Zinc Deficiency And Stnf-Rii Are Associated With Worse Covid-19 Outcomes.


Journal

The Journal of nutrition
ISSN: 1541-6100
Titre abrégé: J Nutr
Pays: United States
ID NLM: 0404243

Informations de publication

Date de publication:
01 Dec 2023
Historique:
received: 28 09 2023
revised: 07 11 2023
accepted: 21 11 2023
medline: 4 12 2023
pubmed: 4 12 2023
entrez: 3 12 2023
Statut: aheadofprint

Résumé

Zinc (Zn) is known for its substantial involvement in immune response as an antioxidant and anti-inflammatory agent. Zinc plasma levels' clinical significance at COVID diagnosis is not yet fully established. We assessed the association between Zn deficiency, gut integrity, inflammation, and COVID-19 outcomes. A prospective observational cohort in which plasma zinc (Zn), soluble tumor necrosis factor alpha receptor II (sTNF-RII) intestinal fatty-acid binding protein (IFABP; marker of intestinal integrity), and zonulin levels (intestinal permeability) were collected from participants during the acute phase of a confirmed COVID-19 diagnosis. Zinc was modeled as continuous and binary, categorized as Zn deficiency (Zn<75 μg/dL) and Zn sufficiency (Zn ≥75 μg/dL). COVID-19 outcomes were classified according to the World Health Organization (WHO) clinical progression scale. We used cumulative probit regression to assess if suboptimal zinc levels, gut, and inflammatory markers increase the likelihood of worse COVID-19 outcomes. Zn deficiency was independently associated with 63% higher predicted odds of worse COVID outcomes. Increases in sTNF-RII [UOR: 3.43 (95%CI: 2.02, 5.82)] and zonulin [UOR: 1.83 (95%CI: 1.21, 2.76)] levels were associated with greater odds of worse COVID outcomes. IFABP was not associated with worse COVID outcomes [UOR: 1.12 (95%CI: 0.82, 1.53)] or acute zinc deficiency [UOR: 0.74 (95%CI: 0.43, 1.27)]. The adjusted predicted odds of worse COVID outcomes are 3-fold higher (p=0.04) for every one-unit decrease in zinc and is more than two times greater odds of COVID severity (p=0.01) for every one-unit increase in sTNF-RII. Zn deficiency and inflammation were independently associated with greater odds of worse COVID outcomes.

Sections du résumé

BACKGROUND BACKGROUND
Zinc (Zn) is known for its substantial involvement in immune response as an antioxidant and anti-inflammatory agent. Zinc plasma levels' clinical significance at COVID diagnosis is not yet fully established.
OBJECTIVES OBJECTIVE
We assessed the association between Zn deficiency, gut integrity, inflammation, and COVID-19 outcomes.
METHODS METHODS
A prospective observational cohort in which plasma zinc (Zn), soluble tumor necrosis factor alpha receptor II (sTNF-RII) intestinal fatty-acid binding protein (IFABP; marker of intestinal integrity), and zonulin levels (intestinal permeability) were collected from participants during the acute phase of a confirmed COVID-19 diagnosis. Zinc was modeled as continuous and binary, categorized as Zn deficiency (Zn<75 μg/dL) and Zn sufficiency (Zn ≥75 μg/dL). COVID-19 outcomes were classified according to the World Health Organization (WHO) clinical progression scale. We used cumulative probit regression to assess if suboptimal zinc levels, gut, and inflammatory markers increase the likelihood of worse COVID-19 outcomes.
RESULTS RESULTS
Zn deficiency was independently associated with 63% higher predicted odds of worse COVID outcomes. Increases in sTNF-RII [UOR: 3.43 (95%CI: 2.02, 5.82)] and zonulin [UOR: 1.83 (95%CI: 1.21, 2.76)] levels were associated with greater odds of worse COVID outcomes. IFABP was not associated with worse COVID outcomes [UOR: 1.12 (95%CI: 0.82, 1.53)] or acute zinc deficiency [UOR: 0.74 (95%CI: 0.43, 1.27)]. The adjusted predicted odds of worse COVID outcomes are 3-fold higher (p=0.04) for every one-unit decrease in zinc and is more than two times greater odds of COVID severity (p=0.01) for every one-unit increase in sTNF-RII.
CONCLUSION CONCLUSIONS
Zn deficiency and inflammation were independently associated with greater odds of worse COVID outcomes.

Identifiants

pubmed: 38043624
pii: S0022-3166(23)72747-8
doi: 10.1016/j.tjnut.2023.11.026
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2023. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Potential conflict of interests: G. A. M. has received grant support from ViiV, Tetraphase, Roche, Vanda, Astellas, and Genentech, and has served as a scientific advisor for Gilead, Merck, ViiV/GSK, Theratechnologies, and Janssen. All other authors report no potential conflicts of interest.

Auteurs

Christian Mouchati (C)

School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA. Electronic address: cfm71@case.edu.

Jared C Durieux (JC)

Center for Clinical Research, University Hospitals Cleveland Medical Center, Cleveland, Ohio, USA.

Sokratis N Zisis (SN)

School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA.

Heather Tribout (H)

Center for Clinical Research, University Hospitals Cleveland Medical Center, Cleveland, Ohio, USA.

Sarah Scott (S)

Center for Clinical Research, University Hospitals Cleveland Medical Center, Cleveland, Ohio, USA.

Beth Smith (B)

Center for Clinical Research, University Hospitals Cleveland Medical Center, Cleveland, Ohio, USA.

Danielle Labbato (D)

Center for Clinical Research, University Hospitals Cleveland Medical Center, Cleveland, Ohio, USA.

Grace A McComsey (GA)

School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA; Center for Clinical Research, University Hospitals Cleveland Medical Center, Cleveland, Ohio, USA. Electronic address: gam9@case.edu.

Classifications MeSH