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Abstract Background The role of vitamin D status in COVID-19 patients is a matter of debate. Objectives To assess serum 25-hydroxyvitamin D (25OHD) levels in hospitalized patients with COVID-19 and to analyze the possible influence of vitamin D status on disease severity. Methods Retrospective case–control study of 216 COVID-19 patients and 197 population-based controls. Serum 25OHD levels were measured in both groups. The association of serum 25OHD levels with COVID-19 severity (admission to the intensive care unit, requirements for mechanical ventilation, or mortality) was also evaluated. Results Of the 216 patients, 19 were on vitamin D supplements and were analyzed separately. In COVID-19 patients, mean ± standard deviation 25OHD levels were 13.8 ± 7.2 ng/mL, compared with 20.9 ± 7.4 ng/mL in controls (P < .0001). 25OHD values were lower in men than in women. Vitamin D deficiency was found in 82.2% of COVID-19 cases and 47.2% of population-based controls (P < .0001). 25OHD inversely correlates with serum ferritin (P = .013) and D-dimer levels (P = .027). Vitamin D-deficient COVID-19 patients had a greater prevalence of hypertension and cardiovascular diseases, raised serum ferritin and troponin levels, as well as a longer length of hospital stay than those with serum 25OHD levels ≥20 ng/mL. No causal relationship was found between vitamin D deficiency and COVID-19 severity as a combined endpoint or as its separate components. Conclusions 25OHD levels are lower in hospitalized COVID-19 patients than in population-based controls and these patients had a higher prevalence of deficiency. We did not find any relationship between vitamin D concentrations or vitamin deficiency and the severity of the disease.

Purpose: A high cardiovascular risk has been described in patients with rheumatoid arthritis (RA); the effects of different biological agents have also been described in these patients. The aim of the present study is to examine the effects of tumor necrosis factor inhibitors (TNFi) in the lipoprotein profile of RA patients using a broad laboratory assessment including a large number of non-routine tests. Patients and Methods: RA patients treated with and without TNFi (70 patients in each group) were cross-sectionally compared regarding a broad spectrum of lipoprotein parameters including serum levels of total and HDL, LDL and VLDL cholesterol triglycerides, lipoprotein A (LpA), apolipoprotein A1 (Apo A), B100 (Apo B) and paroxonase. For each lipoprotein subfraction (HDL, LDL and VLDL), we assess specific concentrations of cholesterol, triglycerides, phospholipids and proteins and total mass of each one. Additionally, HDL Apo A, LDL and VLDL Apo B concentrations and number of particles of LDL and VLDL were also determined. Exploratory univariate and multivariate analyses of the different variables were performed. Results: Seventy patients in each subset were enrolled. Patients on treatment with TNFi showed a trend to be younger and to have a longer disease duration. Regarding the lipoprotein analyses, borderline significant higher levels of serum Apo A were detected and an independent association with lower HDL mass, LDL triglyceride, VLDL cholesterol, VLDL Apo B, VLDL mass, number of VLDL cholesterol molecules and number of particles of VLDL was clearly observed. Conclusion: TNFi treatment was associated with beneficial atherogenic effects at the lipoprotein level especially centered in the VLDL-related parameters consistent with a reduction of the atherogenic risk. Keywords: rheumatoid arthritis, lipoproteins, tumor necrosis factor inhibitors

The simplicity and low cost of rapid point-of-care tests greatly facilitate large-scale population testing, which can contribute to controlling the spread of the COVID-19 virus. We evaluated the applicability of a self-testing strategy for SARS-CoV2 in a population-based, cross-sectional study in Cantabria, Spain, between April and May 2020. For the self-testing strategy, participants received the necessary material for the self-collection of blood and performance of a rapid antibody test using lateral flow immunoassay at home without the supervision of healthcare personnel. A total of 1,022 participants were enrolled. Most participants correctly performed the COVID-19 self-test the first time (91.3% [95% CI 89.4–92.9]). Only a minority of the participants (0.7%) needed the help of healthcare personnel, while 6.9% required a second kit delivery, for a total valid test result in 96.9% of the participants. Incorrect use of the self-test was not associated with the educational level, age over 65, or housing area. Prevalence of IgG antibodies against SARS-CoV2 for subjects with a valid rapid test result was 3.1% (95% CI 2.2–4.4), similar to the seroprevalence result obtained using a conventional approach carried out by healthcare professionals. In conclusion, COVID-19 self-testing should be considered as a screening tool.

