A randomized study comparing regular care with a nurse-led clinic based on tight disease activity control and person-centred care in patients with rheumatoid arthritis with moderate/high disease activity: A 6-month evaluation.

INTRODUCTION: A recent survey showed that 27% of rheumatoid arthritis (RA) patients had inadequately controlled disease activity. Hence, there is a need for new strategies aiming at improving patient outcomes. The aim of the present study was to evaluate the effect of a nurse-led clinic with frequent visits, treat-to-target and person-centred care of patients with established RA and moderate-to-high disease activity compared with patients receiving regular care. METHODS: The study was a randomized, controlled trial over 26 weeks, with a nonrandomized extension to week 50. Patients were randomized to an intervention group (IG; nurse-led clinic) based on person-centred care, frequent visits and "treat to target", or to a control group (CG) which visited the clinic according to care as usual. The primary outcome was the difference in the DAS28 change between the IG and the CG groups. RESULTS: A total of 332 patients were screened for eligibility, of which 70 were randomly assigned to either the IG (n = 36) or the CG (n = 34) group. The primary outcome was not met, although patients in the IG group tended to improve more than those in the CG group (difference: 0.43 (95% confidence interval [CI] -0.27, 1.13). In both the IG and CG groups, delta-DAS28 improved significantly. The European League Against Rheumatology moderate or good response was achieved by 76% (95% CI 58, 89) in the IG and 49% (95% CI 32, 65) in the CG group. CONCLUSIONS: Disease activity tended to improve more with the nurse-led intervention compared with regular care, although the difference was not significant, probably partly due to the lack of statistical power.

Soluble E-cadherin in systemic lupus erythematosus.

OBJECTIVE: E-cadherin is a potent adherens junction molecule implicated in tissue morphogenesis, epithelial functioning, and immune regulation. Serum levels of soluble E-cadherin (sE-cadherin), an end product of proteolytic cleavage of E-cadherin, is increased in patients with cancer, infections, and inflammation-related diseases. The aim of our study was to measure serum levels of sE-cadherin in systemic lupus erythematosus (SLE) and to determine associations between serum levels of sE-cadherin and markers of inflammation and organ damage in female patients with SLE. METHODS: Serum levels of sE-cadherin were analyzed by ELISA in 150 female patients with SLE and 31 healthy women. Simple and multiple regression analyses between sE-cadherin levels and disease-related variables were performed in patients with SLE. RESULTS: Serum levels of sE-cadherin were elevated in patients with SLE compared with levels in healthy controls. sE-cadherin levels correlated positively with age, disease duration, SLE Collaborating Clinics Damage Index, erythrocyte sedimentation rate (ESR), s-creatinine, cholesterol, triglycerides, interleukin 6, and matrix metalloproteinase-3. In multiple regression analysis, s-creatinine, age, ESR, and triglycerides remained determinants of sE-cadherin. Within the patients with SLE, higher sE-cadherin levels were found only in patients with renal damage, i.e., s-creatinine > 90 µmol/l, glomerular filtration rate < 50 ml/min, or renal involvement ever by SLE. CONCLUSION: Our study demonstrates significantly elevated serum levels of sE-cadherin in women with SLE compared with healthy women. The levels of sE-cadherin were positively correlated to s-creatinine, age, ESR, and triglycerides. Significantly elevated sE-cadherin levels were observed only in patients with renal damage.

Prevalence and risk factors of vertebral compression fractures in female SLE patients.

INTRODUCTION: Our objective was to determine the frequency of and factors associated with prevalent vertebral compression fractures in female systemic lupus erythematosus (SLE) patients attending rheumatologists in western Sweden. METHODS: In this cross sectional study 150 women were included. They were examined with x-ray of thoracic and lumbar spine (Th4 to L4). A reduction of at least 20% of any vertebral height, assessed by Genant's semiquantitative method, was defined as a fracture. Bone mineral density (BMD) was measured by dual energy x-ray absorptiometry (DXA). RESULTS: Median patient age was 47 years (20 to 82) and disease duration 11 years (1 to 41). Only 6 (4%) women had a history of clinical compressions whereas 43 (29%) had at least one radiological fracture each. The patients with at least one fracture at any site were characterized by older age (P < 0.001), being postmenopausal (P < 0.01), higher Systemic Lupus International Collaborative Clinics Damage Index (P < 0.05), lower BMD total hip and femoral neck (P < 0.05), more peripheral fractures (P < 0.01), medication with bisphosphonates (P <0.05) and calcium and vitamin D3 (P < 0.05). There were no significant differences regarding current or cumulative glucocorticosteroid dose between the groups. In logistic regression analyses high age remained as a risk factor of at least one vertebral fracture at any site whereas low BMD in total hip was associated with vertebral fracture in the lumbar spine. CONCLUSIONS: Radiological compression fractures are common but seldom diagnosed in SLE patients. High age and low BMD in total hip, but not in spine, was associated with vertebral fractures.

Role of resistin as a marker of inflammation in systemic lupus erythematosus.

INTRODUCTION: Resistin is a cystein-rich secretory adipokine. It is proposed to have proinflammatory properties in humans. The aim of this study was to determine associations between serum levels of resistin and markers of inflammation and bone mineral density (BMD) in female patients with systemic lupus erythematosus (SLE). METHODS: One hundred sixty-three female patients with SLE (20 to 82 years old) were examined in a cross-sectional study. Venous blood samples were analyzed for resistin, erythrocyte sedimentation rate (ESR), C-reactive protein, creatinine, fasting lipids, complements, tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6, sIL-6R (soluble IL-6 receptor), ICTP (C-terminal telopeptide of type I collagen), and PINP (N-terminal propeptide of type I procollagen). Simple and multiple regression analyses as well as logistic regression analyses were performed. Resistin in serum was compared with 42 healthy female controls with respect to age. RESULTS: Serum resistin levels in controls were similar to those of patients with SLE. Markers of inflammation and current dose of glucocorticosteroids correlated positively to resistin in serum. Markers of renal function, number of prevalent vertebral fractures, and BMD were also significantly associated with resistin. In a multiple regression model, ESR, creatinine, C3, current glucocorticosteroid dose, high-density lipoprotein, and BMD radius remained significantly associated with resistin. In logistic regression analyses with resistin as the independent variable, a significant association was found with ESR (normal or elevated) but not with S-creatinine or z score for hip and radius total. CONCLUSION: Although resistin measurements did not differ between patients and controls, resistin was clearly associated with general inflammation, renal disease, treatment with glucocorticosteroids, and bone loss. We hypothesize that resistin has proinflammatory and disease-promoting properties in SLE. Further studies are needed to elucidate the mechanism behind these associations.