C-reactive protein rise in response to macronutrient deficit early in critical illness: sign of inflammation or mediator of infection prevention and recovery.

CRP Critical illness Cytokines Early macronutrient restriction Infection Inflammation

Journal

Intensive care medicine
ISSN: 1432-1238
Titre abrégé: Intensive Care Med
Pays: United States
ID NLM: 7704851

Informations de publication

Date de publication:
Jan 2022
Historique:
received: 17 06 2021
accepted: 22 10 2021
pubmed: 25 11 2021
medline: 31 3 2022
entrez: 24 11 2021
Statut: ppublish

Résumé

Withholding parenteral nutrition (PN) early in critical illness, late-PN, has shown to prevent infections despite a higher peak C-reactive protein (CRP). We investigated whether the accentuated CRP rise was caused by a systemic inflammatory effect mediated by cytokines or arose as a consequence of the different feeding regimens, and whether it related to improved outcome with late-PN. This secondary analysis of the EPaNIC-RCT first investigated, with multivariable linear regression analyses, determinants of late-PN-induced CRP rise and its association with cytokine responses (IL-6, IL-10, TNF-α) in matched early-PN and late-PN patients requiring intensive care for ≥ 3 days. Secondly, with multivariable logistic regression and Cox proportional-hazard analyses, we investigated whether late-PN-induced CRP rises mediated infection prevention and enhanced recovery or reflected an adverse effect counteracting such benefits of late-PN. CRP peaked on day 3, higher with late-PN [216(152-274)mg/l] (n = 946) than with early-PN [181(122-239)mg/l] (n = 946) (p < 0.0001). Independent determinants of higher CRP rise were lower carbohydrate and protein intakes (p ≤ 0.04) with late-PN, besides higher blood glucose and serum insulin concentrations (p ≤ 0.01). Late-PN did not affect cytokines. Higher CRP rises were independently associated with more infections and lower likelihood of early ICU discharge (p ≤ 0.002), and the effect size of late-PN versus early-PN on these outcomes was increased rather than reduced after adjusting for CRP rise, not confirming a mediating role. The higher CRP rise with late-PN, explained by the early macronutrient deficits, did not relate to cytokine responses and thus did not reflect more systemic inflammation. Instead of mediating clinical benefit on infection or recovery, the accentuated CRP rise appeared an adverse effect reducing such late-PN benefits.

Identifiants

pubmed: 34816288
doi: 10.1007/s00134-021-06565-1
pii: 10.1007/s00134-021-06565-1
doi:

Substances chimiques

C-Reactive Protein 9007-41-4

Banques de données

ClinicalTrials.gov
['NCT00512122']

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

25-35

Subventions

Organisme : ku leuven
ID : C24/17/070
Organisme : flemish government, methusalem program
ID : METH14/06
Organisme : european research council advanced grants
ID : AdvG-2012-321670
Organisme : european research council advanced grants
ID : AdvG-2017-785809

Informations de copyright

© 2021. Springer-Verlag GmbH Germany, part of Springer Nature.

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Auteurs

Catherine Ingels (C)

Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, 3000, Leuven, Belgium. catherine.ingels@kuleuven.be.

Lies Langouche (L)

Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, 3000, Leuven, Belgium.

Jasperina Dubois (J)

Department of Anesthesia and Intensive Care, Jessa Hospital, Salvatorstraat 20, 3500, Hasselt, Belgium.

Inge Derese (I)

Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, 3000, Leuven, Belgium.

Sarah Vander Perre (S)

Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, 3000, Leuven, Belgium.

Pieter J Wouters (PJ)

Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, 3000, Leuven, Belgium.

Jan Gunst (J)

Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, 3000, Leuven, Belgium.

Michaël Casaer (M)

Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, 3000, Leuven, Belgium.

Fabian Güiza (F)

Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, 3000, Leuven, Belgium.

Ilse Vanhorebeek (I)

Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, 3000, Leuven, Belgium.

Greet Van den Berghe (G)

Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, 3000, Leuven, Belgium.

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