ORCID Profile
0000-0001-8227-0909
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Publisher: Wiley
Date: 17-02-2021
DOI: 10.1111/ANS.16592
Publisher: Wiley
Date: 09-03-2021
DOI: 10.1111/ANAE.15458
Abstract: Peri‐operative SARS‐CoV‐2 infection increases postoperative mortality. The aim of this study was to determine the optimal duration of planned delay before surgery in patients who have had SARS‐CoV‐2 infection. This international, multicentre, prospective cohort study included patients undergoing elective or emergency surgery during October 2020. Surgical patients with pre‐operative SARS‐CoV‐2 infection were compared with those without previous SARS‐CoV‐2 infection. The primary outcome measure was 30‐day postoperative mortality. Logistic regression models were used to calculate adjusted 30‐day mortality rates stratified by time from diagnosis of SARS‐CoV‐2 infection to surgery. Among 140,231 patients (116 countries), 3127 patients (2.2%) had a pre‐operative SARS‐CoV‐2 diagnosis. Adjusted 30‐day mortality in patients without SARS‐CoV‐2 infection was 1.5% (95%CI 1.4–1.5). In patients with a pre‐operative SARS‐CoV‐2 diagnosis, mortality was increased in patients having surgery within 0–2 weeks, 3–4 weeks and 5–6 weeks of the diagnosis (odds ratio (95%CI) 4.1 (3.3–4.8), 3.9 (2.6–5.1) and 3.6 (2.0–5.2), respectively). Surgery performed ≥ 7 weeks after SARS‐CoV‐2 diagnosis was associated with a similar mortality risk to baseline (odds ratio (95%CI) 1.5 (0.9–2.1)). After a ≥ 7 week delay in undertaking surgery following SARS‐CoV‐2 infection, patients with ongoing symptoms had a higher mortality than patients whose symptoms had resolved or who had been asymptomatic (6.0% (95%CI 3.2–8.7) vs. 2.4% (95%CI 1.4–3.4) vs. 1.3% (95%CI 0.6–2.0), respectively). Where possible, surgery should be delayed for at least 7 weeks following SARS‐CoV‐2 infection. Patients with ongoing symptoms ≥ 7 weeks from diagnosis may benefit from further delay.
Publisher: Oxford University Press (OUP)
Date: 24-03-2021
DOI: 10.1093/BJS/ZNAB101
Abstract: Preoperative SARS-CoV-2 vaccination could support safer elective surgery. Vaccine numbers are limited so this study aimed to inform their prioritization by modelling. The primary outcome was the number needed to vaccinate (NNV) to prevent one COVID-19-related death in 1 year. NNVs were based on postoperative SARS-CoV-2 rates and mortality in an international cohort study (surgical patients), and community SARS-CoV-2 incidence and case fatality data (general population). NNV estimates were stratified by age (18–49, 50–69, 70 or more years) and type of surgery. Best- and worst-case scenarios were used to describe uncertainty. NNVs were more favourable in surgical patients than the general population. The most favourable NNVs were in patients aged 70 years or more needing cancer surgery (351 best case 196, worst case 816) or non-cancer surgery (733 best case 407, worst case 1664). Both exceeded the NNV in the general population (1840 best case 1196, worst case 3066). NNVs for surgical patients remained favourable at a range of SARS-CoV-2 incidence rates in sensitivity analysis modelling. Globally, prioritizing preoperative vaccination of patients needing elective surgery ahead of the general population could prevent an additional 58 687 (best case 115 007, worst case 20 177) COVID-19-related deaths in 1 year. As global roll out of SARS-CoV-2 vaccination proceeds, patients needing elective surgery should be prioritized ahead of the general population.
Publisher: Springer Science and Business Media LLC
Date: 02-04-2019
Publisher: Elsevier BV
Date: 02-2021
Publisher: American Physiological Society
Date: 03-2008
DOI: 10.1152/AJPRENAL.00372.2007
Abstract: In experimental membranous nephropathy, complement C5b-9-induced glomerular epithelial cell (GEC) injury leads to morphological changes in GEC and proteinuria, in association with phospholipase A 2 (PLA 2 ) activation. The present study addresses the role of calcium-independent PLA 2 (iPLA 2 ) in GEC injury. iPLA 2 β short and iPLA 2 γ were expressed in cultured rat GEC and normal rat glomeruli. To determine whether iPLA 2 is involved in complement-mediated arachidonic acid (AA) release, GEC were stably transfected with iPLA 2 γ or iPLA 2 β cDNAs (GEC-iPLA 2 γ GEC-iPLA 2 β). Compared with control cells (GEC-Neo), GEC-iPLA 2 γ and GEC-iPLA 2 β demonstrated greater expression of iPLA 2 proteins and activities. Complement-mediated release of [ 3 H]AA was augmented significantly in GEC-iPLA 2 γ compared with GEC-Neo, and the augmented [ 3 H]AA release was inhibited by the iPLA 2 -directed inhibitor bromoenol lactone (BEL). For comparison, overexpression of iPLA 2 γ also lified [ 3 H]AA release after incubation of GEC with H 2 O 2 , or chemical anoxia followed by reexposure to glucose (in vitro ischemia-reperfusion injury). In parallel with release of [ 3 H]AA, complement-mediated production of prostaglandin E 2 was lified in GEC-iPLA 2 γ. Complement-mediated cytotoxicity was attenuated significantly in GEC-iPLA 2 γ compared with GEC-Neo, and the cytoprotective effect of iPLA 2 γ was reversed by BEL, and in part by indomethacin. Overexpression of iPLA 2 β did not lify complement-dependent [ 3 H]AA release, but nonetheless attenuated complement-mediated cytotoxicity. Thus iPLA 2 γ may be involved in complement-mediated release of AA. Expression of iPLA 2 γ or iPLA 2 β induces cytoprotection against complement-dependent GEC injury. Modulation of iPLA 2 activity may prove to be a novel approach to reducing GEC injury.
No related grants have been discovered for Daniel Cohen.