Background Environmental factors play a central role in seasonal epidemics. SARS-CoV-2 infection in Spain has shown a heterogeneous geographical pattern This study aimed to assess the influence of several climatic factors on the infectivity of SARS-CoV-2 and the severity of COVID-19 among the Spanish Autonomous Communities (AA.CC.). Methods Data on coronavirus infectivity and severity of COVID-19 disease, as well as the climatic variables were obtained from official sources (Ministry of Health and Spanish Meteorological Agency, respectively). To assess the possible influence of climate on the development of the disease, data on ultraviolet radiation (UVR) were collected during the months before the start of the pandemic. To analyze its influence on the infectivity of SARS-CoV-2, data on UVR, temperature, and humidity were obtained from the months of highest contagiousness to the peak of the pandemic. Results From October 2019 to January 2020, mean UVR was significantly related not only to SARS-CoV-2 infection (cumulative incidence -previous 14 days- × 10 5 habitants, rho  = − 0.0,666; p  = 0.009), but also with COVID-19 severity, assessed as hospital admissions ( rho  = − 0.626; p  = 0.017) and ICU admissions ( rho  = − 0.565; p  = 0.035). Besides, temperature (February: rho  = − 0.832; p  < 0.001 and March: rho  = − 0.904; p  < 0.001), was the main climatic factor responsible for the infectivity of the coronavirus and directly contributed to a different spread of SARS-CoV-2 across the Spanish regions. Conclusions Climatic factors may partially explain the differences in COVID-19 incidence and severity across the different Spanish regions. The knowledge of these factors could help to develop preventive and public health actions against upcoming outbreaks of the disease.

The role of antiphospholipid (aPL) and antinuclear antibodies (ANA) in the progression of coronary artery disease (CAD) remains uncertain. We aimed to determine whether the presence of aPL or ANA predicts CAD progression. We conducted a retrospective, single-center, case-control study including patients with CAD classified as either rapid clinical progressors (RCP) or long-standing stable (LSS), and a population-based control group. Autoantibodies analyzed included anticardiolipin (aCL), anti-β2 glycoprotein I (aB2GPI), anti-phosphatidylserine/prothrombin (anti-PS/PT), and ANA. We included 180 CAD patients (58 RCP, 122 LSS) and 210 matched controls. CAD patients more frequently exhibited positive aCL (p<0.05), whereas aB2GPI IgA was higher among controls. The only significant difference between RCP and LSS was an increased prevalence of aCL IgA in RCP (p<0.05). No consistent differences were found in ANA positivity, antibody subtypes, or overall autoantibody load between groups. This study does not support a significant role for aPL or ANA in the development or progression of CAD. These findings should be interpreted as hypothesis-generating, and larger, prospective multicenter studies with repeated antibody measurements are required to clarify these associations.

The role of the immune response in the pathogenesis of antiphospholipid syndrome (APS) remains elusive. It is possible that differences in the frequencies of Th17 cells and/or defects in the immunoregulatory mechanisms are involved in the pathogenesis of APS. Our aim was to determine the peripheral blood Th cells phenotype and the circulating cytokine profile in patients with primary APS (pAPS) and compare it with systemic lupus erythemathosus (SLE) as disease control group. The frequencies of circulating regulatory T cells (Tregs) were determined in PBMCs from 36 patients with pAPS by flow cytometry. As control groups we included 21 age- and gender-matched healthy controls (HC) and 11 patients with SLE. The suppressive capacity of Tregs was evaluated by coculture assay. On the other hand, intracellular cytokine production was assessed in Th1, Th2, and Th17 cells and circulating IL-6, IL-10, and IL-35 were measured by Cytometric Bead Array and ELISA. The quantification of Th master gene expression levels was performed by real time quantitative PCR. pAPS patients and SLE patients did not show differences in the percentage or number of Tregs compared to HC. The suppressive capacity of Tregs was also similar in the three study group. Instead, we found higher FoxP3·mRNA expression levels in pAPS patients and HC than SLE patients. Regarding the Th17 response, patients with pAPS and HC showed a significantly lower frequency of circulating Th17 cells than SLE. However, no differences were observed in the Th1 response between patients and controls. Thus, increased Th17/Th1 and Th17/Treg ratios were found in SLE patients but not in pAPS patients. pAPS and SLE patients had higher serum IL-6 levels than HC but there was not difference between both disease groups. Besides, a significant increase in the immunosuppressive cytokine levels was observed only in pAPS as compared to HC. Our data demonstrate an increased inflammatory profile of peripheral blood CD4 T cells from SLE as compared with pAPS mostly due to an increased Th17 response. In conclusion, there seems not to be a direct pathogenic role for Th cells in pAPS but in SLE.

