joints (1 point), absence of an increase in the level of rheumatoid factor in the blood serum (2 points), and the presence of ultrasound signs of synovitis and tenosynovitis of the long head of the biceps muscle in both shoulder joints (1 point). A positive trend in clinical condition and laboratory parameters was observed during the treatment of PMR with methylprednisolone. The monitored parameters of bone mineral density of the spine and femoral neck indicated that continuation of denosumab therapy for the prevention of recurrent fractures, initiated even before the diagnosis of PMR due to concomitant postmenopausal osteoporosis, was advisable during glucocorticoid administration.

Immune dysfunction in rheumatoid arthritis (RA) is a contributing factor to the development of peripheral neuropathy (PN). The objective of our study was to investigate the biological and clinical factors associated with PN in patients with RA. We conducted a retro-prospective cross-sectional study. A total of 63 patients with RA were included. They were divided into two groups, 18 with PN and 45 without PN. Participants with PN were those with a pathological electroneuromyogram (ENMG) with or without signs and symptoms of PN. Blood samples were taken for the measurement of rheumatoid factor (RF) and C-reactive protein (CRP). The concentration of anti-citrullinated peptide antibodies (ACPA) were collected from patient records. The significance threshold was set at a p-value <0.05. The majority of participants, 82.5% were female. The mean age was 51.86 ± 13.07 years. PN was present in 28.6% of the participants. RF and ACPA were positive in 71.4 and 77.8% of the participants, respectively. Severely active RA was significantly associated with the presence of PN (p < 0.001, OR = 55.13). RF concentrations were significantly higher in patients with PN. The area under the ROC curve for RF concentration in predicting PN in patients with RA was 0.7 (AUC = 0.7), patients with an RF > 169.10 IU/mL had a significant risk of presenting PN (p = 0.003, OR = 8.20). Severe rheumatoid arthritis is associated with PN. Inflammatory markers may play a key role in the pathogenesis and may provide valuable guidance for the early diagnosis of PN in RA.