Fatima K. Alduraibi

Cutaneous lupus erythematosus (CLE) is the most common organ manifestation in individuals diagnosed with systemic lupus erythematosus (SLE). CLE can occur either alone or in association with SLE; in the latter case, it substantially increases the occurrence of disease flares and can cause disfigurement. The clinical pathogenesis of CLE is well established, as exposure to ultraviolet (UV) light and/or other environmental triggers, such as smoking or drug use, can lead to keratinocyte death in genetically susceptible individuals. This in turn activates cytotoxic T cells, plasmacytoid dendritic cells (pDCs), and B cells, creating a continuous interaction between the innate and adaptive immune systems. This interaction plays a pivotal role in CLE development, driving the formation of skin lesions. However, the molecular mechanisms underlying these cutaneous manifestations are not yet fully understood. While significant advances have been made in SLE treatment over the past few decades, U.S. Food and Drug Administration (FDA)-approved therapies remain limited to hydroxychloroquine, glucocorticoids, belimumab, and anifrolumab. Although new therapies for CLE have emerged, given the highly heterogeneous nature of the condition, personalized medicine is essential to prevent disfigurement and systemic disease flares. Understanding the molecular pathogenesis of CLE is crucial for developing targeted therapies and improving patient outcomes. This review presents current insights into CLE pathogenesis, highlighting key mechanisms driving the disease and exploring recent advances in treatments that have shown promise in clinical practice.

Connective tissue disease-associated pulmonary arterial hypertension (CTD-PAH) is a progressive and high-risk subtype of PAH, with outcomes generally worse than those seen in idiopathic PAH. Early recognition and treatment are essential for improving survival, yet early-stage CTD-PAH remains challenging to identify, particularly for non-specialist clinicians. The 2022 ESC/ERS guidelines introduced several key updates that support an earlier diagnosis and more targeted management. These include a revised echocardiographic threshold for pulmonary hypertension probability (tricuspid regurgitation velocity >2.8 m/s), a lowered hemodynamic definition of PAH (mean pulmonary artery pressure >20 mmHg and pulmonary vascular resistance >2 WU), and a preference for annual screening using the DETECT algorithm in asymptomatic systemic sclerosis (SSc) patients. Additionally, novel therapeutic targets such as the activin/TGF-β pathway have been incorporated into updated treatment algorithms. Although CTD-PAH remains associated with worse outcomes than idiopathic PAH, recent advances in screening, risk assessment, and targeted therapies have begun to improve the trajectory of the disease. Early detection, personalized treatment, and comprehensive care are now key to transforming this high-risk condition into a more manageable one.

Background: Rheumatoid arthritis-associated interstitial lung disease (RA-ILD) is a well-described complication of rheumatoid arthritis (RA). The authors sought to describe the characteristics, treatment strategies, and outcomes of RA-ILD patients at 6 and 12 months. Methods: Patients treated at the medical center between 2010 and 2019 with ICD9 and ICD10 codes for RA and interstitial lung disease (ILD) meeting American College of Rheumatology 1987 or 2010 ACR/European League Against Rheumatism classification criteria were considered for inclusion. The diagnosis of RA-ILD was based on clinical features, pulmonary function testing (PFT), and high-resolution computed tomography (HRCT) findings. Baseline demographics, body mass index , serologic status, tobacco use, PFT and HRCT findings, and RA-ILD treatments at 0, 6, and 12 months were extracted and analyzed. Results: Forty-seven patients diagnosed with RA-ILD were included in this analysis. The median age at diagnosis was 64.7 years, and the median duration of follow-up was 30 months. Thirty-two patients (68.09%) had follow-up data available at 6 months and 27 (57.45%) had follow-up data at 12 months. Twenty-three (48.9%) patients received treatment for RA-ILD. Forty-three (90.6%) and 42 (88.9%) patients exhibited stability/improvement of RA-ILD at 6 and 12 months of follow-up, respectively. Progression of RA-ILD at 6 months was associated with tobacco use (P=.025); however, no specific variable was associated with RA-ILD progression at 12 months. Conclusions: Patients with RA-ILD receiving treatment tend to show improvement or stability in lung disease at 6 and 12 months, although high attrition rate and short follow-up preclude finding of additional factors associated with ILD. Trial registration: Not applicable. Cite this article as: Alduraibi FK, Haigney J, Surmachevska N, Sun D, Osborne JD, Danila MI. Profile of patients with rheumatoid arthritis-associated interstitial lung disease: A single-center. Eur J Rheumatol. 2025, 12(3), 0087, doi: 10.5152/eurjrheum.2025.24087.

Systemic lupus erythematosus (SLE) is a complex autoimmune disorder characterized by the production of autoreactive B and T cells and cytokines, leading to chronic inflammation affecting multiple organs. SLE is associated with significant complications that substantially increase morbidity and mortality. Given its complex pathogenesis, conventional treatments for SLE often have significant side effects and limited efficacy, necessitating the exploration of novel therapeutic strategies. One promising approach is the use of chimeric antigen receptor (CAR)-T-cell therapy, which has shown remarkable success in treating refractory hematological malignancies. This review provides a comprehensive analysis of the current use of CAR-T-cell therapy in SLE.

Lupus nephritis (LN), a major complication in individuals diagnosed with systemic lupus erythematosus, substantially increases morbidity and mortality. Despite marked improvements in the survival of patients with severe LN over the past 50 years, complete clinical remission after immunosuppressive therapy is achieved in only half of the patients. Therefore, timely detection of LN is vital for initiating prompt therapeutic interventions and improving patient outcomes. Biomarkers have emerged as valuable tools for LN detection and monitoring; however, the complex role of these biomarkers in LN pathogenesis remains unclear. Renal biopsy remains the gold standard for the identification of the histological phenotypes of LN and guides disease management. However, the molecular pathophysiology of specific renal lesions remains poorly understood. In this review, we provide a critical, up-to-date overview of the latest developments in the field of LN biomarkers.

Purpose of Review To provide an updated understanding of risks and benefits of Janus kinase inhibitors (JAKi) versus biologic disease-modifying antirheumatic drugs (bDMARDs) in the management of rheumatoid arthritis (RA). Recent Findings Shared decision-making is needed in choosing between JAKi and bDMARDs. Cardiovascular disease, malignancy, and thromboembolic events guide this choice. In patients with active RA despite methotrexate use, tumor necrosis factor inhibitor is conditionally favored over JAKi for low-cardiovascular-risk patients and strongly favored in those with pre-existing cardiovascular disease or multiple cardiovascular risk factors. Suboptimal treatment of treatment-refractory RA patients may pose a greater absolute cardiovascular risk than with JAKi use. Use of aspirin and statin may be considered to reduce cardiovascular risk. Summary New safety data on JAKi has redefined the treatment approach in RA. JAKi remains an important oral medication option in active RA despite treatment with bDMARDs, especially in those with low cardiovascular risk.