Background Systemic lupus erythematosus (SLE) is a common systemic autoimmune disease with a complex genetic inheritance. Genome-wide association studies (GWAS) have significantly increased the number of significant loci associated with SLE risk. To date, however, established loci account for less than 30% of the disease heritability and additional risk variants have yet to be identified. Here we performed a GWAS followed by a meta-analysis to identify new genome-wide significant loci for SLE. Methods We genotyped a cohort of 907 patients with SLE (cases) and 1524 healthy controls from Spain and performed imputation using the 1000 Genomes reference data. We tested for association using logistic regression with correction for the principal components of variation. Meta-analysis of the association results was subsequently performed on 7,110,321 variants using genetic data from a large cohort of 4036 patients with SLE and 6959 controls of Northern European ancestry. Genetic association was also tested at the pathway level after removing the effect of known risk loci using PASCAL software. Results We identified five new loci associated with SLE at the genome-wide level of significance ( p  < 5 × 10 − 8 ): GRB2 , SMYD3 , ST8SIA4 , LAT2 and ARHGAP27 . Pathway analysis revealed several biological processes significantly associated with SLE risk: B cell receptor signaling ( p  = 5.28 × 10 − 6 ), CTLA4 co-stimulation during T cell activation ( p  = 3.06 × 10 − 5 ), interleukin-4 signaling ( p  = 3.97 × 10 − 5 ) and cell surface interactions at the vascular wall ( p  = 4.63 × 10 − 5 ). Conclusions Our results identify five novel loci for SLE susceptibility, and biologic pathways associated via multiple low-effect-size loci.

BackgroundDiffuse idiopathic skeletal hyperostosis (DISH) is considered a slowly progressive condition, typically requiring a decade to achieve full radiographic development. However, some individuals exhibit accelerated ossification. This study aimed to characterise the clinical profile of these patients, referred to as Fast Ossifiers (FO).MethodsStudy nested within the Camargo Cohort, integrating cross-sectional and longitudinal data (baseline (E0), 5 year (E1) and 10 year assessments (E2)). Propensity Score matching was applied. FO was defined as progression of ≥2 grades in Schlapbach’s Scale between consecutive assessments. We evaluated inflammation, insulin resistance (via Triglyceride-Glucose Index (TyG)), Visceral Adiposity Index (VAI), intact parathormone (iPTH), bone turnover markers and Trabecular Bone Score (TBS).ResultsWe analysed 455 DISH cases and 455 matched controls. During follow-up, 61 individuals fulfilled FO criteria (18%<60 years; 49% female; 65.6% obese; 72.1% hypertensive). Compared with controls, FO subjects had higher TyG (8.65±0.9 vs 8.39±0.4; p=0.002), FO-females showed higher visceral adiposity (VAI 2.30±2 vs 1.44±0.1; p=0.024), and both sexes presented elevated iPTH at E2. In multivariable models, FO was associated with high TyG (adjusted OR=9.31; 95% CI: 1.04 to 36; p=0.046), low TBS (adjusted OR=0.002; 95% CI: 0.001 to 0.61) and higher alkaline phosphatase levels (79 vs 69 (U/L); p=0.043).ConclusionsFO represents an active variant that challenges the view of DISH as a quiescent disease affecting older men. Rather than a single entity, FO emerges as a convergent phenotype driven by diverse metabolic pathways and linked to accelerated skeletal changes, including ossification and early trabecular impairment.

