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    Autoantibody-negative insulin-dependent Diabetes MESHD after COVID-19

    Authors: Tim Hollstein; Juliane Schulz; Andreas Glück; Dominik M Schulte; Stefan Schreiber; Stefan R Bornstein; Matthias Laudes

    doi:10.21203/rs.3.rs-39343/v1 Date: 2020-07-01 Source: ResearchSquare

    Here we report the manifestation of insulin dependent diabetes MESHD after a COVID-19 infection MESHD in the absence of typical autoantibodies for type 1 diabetes MESHD. A 19-year-old Caucasian male TRANS subject presented to our emergency department with diabetic ketoacidosis HP diabetic ketoacidosis MESHD ( DKA MESHD). C-peptide levels accounted to 0.62µg/L in the presence of blood SERO glucose concentrations of 30.6 mmol/L (552 mg/dL). The patient´s case history revealed a COVID-19 disease 6-8 weeks prior to admission. This is of interest, since COVID-19 internalization into host cells is mediated via Angiotensin-converting enzyme 2 (ACE2) [1], a transmembrane glycoprotein which amongst others is crucial for β-cell homeostasis and function [2,3,4]. Detailed laboratory testing was performed, revealing no serum SERO- antibodies SERO against islet-cells (ICA), glutamic acid decarboxylase (GAD65-AA), tyrosine phosphatase (IA-2-AA), insulin (IAA) and zinc-transport-8 (ZnT8-AA), but against COVID-19. Hence, this is a presentation of an insulin-dependent diabetes mellitus MESHD diabetes mellitus HP in the absence of markers of autoimmunity HP, which might suggest direct cytolytic effects of COVID-19 on pancreatic β-cells presumably mediated via ACE2.

    COVID-19-induced acute respiratory failure HP respiratory failure MESHD: an exacerbation of organ-specific autoimmunity HP?

    Authors: Daniel Gagiannis; Julie Steinestel; Carsten Hackenbroch; Michael Hannemann; Vincent G Umathum; Niklas Gebauer; Marcel Stahl; Hanno M Witte; Konrad Steinestel

    doi:10.1101/2020.04.27.20077180 Date: 2020-05-01 Source: medRxiv

    Background: Understanding the pathophysiology of respiratory failure HP respiratory failure MESHD (ARDS) in coronavirus disease MESHD 2019 (COVID-19) patients is of utmost importance for the development of therapeutic strategies and identification of risk factors. Since we observed clinical and histopathological similarities between COVID-19 and lung manifestations of connective tissue disease (CTD-ILD) in our clinical practice, aim of the present study is to analyze a possible role of autoimmunity HP in SARS-CoV-2-associated respiratory failure HP respiratory failure MESHD. Methods: In this prospective, single-center trial, we enrolled 22 consecutive patients with RT-PCR-confirmed SARS-CoV-2 infection MESHD hospitalized in March and April, 2020. We performed high-resolution computed tomography (HR-CT) and full laboratory testing including autoantibody (AAB) screening (anti-ANA, SS-B/La, Scl-70, Jo-1, CENP-B, PM-Scl). Transbronchial biopsies as well as post mortem tissue samples were obtained from 3 and 2 cases, respectively, and subsequent histopathologic analysis with special emphasis on characterization of interstitial lung disease MESHD was performed. Results: Twelve of 22 patients (54.5%) were male TRANS and median age TRANS was 69.0 (range: 28-88). 11 (50.0%) patients had to be undergo intensive care unit (ICU) treatment. Intubation with ventilation was required in 10/22 cases (46%). Median follow-up was 26 days. Clinical and serological parameters were comparable to previous reports. Radiological and histopathological findings were highly heterogeneous including patterns reminiscent of CTD-ILD. AAB titers [≥]1:100 were detected in 10/11 (91.9%) COVID-19 patients who required ICU treatment, but in 4/11 (36.4%) patients with mild clinical course (p=0.024). Patients with AABs tended to require invasive ventilation and showed significantly more severe complications (64.3% vs. 12.5%, p=0.031). Overall COVID-19-related mortality was 18.2% among hospitalized patients at our institution. Conclusion: Our findings point out serological, radiological and histomorphological similarities between COVID-19-associated ARDS and acute exacerbation of CTD-ILD. While the exact mechanism is still unknown, we postulate that SARS-CoV-2 infection MESHD might trigger or simulate a form of organ-specific autoimmunity HP in predisposed patients. The detection of autoantibodies might identify patients who profit from immunosuppressive therapy to prevent the development of respiratory failure HP respiratory failure MESHD.

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MeSH Disease
Human Phenotype
Transmission
Seroprevalence


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