Rheumatology International最新文献

Stroke represents a major complication in Takayasu arteritis (TA). We aimed to determine clinical characteristics and neurological outcomes in TA patients with stroke compared to those without. We retrospectively analyzed 35 patients (27F/8 M) with documented stroke to 50 consecutive patients (47F/3 M) without stroke followed by the Istanbul University-Cerrahpasa Medical Faculty. Demographic data, clinical manifestations, arterial involvement patterns, treatments, and neurological outcomes were evaluated. Disability was assessed using the Expanded Disability Status Scale (EDSS), Barthel Index, and Modified Rankin Scale. Mean age at diagnosis among patients with stroke and non-stroke was similar (38.5 ± 10.7 vs. 35.6 ± 11.6 years). The mean age at stroke was 43.1 ± 10.3 years. Patients with stroke were more likely to be male (22.9% vs. 6.0%, p = 0.023). Strokes were predominantly ischemic (91.4%), affecting anterior circulation (82.8%) with left hemisphere predominance (72.4%). Internal carotid artery (ICA) involvement was significantly associated with stroke (right ICA: 51.4% vs 18.0%, p = 0.001; left ICA: 37.1% vs 18.0%, p = 0.047), while abdominal aorta involvement seemed to be protective (20.0% vs 42.0%, p = 0.028). Male gender (OR = 5.70, p = 0.038) and any ICA involvement (OR = 5.98, p = 0.004) were identified as independent predictors of stroke. Importantly, 40% experienced stroke as the initial TA manifestation. Among those developing stroke after TA diagnosis, 85.7% were already receiving immunosuppression and 47.6% antiplatelet therapy. Stroke patients demonstrated significant disability (mean EDSS: 3.63 ± 3.36 vs 0.02 ± 0.14, p < 0.001) and 11.4% mortality, median 5 years after stroke. Male patients and those with ICA involvement face the highest risk for stroke in TA. Long-term consequences are devastating with increased mortality, severe disability and high recurrence rates. The failure of immunosuppressive therapy to prevent stroke in the majority of treated patients, combined with substantial perioperative mortality, stress the inadequacy of current management strategies.

Women with autoimmune rheumatic diseases (ARDs) require effective contraception to prevent unplanned pregnancies and minimize risks associated with disease activity and teratogenic medications. Despite established guidelines, contraception counseling and use remain suboptimal. This study aimed to assess contraception use and patient preferences for reproductive health counseling in a cohort of women with ARDs. We conducted a cross-sectional survey between January 2023 and February 2024 at a tertiary rheumatology center in Italy. Consecutive women aged 18-50 years with a confirmed autoimmune rheumatic disease (ARD) diagnosis were invited to complete a 47-item anonymous questionnaire covering sexuality, contraception, fertility, pregnancy, breastfeeding, medication safety, and disease transmissibility. Descriptive statistics and subgroup comparisons were performed using chi-square, Fisher's exact test, and Mann-Whitney U test, with significance set at p < 0.05. A total of 189 women participated, of whom 156 were premenopausal (mean age 31 years, mean disease duration 7 years). Among them, 37.8% (n = 59) reported not using any contraception, 40.4% (n = 63) used barrier methods, and 23.1% (n = 36) relied on effective or highly effective methods, including only 5.8% (n = 9) using long-acting reversible contraceptives. Alarmingly, 71.0% of women treated with teratogenic drugs were not using contraception. While 64.7% (n = 101) had discussed contraception with their partner, only 13.5% (n = 21) had spoken with a healthcare provider, and merely 6.3% (n = 2) of those on teratogenic medications expressed interest in dedicated counseling. Our findings highlight significant gaps in contraception counseling and adherence among women with ARDs, particularly those at high risk for medication-related fetal harm. Given the potential impact on maternal-fetal health, rheumatologists should routinely integrate reproductive health discussions into patient care and collaborate with gynecologists to improve contraception uptake. Targeted educational programs may enhance awareness and adherence to contraception guidelines, ultimately optimizing pregnancy outcomes in women with ARDs.

