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Objectives. This study aimed to estimate the prevalence of US-detected tenosynovitis in RA patients in clinical remission and to explore its clinical correlates. Methods. A total of 427 RA patients in clinical remission were consecutively enrolled from 25 Italian rheumatology centres. Tenosynovitis and synovitis were scored by US grey scale (GS) and power Doppler (PD) semi-quantitative scoring systems at wrist and hand joints. Complete clinical assessment was performed by rheumatologists blinded to the US results. A flare questionnaire was used to assess unstable remission (primary outcome), HAQ for functional disability and radiographic erosions for damage (secondary outcomes). Cross-sectional relationships between the presence of each US finding and outcome variables are presented as odds ratios (ORs) and 95% CIs, both crude and adjusted for pre-specified confounders. Results. The prevalence of tenosynovitis in clinical remission was 52.5% (95% CI 0.48, 0.57) for GS and 22.7% (95% CI 0.19, 0.27) for PD, while the prevalence of synovitis was 71.6% (95% CI 0.67, 0.76) for GS and 42% (95% CI 0.37, 0.47) for PD. Among clinical correlates, PD tenosynovitis associated with lower remission duration and morning stiffness while PD synovitis did not. Only PD tenosynovitis showed a significant association with the flare questionnaire [OR 1.95 (95% CI 1.17, 3.26)]. No cross-sectional associations were found with the HAQ. The presence of radiographic erosions associated with GS and PD synovitis but not with tenosynovitis. Conclusions. US-detected tenosynovitis is a frequent finding in RA patients in clinical remission and associates with unstable remission. [ABSTRACT FROM AUTHOR]

Objective. Chronic autoimmune diseases are associated with increased risk of cardiovascular death. Endothelial dysfunction represents the first stage of subclinical atherosclerosis and multiple factors contribute to endothelial injury. Among these, an altered balance between endothelial microparticle (EMP) release and endothelial progenitor cell (EPC) generation promotes endothelial dysfunction. The role of EMPs and EPCs in promoting endothelial damage in primary SS (pSS) has never been investigated. Our aim was to evaluate the role of EMPs and EPCs as markers of endothelial damage in pSS and their correlation with disease clinical and immunological features. Methods. Circulating EMPs (CD31 + /CD42 − ), true EPCs (CD34 + /KDR + /CD133 + ) and mature EPCs (CD34 + /KDR + /CD133 − ) were quantified by FACS analysis in 34 pSS patients and 18 age- and sex-matched controls. Correlation between EMP and EPC levels and parameters of disease activity and damage, clinical features and markers of immunological dysfunction was performed. Results. Patients displayed higher EMP numbers with respect to healthy controls [HCs; mean 450 n /μl ( s.d. 155) vs 231 (110) ,P < 0.0001]. EPC and mature EPC levels were higher in patients compared with HCs [mean 226 n /ml ( s.d. 181) vs 69 (53), P < 0.001 and 166 (161) vs 36 (32), P < 0.0001, respectively). EMP levels directly correlated with disease duration from symptoms and diagnosis (ρ = 0.5, P < 0.01). Early EPCs inversely correlated with disease duration from symptoms (ρ = −0.5, P < 0.01) and diagnosis (ρ = −0.4, P < 0.05). Conclusion. This is the first demonstration of chronic endothelial fragmentation characterizing pSS. The reparative potentiality of the endothelial layer appears to be preserved in the earliest stages of disease. During the course of the disease, progressive exhaustion of the precursor endothelial pool may be hypothesized, leading to defective vascular layer restoration and endothelial dysfunction. [ABSTRACT FROM AUTHOR]

