Corpus overview


MeSH Disease

Human Phenotype


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    Changes in Cause-of- Death MESHD Attribution During the Covid-19 Pandemic: Association with Hospital Quality Metrics and Implications for Future Research

    Authors: Kathleen A. Fairman; Kellie J. Goodlet; James D. Rucker

    doi:10.1101/2020.07.25.20162198 Date: 2020-07-28 Source: medRxiv

    Background: Severe acute respiratory syndrome MESHD coronavirus 2 (SARS-CoV-2) is often comorbid with conditions subject to quality metrics (QM) used for hospital performance SERO assessment and rate-setting. Although diagnostic coding change in response to financial incentives is well documented, no study has examined the association of QM with SARS-CoV-2 cause-of- death MESHD attribution (CODA). Calculations of excess all-cause deaths MESHD overlook the importance of accurate CODA and of distinguishing policy-related from virus-related mortality. Objective: Examine CODA, overall and for QM and non-QM diagnoses, in 3 pandemic periods: awareness (January 19-March 14), height (March 15-May 16), and late (May 17-June 20). Methods: Retrospective analysis of publicly available national weekly COD data, adjusted for population growth and reporting lags, October 2014-June 20, 2020. CODA in 5 pre-pandemic influenza seasons was compared with 2019-20. Suitability of the data to distinguish policy-related from virus-related effects was assessed. Results: Following federal guidance permitting SARS-CoV-2 CODA without laboratory testing, mortality from the QM diagnoses cancer and chronic lower respiratory disease MESHD declined steadily relative to prior-season means, reaching 4.4% less and 12.1% less, respectively, in late pandemic. Deaths MESHD for non-QM diagnoses increased, by 21.0% for Alzheimers disease MESHD Alzheimers disease HP and 29.0% for diabetes during pandemic height. Increases in competing CODs over historical experience, suggesting SARS-CoV-2 underreporting, more than offset declines during pandemic height. However, in the late-pandemic period, declines slightly numerically exceeded increases, suggesting SARS-CoV-2 overreporting. In pandemic-height and late-pandemic periods, respectively, only 83.5% and 69.7% of increases in all-cause deaths MESHD were explained by changes in the reported CODs, including SARS-CoV-2, preventing assessment of policy-related mortality or of factors contributing to increased all-cause deaths MESHD. Conclusions: Substitution of SARS-CoV-2 for competing CODs may have occurred, particularly for QM diagnoses and late in the pandemic. Continued monitoring of these trends, qualitative research on pandemic CODA, and the addition of place-of- death MESHD data and psychiatric CODs to the file would facilitate assessment of policy-related and virus-related effects on mortality.

    Potential involvement of monoamine oxidase activity in SARS-COV2 infection MESHD and delirium MESHD delirium HP onset

    Authors: Miroslava Cuperlovic-Culf; Emma L Cunningham; Anuradha Surendra; Xiaobei Pan; Steffany A.L. Bennett; Mijin Jung; Bernadette McGuiness; Anthony Peter Passmore; Danny McAuley; David Beverland; Brian D. Green

    doi:10.1101/2020.06.16.20128660 Date: 2020-06-19 Source: medRxiv

    Abstract Severe acute respiratory syndrome MESHD coronavirus 2 (SARS-CoV-2) causes a range of extra- respiratory signs and symptoms MESHD. One such manifestation is delirium MESHD delirium HP, an acute confusional state occurring in 60-70% of severe SARS-CoV-2 cases. Delirium MESHD Delirium HP is also a common clinical syndrome MESHD following planned orthopedic surgery. This investigation initially explored the underlying role of metabolism in delirium MESHD delirium HP-susceptibility in this setting. Metabolomics profiles of cerebrospinal fluid (CSF) and blood SERO taken prior to surgery found significant concentration differences of several amino acids, acylcarnitines and polyamines were observed in delirium MESHD delirium HP-prone patients. Phenethylamine (PEA) concentrations in delirium MESHD delirium HP-prone patients was significantly lower in CSF than in blood SERO, whilst in age TRANS- and gender TRANS-matched controls the opposite was observed (adjusted p values: 1.8x10-6 (control) and 1.788x10-10 ( delirium MESHD delirium HP)). PEA is metabolised by monoamine oxidase B (MAOB), a putative enzyme target for the treatment of Alzheimers disease MESHD Alzheimers disease HP, Parkinsons disease MESHD and depression. Our computational structural comparisons of MAOB and angiotensin converting enzyme (ACE) 2 found high similarity, specifically within the SARS-CoV-2 spike protein. MAOB structural alignment to ACE2 was 51% overall, but this was over 95% in the ACE2-spike protein binding region. Thus, it is possible that the spike protein interacts with MAOB on a molecular level. A previously published metabolomic dataset of control subjects and patients with either mild or severe COVID-19 was then analysed. Major concentration differences in some metabolites attributed to altered MAO activity were detected. Therefore, our hypothesis is that the SARS-CoV-2 influences MAOB activity, which is one potential cause for the many observed neurological and platelet based complications of SARS-CoV-2 infection MESHD. Further research is required to establish what effect MAOB inhibitors might have on these pathways. There is no evidence at present to support the withholding of MAOB inhibitors.

    Deaths MESHD from Covid-19: Who are the forgotten victims?

    Authors: Kieran Docherty; Jawad Butt; Rudolf de Boer; Pooja Dewan; Lars Koeber; Aldo Maggioni; John McMurray; Scott Solomon; Pardeep Singh Jhund

    doi:10.1101/2020.04.21.20073114 Date: 2020-04-24 Source: medRxiv

    Background: With the global pandemic of coronavirus disease MESHD 2019 (Covid-19) there has been disruption to normal clinical activity in response to the increased demand on health services. There are reports of a reduction in non-Covid-19 emergency MESHD presentations. Consequentially, there are concerns that deaths MESHD from non-Covid-19 causes could increase. We examined recent reported population-based mortality rates, compared with expected rates, and compared any excess in deaths MESHD with the number of deaths MESHD attributed to Covid-19. Methods: National agency and death MESHD registration reports were searched for numbers of deaths MESHD attributed to Covid-19 and overall mortality that had been publicly reported by 06 May 2020. Data on the number of deaths MESHD attributed to Covid-19, the total number of deaths MESHD registered in the population and the historical average over at least 3 years were collected. Data were available for 4 European countries (England & Wales, Scotland, Netherlands and Italy) and New York State, United States of America. Results: There was an increase in observed, compared with expected, mortality in Scotland (+68%), England and Wales (+74%), the Netherlands (+58%), Italy (+39%) and New York state (+49%). Of these deaths MESHD, only 73% in Scotland, 71 % in England and Wales, 53% in the Netherlands, 54% in Italy and 79% in New York state were attributed to Covid-19 leaving a number of excess deaths MESHD not attributed to Covid-19. In the 5-week period of study, Scotland, 10% of the excess of deaths MESHD were attributed to dementia MESHD dementia HP/ Alzheimers disease MESHD Alzheimers disease HP and 7% to cardiovascular causes. Conclusion: A substantial proportion of excess deaths MESHD observed during the current COVID-19 pandemic are not attributed to COVID-19 and may represent unrecognised deaths MESHD due to Covid-19, an excess of deaths MESHD due to other causes, or both. The impact of Covid-19 on mortality and morbidity from other causes needs to be quantified and addressed in public health planning.

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MeSH Disease
Human Phenotype

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