Effects of Renin-Angiotensin System Inhibitors on Atrial Mechanics Parameters in Patients with Metabolic Syndrome.

INTRODUCTION: Metabolic syndrome (MS) is associated with abnormalities in atrial mechanics, atrial remodeling, and an increased risk of heart rhythm disorders. One of the most commonly used approaches to the prevention of cardiac remodeling in arterial hypertension is the administration of renin-angiotensin system (RAS) inhibitors. Therefore, this study aimed to investigate the effects of RAS inhibitors on atrial mechanics parameters in patients with MS. METHODS AND MATERIALS: This longitudinal observational study included 55 patients with hypertension and MS, as defined by the ATP III criteria. The patients were evaluated at the start of antihypertensive treatment with an RAS inhibitor. The patients' clinical characteristics, chosen pharmacological treatment, and transthoracic echocardiography findings were recorded at baseline and 6 months thereafter. A student's dependent sample t-test was used for comparisons between groups. Pearson correlation was used to evaluate the relationships between variables. RESULTS: Patients with MS had higher peak atrial longitudinal strain (PALS) values at 6 months than at baseline. Meanwhile, systolic strain and peak late strain rates were lower at follow-up than at baseline. The different antihypertensive treatments had comparable effects on the PALS changes during the follow-up period. Higher high-density lipoprotein levels at baseline were correlated with changes in PALS. CONCLUSION: The administration of RAS inhibitors improved atrial mechanics parameters in the early stages of antihypertensive management in MS.

Risk Factors of Muscle Wasting in Women with Rheumatoid Arthritis: Relevance of the Persistent Failure of Conventional Combination Therapy.

Background: Muscle wasting, also known as myopenia, is frequent in rheumatoid arthritis (RA). To date, it is still unknown if the failure of pharmacologic therapies increases the risk of myopenia in RA. Objective: To identify if treatment failure with conventional synthetic DMARDs (csDMARDs) constitutes an independent risk factor of muscle wasting in women with RA. Methods: This was a cross-sectional study. We included 277 women with RA. Assessments in RA patients included: clinical, epidemiological, and therapeutic variables. The skeletal muscle index (SMI) was estimated by DXA, and myopenia was diagnosed if they had an SMI < 5.45 kg/m2. Multivariable logistic regression models identified risk factors of myopenia. Results: Muscle wasting was observed in 28.2% of patients with RA. The risk factors of myopenia in RA were menopausal (OR: 4.45, 95% CI: 1.86 to 10.64) and failure of combined therapy with csDMARDs (OR: 2.42, 95% CI: 1.15 to 5.07). The increased body mass index was protective (OR:0.81, 95% CI: 0.75 to 0.87). Conclusions: Around one of four patients with RA presented muscle wasting. Muscle wasting is related to treatment failure of combined csDMARDs; other factors influencing the presence of muscle wasting is being postmenopausal, whereas, the body mass index was a protective factor.

Risk factors associated with permanent disability in neuromyelitis optica spectrum disorders.

BACKGROUND: Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune inflammatory disease of the central nervous system. In NMOSD, a relapse results in increased disability. OBJECTIVE: To assess risk factors associated with permanent disability (PD) in patients with neuromyelitis optica spectrum disorders (NMOSD). METHODS: We evaluated 34 cases (who developed permanent disability) and 33 controls. The assessment included the following variables: sociodemographic data and characteristics of the disease. Logistic regression analysis was performed to adjust variables associated with PD. RESULTS: fifty-one percent developed PD during follow-up; 15 (22%) developed permanent visual disability, 13 (19%) developed permanent motor disability and 6 (9%) were restricted to wheelchair. Factors associated with PD in the crude analysis were: age at onset ≥ 50 years (OR 3.95, 95% IC 1.12-13.94, p= 0.032), time from onset to diagnosis ≥ 12 months (OR 3.30, 95% IC 1.13-9.64, p= 0.029), time from onset to treatment ≥ 60 months (OR 4.16, 95% IC 1.03-16.85, p= 0.045), EDSS ≥ 4.0 at the first appointment (OR 3.21, 95% IC 1.18-8.76, p= 0.022) and severe relapses during disease evolution (OR 5.72, 95% IC 1.98-16.57, p= 0.001). Factors associated with PD in the adjusted analysis were: age at onset ≥ 50 years (OR 5.82, 95% IC 1.30-26.05, p= 0.021), time from onset to diagnosis ≥ 12 months (OR 5.43, 95% IC 1.47-20.08, p= 0.011) and severe relapses during disease evolution (OR 6.65, 95% IC 1.98-22.31, p= 0.002). CONCLUSION: Half of patients with NMOSD may develop PD during disease evolution. Age of onset ≥ 50 years, delay to diagnosis ≥12 months and initial EDSS ≥ 4.0 constitute the strongest risk factors for PD.

Serum chemerin levels: A potential biomarker of joint inflammation in women with rheumatoid arthritis.

