Obesity is a modifiable major cause of morbidity and mortality in the general population, but little is known about the association of obesity and quality of life in patients with rheumatoid arthritis (RA). Thus, we set out a study to test the hypothesis that obesity is independently associated with lower quality of life in patients with RA. Three hundred and fifty nine patients with RA underwent an interview, physical exam, and all clinical charts were reviewed. Based on body mass index (BMI), patients were classified as normal (BMI < 25 kg/m(2)), overweight (BMI = 25-29.9 kg/m(2)), and obese (BMI > or = 30 kg/m(2)). Quality of life was quantified with the Medical Outcomes Study Short Form 36 (SF-36). Data obtained included demographic variables, extra-articular disease, comorbidities, presence of X-ray erosions, rheumatoid factor, and depression. The association between obesity and quality of life was examined with the use of multiple lineal regression models. One hundred and seventy-two patients (47.9%) had normal BMI, 126 (35.1%) were overweight, and 61 patients (17%) were obese. Obese patients had lower quality of life (30.8 +/- 18.1) than overweight patients (43.3 +/- 20.1) and patients with normal weight (43.8 +/- 22.2), P < 0.001. The association between obesity and impaired quality of life was confirmed with a linear regression model (Coef = -12.9, P < 0.001) and remained significant after adjustment for age, sex, disease activity, extra-articular disease, comorbidities, X-ray erosions, presence of rheumatoid factor, depression, education, and disease duration (Coef = -5.3, P = 0.039). In conclusion, obesity is independently associated with the impaired quality of life in patients with rheumatoid arthritis.

Mestizo patients are at increased risk of developing renal disease, whereas anti-malarial use protects patients from such an occurrence.

Objective In this paper, we aim to define factors associated with health-related quality of life (HRQoL) in Mestizo patients with systemic lupus erythematosus (SLE). Methods We evaluated patients with SLE from Peru's two largest hospitals between October 2012 and July 2015 to ascertain HRQoL. Using a standard protocol, we incorporated demographic characteristics, clinical manifestations and treatment in our analysis. HRQoL was measured with the LupusQoL, disease activity was ascertained with the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI), and damage was appraised with the Systemic Lupus International Collaborating Clinics (SLICC)/American College of Rheumatology (ACR) damage index (SDI). The associations between the LupusQoL and these variables were examined using linear regression models. Model selection was based on backward elimination. Results A total of 277 patients fit the inclusion criterion. Of these, 254 (91.7%) were female, the median (interquartile range, IQR) age at diagnosis was 41.5 (33.8-51.8) years, disease duration was 6.5 (2.7-11.3) years. The HRQoL domains most affected were the following: burden to others, fatigue, and intimate relationships. Through multivariate analysis, we determined that older age at diagnosis, higher disease activity, damage, and immunosuppressive drug use were negatively associated with HRQoL. Further, we found that higher socioeconomic status, disease duration, and antimalarial use were positively associated with HRQoL. Conclusion Age at diagnosis, disease activity, damage, and use of immunosuppressive drugs were negatively associated with HRQoL; high socioeconomic status, disease duration, and use of antimalarials were positively associated with HRQoL.

Although endothelium-derived hyperpolarizing factor (EDHF) is thought to be a cytochrome P-450 product (arachidonic acid metabolite) in some tissues, in porcine coronary arteries (PCAs) its nature remains unclear. Because phospholipase A2 and C are involved in the synthesis and/or release of EDHF in the PCA, the arachidonic acid (AA) pathway may be involved. In the presence of the cyclooxygenase inhibitor indomethacin (10(-5) M) and the NOS inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME; 10(-4) M), both bradykinin (BK; 10(-9)-10(-6) M) and AA (10(-7)-10(-4) M) induced dose-dependent relaxation of PGF2alpha-contracted PCA rings, which was blocked by a high extracellular concentration of KCl (30 mM) or pretreatment with ouabain, a Na+/K+-adenosine triphosphatase (ATPase) inhibitor (5 x 10(-7) M). Eicosatetraynoic acid (ETYA; 20 microM), which inhibits all AA pathways, slightly affected the response to BK and AA; however, lipoxygenase or cytochrome P-450 inhibitors had no effect, suggesting that relaxation is independent of these enzymatic pathways. Because endothelial cells can generate reactive oxygen species (ROS) via metabolism of AA and independent of cyclooxygenase activity, we also studied (a) whether ROS can relax the PCA, as well as the mechanism(s) involved, and (b) the role of ROS in BK- and AA-induced relaxation. Xanthine (X; 100 microM) plus xanthine oxidase (XO; 0.02 U/ml) induced time-dependent relaxation of PGF2alpha-contracted PCA rings in the presence of indomethacin and L-NAME. Dilatation was not affected by superoxide dismutase (SOD; 500 U/ml) but was abolished by catalase (300 U/ml), suggesting that hydrogen peroxide (H2O2) is involved. When rings were contracted by depolarizing them with 30 mM KCl, X/XO failed to elicit relaxation. Ouabain abolished the response to X/XO, suggesting that X/XO may induce relaxation by hyperpolarizing vascular smooth muscle cells via stimulation of the Na+/K+-ATPase pump. We therefore questioned whether ROS might be involved in BK- and AA-induced relaxation. Because catalase combined with SOD had little or no effect, we concluded that in the PCA, the relaxation induced by BK via EDHF involves some mechanism independent of NO, AA metabolism, or ROS.