15 research outputs found

    Treatment with tocilizumab or corticosteroids for COVID-19 patients with hyperinflammatory state: a multicentre cohort study (SAM-COVID-19)

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    Objectives: The objective of this study was to estimate the association between tocilizumab or corticosteroids and the risk of intubation or death in patients with coronavirus disease 19 (COVID-19) with a hyperinflammatory state according to clinical and laboratory parameters. Methods: A cohort study was performed in 60 Spanish hospitals including 778 patients with COVID-19 and clinical and laboratory data indicative of a hyperinflammatory state. Treatment was mainly with tocilizumab, an intermediate-high dose of corticosteroids (IHDC), a pulse dose of corticosteroids (PDC), combination therapy, or no treatment. Primary outcome was intubation or death; follow-up was 21 days. Propensity score-adjusted estimations using Cox regression (logistic regression if needed) were calculated. Propensity scores were used as confounders, matching variables and for the inverse probability of treatment weights (IPTWs). Results: In all, 88, 117, 78 and 151 patients treated with tocilizumab, IHDC, PDC, and combination therapy, respectively, were compared with 344 untreated patients. The primary endpoint occurred in 10 (11.4%), 27 (23.1%), 12 (15.4%), 40 (25.6%) and 69 (21.1%), respectively. The IPTW-based hazard ratios (odds ratio for combination therapy) for the primary endpoint were 0.32 (95%CI 0.22-0.47; p < 0.001) for tocilizumab, 0.82 (0.71-1.30; p 0.82) for IHDC, 0.61 (0.43-0.86; p 0.006) for PDC, and 1.17 (0.86-1.58; p 0.30) for combination therapy. Other applications of the propensity score provided similar results, but were not significant for PDC. Tocilizumab was also associated with lower hazard of death alone in IPTW analysis (0.07; 0.02-0.17; p < 0.001). Conclusions: Tocilizumab might be useful in COVID-19 patients with a hyperinflammatory state and should be prioritized for randomized trials in this situatio

    Supplementary Materials - Exploring the anti-Inflammatory effect of Inulin by integrating transcriptomic and proteomic analyses in a murine macrophage cell model

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    Supplementary Table S1. Amplification system for the genes of interest and for the genes used for normalization in the qPCR validation. Supplementary Table S2. Normalized counts of all mapped genes from the RNA-Seq assay. Supplementary Table S3. Differentially expressed genes according to the differential expression analysis with DESeq2. Supplementary Table S4. diaPASEF-based protein quantification data for all the samples. A total of 6839 proteins were quantified by diaPASEF LC-MS/MS after processing of the runs as described in the Section 2 and Section 2.5.4. Supplementary Table S5. Differential abundance test for comparison of the LPS + I1 vs. LPS groups. Proteins with CV ≤ 20.0% and quantified in at least 50% of the samples of each group were considered. Fold changes, resulting p-values, and Benjamini–Hochberg corrected p-values for each of the 6065 considered proteins are shown. Supplementary Figure S1. Effect of inulin on the lysosome pathway (KEGG: 04142) from RAW 264.7 LPS-induced inflammation model cells. Pathway diagrams overlayed with the measured protein fold change showing coherent cascades. Differentially expressed genes are represented with positive values in red. Supplementary Figure S2. Effect of inulin on the NF-κB signaling pathway showing integrated transcriptomics data. Genes overexpressed (in red) or underexpressed (green) according to the transcriptomic analysis are highlighted. Supplementary Figure S3. Effect of Inulin on the IL-17 signaling pathway (KEGG: 04657) from RAW 264.7 LPS-induced inflammation model cells. Pathway diagram, overlayed with the measured protein perturbation showing coherent cascades. Differentially expressed genes are represented with negative fold-change values in blue and positive values in red.Peer reviewe
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