(1) Background: Telerehabilitation is an approach that uses digital technology to provide remote medical recovery services. It can be an option for cardiovascular recovery at home in patients with peripheral arterial disease (PAD) of the lower limbs. (2) Methods: We performed literature research through two databases: PubMed and Embase. We included randomized controlled trials and cohort studies that evaluated the effectiveness of a technology-assisted home exercise intervention compared with conventional rehabilitation or the usual care in patients with PAD. We analyzed population, intervention, and outcome data. (3) Results: We identified 2468 studies. After rigorous screening, we included 25 articles in the review. The following results were evaluated: dissemination and acceptance of digital technologies among these people, functional capacity, exercise intensity, patient motivation, sex-specific response differences in mortality and clinical outcomes, quality of life assessment, and changes in values of inflammatory biomarkers. All of these were correlated with the type of intervention and the dose of the exercise. (4) Conclusions: Home-based exercise therapy supervised with the help of specific devices could be successfully implemented in the therapeutic management of the PAD population. Health specialists should take into account the clinical–paraclinical profile and the emotional status of the patients. Such individualized interventions could bring significant benefits for the people with this disease and for the healthcare system, including increasing exercise adherence, engagement, self-care capacity, life expectancy, and quality of life for these patients, as well as reducing their symptoms, cardiovascular complications, and hospitalizations.

Background: Cardiovascular implications in systemic lupus erythematosus (SLE) are common and varied, including impacts on the pericardium, myocardium, valves, coronary arteries, and conduction system; all of these could be potential substrates or triggers of cardiac arrhythmias by interfering with disease severity and specific medication. Therefore, this narrative review aimed to assess the cardiac involvement in SLE underlying, mainly, cardiac arrhythmias. Methods: We analyzed studies, published between 2015 and 2025 on PubMed, which explore cardiovascular involvement with a focus on arrhythmias in SLE from the perspectives of epidemiology, underlying mechanisms, diagnostic techniques, and the impact of standard and biologic therapies. Results: The cardiac manifestation of LES (lupus pericarditis, lupus myocarditis, Libman–Sacks endocarditis, coronary artery disease, coronary vasculitis or myocardial fibrosis) represents a substrate for arrhythmia risk. These substrates, in association with other arrhythmias mechanisms considered as triggers or conduction abnormalities, determined arrhythmogenic conditions in these patients. In addition to structural heart disease, arrhythmias in SLE are caused by ongoing inflammation, immune system irregularities, microvascular problems, autonomic imbalance, oxidative stress, and side effects from treatments. Despite this complex background, arrhythmias are often overlooked and not routinely investigated in SLE care. Data that show how disease-modifying drugs may affect arrhythmias are limited and inconsistent, highlighting significant gaps in knowledge. Cardiac arrhythmias are a significant but, as yet, insufficiently underrecognized aspect of SLE, with serious implications for prognosis. Conclusions: Systemic lupus erythematosus causes cardiovascular involvement that is associated with arrhythmias through various and complexes mechanisms, mainly related to direct cardiovascular structural damage, systemic inflammation or specific therapies. Data on arrhythmias secondary to cardiovascular damage in patients with SLE in the literature are limited. Therefore, early detection of electrical issues, regular cardiovascular evaluation in high-risk patients, and careful management of treatment effects are vital. A coordinated, multidisciplinary cardio-rheumatology approach is essential to improving arrhythmia detection, tailoring treatments, and ultimately decreasing cardiovascular complications and deaths in SLE patients.

