The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and its associated coagulopathy are particularly worrisome in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS), as these diseases carry an increased risk of thrombotic complications. Mathian et al recently reported the clinical course of COVID-19 in a series of 17 patients with SLE under chronic hydroxychloroquine therapy. 1 Of note, only one patient (6%) presented thrombosis despite the fact that four patients (24%) had a history of secondary APS, and five patients (29%) were receiving oral anticoagulants. Antiphospholipid (aPL) antibodies were not measured in these patients during active SARS-CoV-2 infection. 1 The American Society of Hematology recently stated that 'at the current time, there are only very limited data on aPL antibodies in COVID-19 and it is unclear if they represent an epiphenomenon or are actually involved in any haemostatic abnormalities seen in COVID-19 disease'. 2 Furthermore, almost all the available information refers to the lupus anticoagulant, with frequencies ranging from 45% to 87%. 3 4 This paucity of data led us to test a panel of aPL antibodies in blood specimens from 21 patients hospitalised in the intensive care unit between 12 and 19 April, due to severe or critical COVID-19, and received at our laboratory on 20 April to measure interleukin-6 levels. Anticardiolipin, anti-β 2 glycoprotein I, antiprothrombin, antiphosphatidylserine, antiphosphatidylinositol and antiannexin V antibodies were measured, each in IgM and IgG isotypes. Subsequently, demographic and clinical data were obtained from electronic medical records. Sera collected before the SARS-CoV-2 pandemic from 12 healthy individuals, matched for age and sex, were tested as controls.Pertinent results are summarised in table 1. The median age of patients was 62 years; 43% were men; and a high number of comorbidities were observed (median Charlson Comorbidity Index of 3). A total of 19 patients (90%) had shortness of breath on admission, and 12 (57%) eventually required invasive mechanical ventilation during hospitalisation. Elevated levels of D-dimer, ferritin and C reactive protein were found at presentation.Of the 21 patients with COVID-19 studied, 12 had at least one circulating aPL antibody, whereas only 1 of the 12 controls yielded a positive result (57% vs 8%; Fisher's exact test, p=0.009). The most frequently detected aPL antibodies were antiannexin V IgM (19%), anticardiolipin IgM (14%), antiphosphatidylserine IgM (14%), anticardiolipin IgG (10%) and antiphosphatidylserine IgG (10%) antibodies. One patient had triple positivity (8%); three patients had double positivity (25%); and the remaining eight had a single positivity (67%). Age and number of comorbidities tended to be lower in patients with aPL antibodies. In contrast, levels of D-dimer, ferritin and C reactive protein were higher both on admission and throughout the hospital stay in these patients. Elevated levels of interleukin-6 (>40 pg/mL) wer...
Recently, different microRNA (miRNA) gene polymorphisms have been evaluated in patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and Graves’ disease (GD). In the present study, we examined three single-nucleotide polymorphisms (SNPs) located in the pre-miR-146a (rs2910164G/C), pre-miR-196a-2 (rs11614913C/T), and pre-miR-499 (rs3746444A/G) genes. Our study population included 900 Mexican patients with RA, SLE, or GD, as well as 486 healthy control individuals with no family history of inflammatory or autoimmune diseases. Genotyping was performed using TaqMan probes and a 5′ exonuclease assay. None of the investigated SNPs were associated with RA or GD susceptibility under any genetic model (co-dominant, recessive, or dominant). Genotype and allele frequencies of the miR-196a-2 rs11614913C/T polymorphism were similar between SLE cases and controls. In contrast, the miR-146a rs2910164G/C and miR-499 rs3746444A/G polymorphisms were associated with SLE susceptibility. These SNPs were not associated with lupus nephritis (LN). Our results suggest that polymorphisms in miR-146a, miR-196a-2, and miR-499 are not associated with RA or GD susceptibility. This is the first report documenting that the miR-146a rs2910164G/C and miR-499 rs3746444 polymorphisms are associated with SLE susceptibility but not with LN.
Our data provide the first demonstration that PTPN22 R620W confers GD susceptibility among Latin-American patients. Moreover, this is the second report documenting the association of PTPN22 R263Q with protection against SLE and RA.
Background: Information about angiotensin II (Ang II), angiotensin-converting enzyme 2 (ACE2), and Ang-(1–7) levels in patients with COVID-19 is scarce. Objective: To characterize the Ang II–ACE2–Ang-(1–7) axis in patients with SARS-CoV-2 infection to understand its role in pathogenesis and prognosis. Methods: Patients greater than 18 years diagnosed with COVID-19, based on clinical findings and positive RT-PCR test, who required hospitalization and treatment were included. We compared Ang II, aldosterone, Ang-(1–7), and Ang-(1–9) concentrations and ACE2 concentration and activity between COVID-19 patients and historic controls. We compared baseline demographics, laboratory results (enzyme, peptide, and inflammatory marker levels), and outcome (patients who survived versus those who died). Results: Serum from 74 patients [age: 58 (48–67.2) years; 68% men] with moderate (20%) or severe (80%) COVID-19 were analyzed. During 13 (10–21) days of hospitalization, 25 patients died from COVID-19 and 49 patients survived. Compared with controls, Ang II concentration was higher and Ang-(1–7) concentration was lower, despite significantly higher ACE2 activity in patients. Ang II concentration was higher and Ang-(1–7) concentration was lower in patients who died. The Ang II/Ang-(1–7) ratio was significantly higher in patients who died. In multivariate analysis, Ang II/Ang-(1–7) ratio greater than 3.45 (OR = 5.87) and lymphocyte count ⩽0.65 × 103/µl (OR = 8.43) were independent predictors of mortality from COVID-19. Conclusion: In patients with severe SARS-CoV-2 infection, imbalance in the Ang II–ACE2–Ang-(1–7) axis may reflect deleterious effects of Ang II and may indicate a worse outcome.
Circulating microRNAs (miRNAs) and the functional implications of miRNAs contained in extracellular vesicles (EVs) have gained attention in the last decade. Little is known about the regulation of the abundance of plasma miRNAs in response to chronic ingestion of carbohydrates. Therefore, we explored the circulating levels of miR-21, miR-146a, miR-155, and miR-223 in rats consuming sucrose in drinking water. Weanling Wistar rats were 25 weeks with 30% sucrose in drinking water, and miRNAs expression was determined in total plasma and in microvesicles, by RT-qPCR with TaqMan probe based assays for miR-21, miR-146a, miR-155, and miR-223, using cel-miR-39 (as spike in control and reference). Endotoxemia was also measured. Sucrose-fed animals showed higher body weight and retroperitoneal adipose tissue as well as higher glucose and triglyceride plasma levels than controls. Plasma endotoxin levels were low and not different among groups. Plasma miR-21 and miR-223 were higher in the sucrose group (p < 0.05), whereas miR-155 tended to be lower (p = 0.0661), and miR-146a did not show significant differences. In the plasma EVs the same trend was found except for miR-146a that showed significantly higher levels (p < 0.05). Overall, our results show that high carbohydrate ingestion modulates circulating miRNAs levels related to an inflammatory response.
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