Serum 25(OH) Vitamin D Levels in Pregnant Women with Coronavirus Disease 2019 (COVID-19): A Case-Control Study.

The physiological changes during pregnancy may increase the risk of complications in pregnant women with coronavirus disease 2019 (COVID-19). Vitamin D is a fat-soluble secosteroid hormone and its role in immunity is appears to be of particular importance in this recent pandemic. Nevertheless, there is little research about the role of vitamin D levels regarding COVID-19 in pregnant women to date. This study aimed to establish a relationship between serum 25-hydroxyvitamin D (25(OH)D) levels in pregnant women and COVID-19. A comparative case-control study was performed with a study population of 256 pregnant women (82 pregnant women with infection and 174 women in control group). Serum 25(OH)D levels were significantly lower in pregnant women with COVID-19 infection than in those without infection. In addition, 89% of COVID-19-positive pregnant women had 25(OH)D deficiency, while in the control group the percentage was 75.30%, finding statistically significant differences (ORa = 2.68; 95% CI 1.19-6.06; p = 0.01). Our results find a relationship between vitamin D deficiency in pregnant women and COVID-19 infection. This finding could be relevant for actual clinical practice. Thus, more research is needed in this field.

Patrones de excreción del virus de la gripe A (H1N1)pdm09 en pacientes hospitalizados pediátricos / Influenza A (H1N1)pdm09 viral clearance kinetics in hospitalized children

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Gut Microbiota Has a Crucial Role in the Development of Hypertension and Vascular Dysfunction in Toll-like Receptor 7-Driven Lupus Autoimmunity.

Our group has investigated the involvement of gut microbiota in hypertension in a murine model of systemic lupus erythematosus induced by Toll-like receptor (TLR)-7 activation. Female BALB/c mice were randomly assigned to four experimental groups: an untreated control (CTR), a group treated with the TLR7 agonist imiquimod (IMQ), IMQ-treated with vancomycin, and IMQ-treated with a cocktail of broad-spectrum antibiotics. We carried out faecal microbiota transplant (FMT) from donor CTR or IMQ mice to recipient IMQ or CTR animals, respectively. Vancomycin inhibited the increase in blood pressure; improved kidney injury, endothelial function, and oxidative stress; and reduced T helper (Th)17 infiltration in aortas from IMQ-treated mice. The rise in blood pressure and vascular complications present in IMQ mice were also observed in the CTR mice recipients of IMQ microbiota. Reduced relative populations of Sutterella and Anaerovibrio were associated with high blood pressure in our animals, which were increased after stool transplantation of healthy microbiota to IMQ mice. The reduced endothelium-dependent vasodilator responses to acetylcholine induced by IMQ microbiota were normalized after interleukin-17 neutralization. In conclusion, gut microbiota plays a role in the TLR7-driven increase in Th17 cell, endothelial dysfunction, vascular inflammation, and hypertension. The vascular changes induced by IMQ microbiota were initiated by Th17 infiltrating the vasculature.

[Autoimmune hemolytic anemia: Case review]. / Anemia hemolítica autoinmune: revisión de casos.

INTRODUCTION: Autoimmune hemolytic anemia (AIHA) is a rare and generally self-limiting disease in children. MATERIAL AND METHODS: A descriptive cross-sectional study was performed in children under 18 years diagnosed with AIHA from January/1997 to July/2019. Clinical variables were collected and AIHA was classified according to the direct antiglobulin test (DAT) in warm AIHA (IgG+/-C3d) and cold AIHA (C3d). Response to treatment and evolution were analyzed. RESULTS: 25 patients were included and 72% were males. The median age at diagnosis was 2 years (range 0.4 to 9). Fever (72%), pallor (68%), jaundice (64%), hepatosplenomegaly and coluria (48%) were the most common presenting symptoms. The median hemoglobin at diagnosis was 5.4 g/dl. DAT was positive in 96%, with detection of IgG antibodies in 76%. A single case presented negative DAT. 20% of the patients associated another cytopenia, one of which was subsequently diagnosed with common variable immunodeficiency. Concomitant viral infection was suspected or documented in 32%. Most of the cases were self-limiting and responded to corticosteroid treatment (72%). Those with partial response (24%), mainly those associated with other cytopenias, required other lines of treatment (rituximab, mycophenolate, immunoglobulins). Complications (32%) and relapses (26%) were detected only in warm AIHA. CONCLUSIONS: Our case series confirms that AIHA is a very rare disease in childhood. Most cases evolve favorably, although up to a quarter of them require second lines of treatment and, in exceptional cases, they need very aggressive treatments. These latter cases generally correspond to patients who present more than one cytopenia in the course of the disease.

Protective Effects of Short-Chain Fatty Acids on Endothelial Dysfunction Induced by Angiotensin II.

Short-chain fatty acids (SCFAs) are among the main classes of bacterial metabolic products and are mainly synthesized in the colon through bacterial fermentation. Short-chain fatty acids, such as acetate, butyrate, and propionate, reduce endothelial activation induced by proinflammatory mediators, at least in part, by activation of G protein-coupled receptors (GPRs): GPR41 and GPR43. The objective of the study was to analyze the possible protective effects of SCFAs on endothelial dysfunction induced by angiotensin II (AngII). Rat aortic endothelial cells (RAECs) and rat aortas were incubated with AngII (1 µM) for 6 h in the presence or absence of SCFAs (5-10 mM). In RAECs, we found that AngII reduces the production of nitric oxide (NO) stimulated by calcium ionophore A23187; increases the production of reactive oxygen species (ROS), both from the nicotinamide adenine dinucleotide phosphate oxidase system and the mitochondria; diminishes vasodilator-stimulated phosphoprotein (VASP) phosphorylation at Ser239; reduces GPR41 and GPR43 mRNA level; and reduces the endothelium-dependent relaxant response to acetylcholine in aorta. Coincubation with butyrate and acetate, but not with propionate, increases both NO production and pSer239-VASP, reduces the concentration of intracellular ROS, and improves relaxation to acetylcholine. The beneficial effects of butyrate were inhibited by the GPR41 receptor antagonist, ß-hydroxybutyrate, and by the GPR43 receptor antagonist, GLPG0794. Butyrate inhibited the down-regulation of GPR41 and GPR43 induced by AngII, being without effect acetate and propionate. Neither ß-hydroxybutyrate nor GLPG0794 affects the protective effect of acetate in endothelial dysfunction. In conclusion, acetate and butyrate improve endothelial dysfunction induced by AngII by increasing the bioavailability of NO. The effect of butyrate seems to be related to GPR41/43 activation, whereas acetate effects were independent of GPR41/43.