Introduction/objectivesDISH has traditionally been considered a non-inflammatory rheumatic disorder. Currently, an inflammatory component has been theorized in the early phases of this condition (EDISH). The study is aimed at investigating a possible relationship between EDISH and chronic inflammation.MethodAnalytical-observational study: participants from the Camargo Cohort Study were enrolled. We collected clinical, radiological, and laboratory data. C-reactive protein (CRP), albumin-to-globulin ratio (AGR), and triglyceride-glucose (TyG) index were assessed. EDISH was defined by Schlapbach’s scale grades I or II. A fuzzy matching with tolerance factor = 0.2 was performed. Subjects without ossification (NDISH), sex- and age-matched with cases (1:4), acted as controls. Definite DISH was an exclusion criterion. Multivariable analyses were performed.ResultsWe evaluated 987 persons (mean age 64 ± 8 years; 191 cases with 63.9% women). EDISH subjects presented more frequently obesity, T2DM, MetS, and the lipid pattern [↑TG ↓TC]. TyG index and alkaline phosphatase (ALP) were higher. Trabecular bone score (TBS) was significantly lower (1.310 [0.2] vs. 1.342 [0.1]; p = 0.025). CRP and ALP showed the highest correlation (r = 0.510; p = 0.0001) at lowest TBS level. AGR was lower, and its correlations with ALP (r =  − 0.219; p = 0.0001) and CTX (r =  − 0.153; p = 0.022), were weaker or non-significant in NDISH. After adjustment for potential confounders, estimated CRP means for EDISH and NDISH were 0.52 (95% CI: 0.43–0.62) and 0.41 (95% CI: 0.36–0.46), respectively (p = 0.038).ConclusionsEDISH was associated with chronic inflammation. Findings revealed an interplay between inflammation, trabecular impairment, and the onset of ossification. Lipid alterations were similar to those observed in chronic-inflammatory diseases. Key Points• An inflammatory component has been theorized in early stages of DISH (EDISH)• In EDISH group compared to non-DISH, we observed significantly higher correlations between biomarkers and some relevant variables. In particular, with alkaline phosphatase (ALP) and with trabecular bone score (TBS)• EDISH has shown to be associated with chronic inflammation• The lipid alterations observed in the EDISH group were similar to those observed in chronic-inflammatory diseases

The adjusted Global Antiphospholipid Syndrome (APS) Score (aGAPSS) is a tool proposed to quantify the risk for antiphospholipid antibody (aPL)-related clinical manifestations. However, aGAPSS has been validated mainly for thrombotic events and studies on APS-related obstetric manifestations are scarce. Furthermore, the majority of them included patients with positive aPL and different autoimmune diseases. Here, we assess the utility of aGAPSS to predict the response to treatment in aPL carriers without other autoimmune disorders. One-hundred and thirty-seven women with aPL ever pregnant were included. Sixty-five meet the APS classification criteria, 61 had APS-related obstetric manifestations, and 11 were asymptomatic carriers. The patients’ aGAPSS risk was grouped as low (< 6, N = 73), medium (6–11, N = 40), and high risk (≥ 12, N = 24). Since vascular risk factors included in the aGAPSS were infrequent in this population (< 10%), the aGAPSS score was mainly determined by the aPL profile. Overall, the live birth rate was 75%, and 37.2% of the patients had at least one adverse pregnancy outcome (APO). When considering patients according to the aGAPSS (high, medium, and low risk), no significant differences were found for pregnancy loss (29.2%, 25%, and 21.9%) or APO (33.3%, 47.5%, and 32.9%). In the present study, including aPL carriers without other autoimmune diseases, aGAPSS is not a valuable tool to identify patients at risk for obstetric complications despite treatment. In these patients with gestational desire, in addition to the aPL profile, other pregnancy-specific factors, such as age or previous obstetric history, should be considered.