This study was conducted to determine the prevalence of subclinical entheseal involvement at the greater trochanter level by ultrasound in patients with spondyloarthritis. Forty-six patients with spondyloarthritis and 46 healthy age- and sex-matched controls were studied. All patients with no clinical evidence of enthesopathy at the greater trochanter underwent an ultrasound examination. The following three entheses were scanned bilaterally: anterior insertion of gluteus minimus, anterior insertion of gluteus medius, and posterior insertion of gluteus medius. Ultrasound findings of enthesopathy were thickening, calcifications, bone erosions, enthesophytes, bursitis, and power Doppler signal. A total of 276 entheses were evaluated in spondyloarthritis patients. In 112 out of 276 (40.5%), grayscale ultrasound found enthesopathy. The enthesis with the highest number of signs of enthesopathy was the anterior insertion of gluteus medius (46/276) (16%), followed by posterior insertion of gluteus medius (37/276) (13.4%) and anterior insertion of gluteus minimus (29/276) (10.5%). In the healthy population, ultrasound found entesopathy in 80 out of 276 (29%) entheseal sites ( p < 0.0001). Posterior insertion of gluteus medius enthesis was the more frequently involved (34/276) (12.3%), followed by anterior insertion of gluteus medius (24/276) (8.6%) and anterior insertion of gluteus minimus (22/276) (7.9%). Power Doppler was found more frequently in patients with spondyloarthritis compared with healthy controls (1% vs 0%). Our results show a higher prevalence of subclinical enthesopathy at the greater trochanter level in patients with spondyloarthritis than in age- and sex-matched healthy controls. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis is a chronic inflammatory disease characterized by a reduced life expectancy mainly due to cardiovascular disease. In long-standing disease, it has been widely demonstrated that both traditional cardiovascular risk and disease-related factors, including chronic inflammation and immune-mediated mechanisms, play a key role in accelerating atherosclerotic damage of the arterial wall. The short- and long-term effects of immunosuppressive treatment on cardiovascular disease outcome is, however, uncertain and a multidisciplinary approach appears to represent the best management of cardiovascular risk in these patients. INSET: Key issues. [ABSTRACT FROM AUTHOR]

Background and aims: In advanced age, the influence of vertebral fractures on quality of life extends well beyond the usual sequelae of osteoporosis. In order to intercept older subjects' distress associated with the clinical, functional, social and psychological consequences of the disease, we developed and validated a multidimensional instrument (the triple-Q questionnaire) tailored to older women with osteoporotic fractures. We also examined specific aspects of the questionnaire correlated with bone mineral density. Methods: 100 osteoporotic women with vertebral fractures and 100 controls aged >65 years, underwent a thorough examination, which also included X-ray of the thoraco-lumbar spine, hip densitometry, the triple-Q questionnaire, and five referral instruments evaluating function, cognition, perception of general health, mood and pain. Results: The questionnaire was repeatable and able to discriminate between older women with and without vertebral fractures. There was a strong association between referral instrument scores and the corresponding single domain score of the questionnaire. Femoral BMD was also associated with scores indicating fear of falling, fear of fracture, and pain. Conclusions: The questionnaire intercepted the influence of osteoporosis on the quality of life of elderly women with vertebral fractures. Subjects who suffered from severe pain and were more fearful of falling were most likely to be severely osteoporotic. [ABSTRACT FROM AUTHOR]

Connective tissue diseases are associated with increased morbidity and mortality related to a higher rate of cardiovascular events and higher prevalence of subclinical atherosclerosis. Atherosclerosis is now considered a multifactorial process where autoimmunity and chronic inflammation play an important pathogenic role. In systemic autoimmune rheumatic diseases in general, and in systemic lupus erythematosus in particular, atherosclerosis cannot be explained by traditional cardiovascular risk factors alone. Cellular and humoral mechanisms, together with specific factors associated with the disease itself and/or its treatments, have been advocated to explain the acceleration of arterial wall organic damage in these patients. Endothelial dysfunction, carotid intima-media thickness and plaque evaluations provide accurate detection of atherosclerotic process at a preclinical stage, before appearance of clinical disease, allowing preventive measure introduction with the aim to modify the cardiovascular risk in subjects with systemic autoimmune rheumatic diseases. [ABSTRACT FROM AUTHOR]