Background/Objectives: Atopy and spondyloarthritis (SpA) are immune-mediated diseases driven by distinct T-helper (Th) cell pathways—Th2 for atopy and Th1/Th17 for SpA. The coexistence of these divergent immune responses is increasingly recognized, particularly in the context of biological therapies that target pro-inflammatory cytokines. This study aimed to investigate Th2 cytokine profiles (IL-4, IL-5, IL-13) in atopic SpA patients receiving biological therapy to better understand how such treatment may influence immune regulation in this complex clinical setting. Methods: We conducted a prospective observational cross-sectional study on 136 SpA patients stratified by biological therapy and atopy status. Serum IL-4, IL-5, and IL-13 levels were quantified using LUMINEX immunoassays. Patients were grouped into biologically treated (BT) and Bio-Naïve (BN) cohorts and further sub-categorized by atopic phenotype (allergic rhinitis, asthma, dermatitis). Statistical comparisons of cytokine levels were made using SPSS IBM version 26 to explore associations with clinical and demographic variables. Results: IL-13 levels were significantly elevated in BT-atopic patients, particularly those with allergic rhinitis and atopic dermatitis, suggesting biological therapy may modulate Th2 responses. IL-5 remained elevated in allergic asthma cases despite treatment, indicating persistent eosinophilic activity. No significant correlation was found between cytokine levels and disease duration or therapy length. Conclusions: Biological therapy in SpA may influence Th2 cytokine expression, notably IL-13, in atopic patients. These findings underscore the importance of immune profiling in guiding personalized treatment strategies and highlight the need for further investigation into the long-term immunomodulatory effects of biologics in patients with overlapping Th1/Th2-driven diseases.

Background/Objectives: Axial spondyloarthritis (axSpA) is a chronic immune-mediated inflammatory disorder affecting the spine and sacroiliac joints, with variable clinical expression. This study assessed serum levels of inflammatory (TNF-α, IL-17A) and metabolic (leptin, adiponectin) biomarkers and their associations with disease activity, inflammation, structural damage, and comorbidities. Methods: This prospective cross-sectional study assessed 89 axSpA patients using clinical, laboratory, and radiological evaluations. Disease activity was measured using ASDAS-CRP and BASDAI scores. Radiographic damage was quantified using the Modified Stoke Ankylosing Spondylitis Spine Score (mSASSS). Serum concentrations of TNF-α, IL-17A, leptin, and adiponectin were quantified by enzyme-linked immunosorbent assay (ELISA). Clinical and imaging correlations were analyzed. Results: Serum leptin levels correlated significantly with higher disease activity scores, inflammatory markers (CRP, ESR), radiographic progression (syndesmophyte formation, mSASSS), and arterial hypertension. Adiponectin levels were inversely associated with disease activity, structural damage, and arterial hypertension, suggesting anti-inflammatory, bone- and cardio-protective properties. TNF-α levels showed an association with inflammatory markers and were higher in patients with peripheral enthesitis. IL-17A levels were weakly correlated with disease activity and structural severity and were significantly lower in patients with a history of anterior uveitis. Conclusions: Leptin and adiponectin may serve as complementary biomarkers in axSpA, reflecting both inflammatory burden and structural damage. While TNF-α and IL-17A remain key therapeutic targets, their correlation with structural changes appears limited. Biomarker profiling could support personalized disease monitoring. Longitudinal studies are needed to validate prognostic implications.