The renin-angiotensin system (RAS), traditionally regarded as a hormonal cascade regulating cardiovascular and renal homeostasis, is increasingly recognized as a locally active, tissue-specific network within joint structures. Accumulating evidence indicates that synovial tissue, synovial fluid, and articular cartilage harbor a functionally active joint-local renin-angiotensin system that operates partially autonomously from the systemic RAS circulation and is implicated in the pathogenesis of both arthritis (RA) and osteoarthritis (OA). This narrative review integrates human, animal, and in vitro evidence to examine the dual-axis organization of the joint RAS, comprising a pathogenic angiotensin-converting enzyme (ACE)/Angiotensin II (Ang II)/ Angiotensin II type 1 receptor (AT1R) axis and a counter-regulatory ACE2/Angiotensin-(1-7) (Ang-(1-7))/Mas receptor-Mas related G protein-coupled receptor D (Mas-MrgD) axis, and to explore how imbalance between these pathways may differentially influence inflammatory and degenerative joint diseases. In RA, experimental and translational studies suggest that enhanced activity of the classical axis within synovial tissue is associated with synovial inflammation, fibroblast-like synoviocyte survival, angiogenesis, and bone erosion through pathways involving nuclear factor kappa B (NF-kB), mitogen-activated protein kinase (MAPK), and receptor activator of nuclear factor kB ligand (RANKL)/Wingless-related integration site (Wnt) signaling pathway. In OA, available data indicate that chondrocyte expression of AT1R/Angiotensin II type 2 receptor (AT2R), together with cytokine-induced receptor upregulation, may sensitize cartilage to Ang II-mediated effects, contributing to matrix metalloproteinase-13 (MMP-13)-mediated matrix degradation and activation of interleukin-6 (IL-6)/janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling. Genetic studies support disease-specific patterns, with the ACE insertion/deletion polymorphism showing a more consistent association with RA susceptibility than with knee OA, although findings vary across populations and do not consistently correlate with disease severity. From a therapeutic perspective, modulation of the joint-local RAS is currently supported mainly by preclinical evidence. Experimental models suggest that classical RAS inhibitors and emerging strategies targeting the protective axis-such as putative ACE2 activators, AT2R agonists, and bone-targeted peptide delivery can influence inflammatory and structural pathways within the joint, while direct clinical evidence remains limited. Overall, current data support the biological relevance of a local joint RAS in arthritis pathophysiology and highlight key gaps between experimental findings and clinical translation.

Giant cell arteritis (GCA) is a medium and large vessel vasculitis. Vision loss is considered the most serious complications traditionally attributed to untreated disease. Urgent corticosteroids (CS) therapy is the standard of care and is considered adequate to prevent blindness. However, in some rare cases blindness may occur despite implementation of the appropriate treatment. We aimed to find patients who went blind despite high dose CS therapy and identify unique features of them together with conducting narrative review of previous case reports to characterize this group in search of common potential risk factors. Cases of blindness prior to treatment induction were not analyzed here. We identified 2 patients in our records who went blind despite high dose CS therapy. We found some repeated common features in patients that went blind in spite of treatment: advanced age, preexisting pronounced arteriosclerosis, thrombocytosis, contraindication to full dose CS therapy resulting in lower doses of CS within the recommended ranges. Defining the subgroup of GCA patients that went blind in spite of proper CS treatment requires further attention as they might potentially benefit from more aggressive therapy (e.g. early introduction of disease-modifying antirheumatic drugs).

Inflammatory rheumatic diseases (IRDs) compromise vascular integrity through systemic inflammation and (auto) immune reactions, which are associated with an increased risk of vascular complications. Venous stasis, endothelial dysfunction, and coagulation imbalance are the primary pathophysiological factors behind thrombotic events in these individuals. The incidence of venous thromboembolism (VTE) in IRDs is higher than in the general population, although the magnitude of this increase varies across diseases. Inflammatory damage to vessel walls, diminished elasticity, and compromised muscle pump function may contribute to the formation of varicose veins (VVs). A sedentary lifestyle, decreased muscular strength, and weight gain worsen the condition, particularly by adversely affecting venous return in the lower extremities. Consequently, the prevention of vascular issues in IRDs should be facilitated by both pharmaceutical interventions and rehabilitation with lifestyle modifications. A multidisciplinary rehabilitation strategy-encompassing regular physical activity, compression therapy, inflammation management, weight control, and patient education-enhances venous return, mitigates thrombosis risk, and improves quality of life.

The aim of this study is to identify factors associated with kinesiophobia in patients with systemic sclerosis (SSc). A total of 72 adult patients diagnosed with SSc were included in this cross-sectional study. Clinical parameters reflecting disease severity, organ involvement, and inflammatory status were recorded. Kinesiophobia level was assessed using the Tampa Scale for Kinesiophobia (TSK). The Berg Balance Scale (BBS), Y Balance Test (YBT), Timed Up and Go Test (TUG), and 10-Meter Walk Test (10MWT) were used to evaluate balance and functional capacity. Factors associated with kinesiophobia was analyzed using multiple linear regression analysis. Kinesiophobia (TSK ≥ 37) was identified in 26 patients (36.1%). Disease related parameters, including disease duration, disease activity, comorbidity burden, skin and other organ involvement (lung, gastrointestinal) were higher in patients with kinesiophobia (p < 0.05, for all). Patients with kinesiophobia had significantly lower BBS score, slower walking speed, longer TUG duration, and were unable to perform the YBT, compared to those without kinesiophobia (all p < 0.001). In the multivariable regression analysis, (β = - 1.26, CI - 1.59 to - 0.94, p < 0.001) and TUG (β = 1.24, CI 0.04-2.43, p = 0.043) showed to be associated with kinesiophobia severity independently. The multivariable model accounted for 65% of the variance in kinesiophobia (adjusted R² = 0.65). In patients with SSc, static imbalance and decreased mobilization capacity are closely associated with kinesiophobia. Monitoring these parameters should be prioritized for the management of kinesiophobia in patients with SSc.