BACKGROUND: Chemerin has a potential role in perpetuating inflammation in autoimmune diseases. Nevertheless, to date, there is no conclusive information on whether high chemerin levels increase the severity of rheumatoid arthritis (RA). Therefore, this study evaluated whether serum chemerin is a biomarker of disease activity in RA patients. METHODS: Study design: cross-sectional. The assessment included clinical and laboratory characteristics, body mass index (BMI) and fat mass. The severity of the disease activity was identified according to the DAS28-CRP index as follows: A) RA with a DAS28-CRP≤2.9 (remission/mild activity) and B) RA with a DAS28-CRP>2.9 (moderate/severe activity). Serum chemerin concentrations were measured by ELISA, and ≥103 ng/mL was considered a high level. Logistic regression analysis was applied to determine whether high chemerin levels were associated with disease activity in RA after adjusting for confounders. Multiple regression analysis was performed to identify variables associated with chemerin levels. RESULTS: Of 210 RA patients, 89 (42%) subjects had moderate/severe disease activity and had higher serum chemerin levels than patients with low disease activity or remission (86 ± 34 vs 73± 27; p = 0.003). Serum chemerin correlated with the number of swollen joints (r = 0.15; p = 0.03), DAS28-CRP (r = 0.22; p = 0.002), and C-reactive protein levels (r = 0.14; p = 0.04), but no correlation was observed with BMI and fat mass. In the adjusted logistic regression analysis, high chemerin levels (≥103 ng/mL) were associated with an increased risk of moderate/severe disease activity (OR: 2.76, 95% CI 1.35-5.62; p = 0.005). In the multiple regression analysis, after adjusting for potential confounders, serum chemerin levels were associated with higher DAS28-CRP (p = 0.002). CONCLUSIONS: Higher chemerin levels increased the risk of moderate and severe disease activity in RA. These results support the role of chemerin as a marker of inflammation in RA. Follow-up studies will identify if maintaining low chemerin levels can be used as a therapeutic target.

Genotypic Analyses of the Sclerostin rs851056 and Dickkopf rs1569198 Polymorphisms in Mexican-Mestizo Postmenopausal Osteoporosis: A Case-Control Study.

Background: The Wnt/ß catenin pathway promotes bone mineralization stimulating proliferation, differentiation, and survival of osteoblasts; it also inhibits osteoclast differentiation and osteocyte activity. Sclerostin (SOST) and Dickkopf 1 (DKK1) are Wnt/ß catenin pathway inhibitors. Genetic variability in the expression of SOST and DKK1 might be involved in the development of postmenopausal osteoporosis (OP). Aim: To determine whether the SOST rs851056 and DKK1 rs1569198 polymorphisms are associated with OP in Mexican-Mestizo postmenopausal women. Materials and Methods: Two hundred and eighty Mexican-Mestizo postmenopausal women were assessed for their bone mineral density by dual-energy X-ray absorptiometry (DXA). Patients were classified as OP or non-OP. Genomic DNA was extracted from peripheral blood leukocytes. Genetic polymorphisms were analyzed by quantitative polymerase chain reaction using TaqMan probes. Results: The frequency of OP was 40% among the study population. Osteoporotic patients were older (p < 0.001), had a higher frequency of smoking (p = 0.01), and lower body mass index (p < 0.001) compared with the non-osteoporotic patients. The genotypic frequencies of the rs851056 locus of the SOST gene were GG 19%, GC 45%, and CC 35%, whereas the genotypic frequencies of the rs1569198 locus of the DKK1 gene were GG 15%, GA 40%, and AA 44%. In relation to rs851056 locus of the SOST gene, no differences were observed between the OP and non-OP cohorts in the frequencies of the GC polymorphism (48.7% vs. 43.1%). Similarly, analyses of the DKK1 rs1569198 does not demonstrate differences in the GA genotypic frequencies between the OP and non-OP cohorts (42.5% vs. 38.9%). Conclusion: Polymorphisms SOST rs851056 and DKK1 rs1569198 polymorphisms are not associated with OP in Mexican-Mestizo postmenopausal women.

Serum Neuropeptide Y Levels Are Associated with TNF-α Levels and Disease Activity in Rheumatoid Arthritis.

BACKGROUND: Neuropeptide Y (NPY) is a sympathetic neurotransmitter with effects on the regulation of inflammatory cells. The role of NPY on autoimmune inflammatory diseases such as rheumatoid arthritis (RA) is not completely understood. Therefore, we evaluate if NPY levels are markers of disease activity in RA and if there is a correlation between NPY levels and tumor necrosis factor-alpha (TNF-α), leptin, and interleukin 6 (IL-6) levels. METHODS: Cross-sectional design, including 108 women with RA. We assessed disease activity by DAS28-ESR (considering active disease a score of ≥2.6). Serum NPY levels and anti-CCP2 antibody, TNF-α, IL-6, and leptin levels were quantified (ELISA). RESULTS: Sixty-eight RA had an active disease (RA-active), and 40 were in remission (RA-remission). RA-active patients had higher NPY levels vs. RA-remission (22.8 ± 13.6 vs. 17.8 ± 10.3; p = 0.04). NPY levels correlated with increased TNF-α levels (r = 0.32, p = 0.001). Leptin or IL-6 did not correlate with NPY levels. In the logistic regression analysis, NPY increased the risk of disease activity (OR: 1.04, 95% CI 1.006-1.09, and p = 0.03). CONCLUSION: Higher NPY levels are an independent marker of disease activity in RA. This study encourages the quantification of NPY levels as a surrogate marker for RA-active. Future studies evaluating the role of NPY levels interacting with other proinflammatory cytokines are required.