Systemic sclerosis-associated interstitial lung disease (SSc-ILD) remains an important cause of morbidity and mortality in systemic sclerosis. Mycophenolate mofetil (MMF) is widely used as first-line immunosuppressive therapy; however, real-world descriptions of pulmonary functional and radiologic evolution during MMF therapy remain limited, particularly according to high-resolution computed tomography (HRCT) pattern. Objectives: To descriptively evaluate pulmonary function evolution, radiologic findings, and safety outcomes in patients with SSc-ILD treated with MMF in routine clinical practice, with exploratory analyses according to HRCT pattern and subsequent antifibrotic use. Materials and Methods: We conducted a retrospective single-center study including 20 patients with SSc-ILD treated with MMF. Clinical, functional (forced vital capacity [FVC]; diffusing capacity for carbon monoxide [DLCO]), and radiologic (HRCT Warrick score) parameters were assessed at baseline, 6 months, and 12 months. Patients were stratified according to nonspecific interstitial pneumonia (NSIP) and usual interstitial pneumonia (UIP) patterns. Statistical analyses were exploratory and descriptive. Results: Pulmonary function remained overall stable during follow-up under MMF therapy, while DLCO improvement was observed at 6 months and remained stable at 12 months. Radiologic progression appeared more limited in patients with NSIP pattern, whereas patients with UIP pattern generally exhibited more frequent radiologic progression during follow-up. Patients who subsequently received nintedanib generally presented with UIP-pattern disease, lower baseline DLCO values, and more advanced pulmonary involvement. MMF was generally well tolerated, with treatment discontinuation due to adverse events observed in a single patient. Conclusions: This small retrospective real-world case series describes pulmonary functional and radiologic evolution in patients with SSc-ILD treated with MMF in routine clinical practice. Overall functional stabilization was observed during follow-up, while radiologic progression was more frequently observed in patients with UIP-pattern disease and more advanced baseline pulmonary involvement. Because of the exploratory descriptive design and limited sample size, these observations should be interpreted cautiously and considered hypothesis-generating only. Further prospective studies with standardized radiologic assessment are required.

Background/Objectives: Children with juvenile idiopathic arthritis (JIA) frequently develop additional autoimmune conditions during follow-up, yet the clinical and diagnostic profile of this comorbid subgroup is incompletely characterised in single-centre paediatric series. We aimed to describe the prevalence, clinical pattern, and diagnostic features of autoimmune comorbidities in a seven-year cohort of children with JIA monitored at a single tertiary paediatric centre, and to document the diagnostic protocols applied for each comorbidity. Methods: We conducted a retrospective descriptive observational study of 103 consecutive children with JIA classified according to the ILAR 2001 criteria and monitored at the Paediatric Rheumatology Unit of St. Mary Children’s Emergency Hospital, Iași, Romania, between 2017 and 2023, with the year 2020 excluded by design owing to the institutional reorganisation during the early COVID-19 pandemic. Autoimmune comorbidities were ascertained from medical records using ICD-10 coding and confirmed by subspecialty evaluation. The diagnostic approach for each comorbidity is reported in detail. Continuous variables are described using mean ± standard deviation, and categorical variables as frequencies (%). No inferential analysis was performed on predictor variables; the study is exploratory and hypothesis-generating. Results: Autoimmune comorbidity was identified in 21 of 103 children (20.4%; 95% confidence interval [CI] 13.1–29.5%), the JIA-AID subgroup. Patients were predominantly female (17 of 21, 81.0%) and aged over 12 years (10 of 21, 47.6%). Autoimmune thyroiditis was the most frequent comorbidity, present in 10 of 21 cases (47.6%) when the euthyroid, hypothyroid, and vitiligo-associated forms were combined, followed by inflammatory bowel disease (4 of 21, 19.0%), alopecia areata (4 of 21, 19.0%), localised scleroderma (2 of 21, 9.5%), and coeliac disease (1 of 21, 4.8%). Three patients (14.3%) had polyautoimmunity, defined as two or more autoimmune diagnoses in addition to JIA. The HLA-B27-positive enthesitis-related arthritis subtype, although small in absolute numbers, was over-represented within the JIA-AID subgroup: 5 of 7 HLA-B27-positive ERA patients (71.4%; 95% CI 29.0–96.3%) carried a coexisting autoimmune diagnosis, compared with 16 of 96 patients in the remainder of the cohort (16.7%; 95% CI 9.8–25.6%); the predominant comorbidity in this subtype was inflammatory bowel disease. Conclusions: Autoimmune comorbidity affected approximately one in five children with JIA in this single-centre cohort, with autoimmune thyroiditis and inflammatory bowel disease as the most frequent associations and a notable concentration of comorbidity within the HLA-B27-positive enthesitis-related arthritis subtype. These descriptive observations are hypothesis-generating and support the case for proactive multidisciplinary screening in selected subgroups. Prospective registry-based studies with explicit exposure classification and standardised functional outcomes will be needed to confirm the patterns reported here.