A multicenter randomized clinical trial of pharmacological vitamin B1 administration to critically ill patients who develop hypophosphatemia during enteral nutrition (The THIAMINE 4 HYPOPHOSPHATEMIA trial).


Journal

Clinical nutrition (Edinburgh, Scotland)
ISSN: 1532-1983
Titre abrégé: Clin Nutr
Pays: England
ID NLM: 8309603

Informations de publication

Date de publication:
08 2021
Historique:
received: 27 05 2021
revised: 02 07 2021
accepted: 17 07 2021
pubmed: 14 8 2021
medline: 28 12 2021
entrez: 13 8 2021
Statut: ppublish

Résumé

Hypophosphatemia may be a useful biomarker to identify thiamine deficiency in critically ill enterally-fed patients. The objective was to determine whether intravenous thiamine affects blood lactate, biochemical and clinical outcomes in this group. This randomized clinical trial was conducted across 5 Intensive Care Units. Ninety critically ill adult patients with a serum phosphate ≤0.65 mmol/L within 72 h of commencing enteral nutrition were randomized to intravenous thiamine (200 mg every 12 h for up to 14 doses) or usual care (control). The primary outcome was blood lactate over time and data are median [IQR] unless specified. Baseline variables were well balanced (thiamine: lactate 1.2 [1.0, 1.6] mmol/L, phosphate 0.56 [0.44, 0.64] mmol/L vs. control: lactate 1.0 [0.8, 1.3], phosphate 0.54 [0.44, 0.61]). Patients randomized to the intervention received a median of 11 [7.5, 13.5] doses for a total of 2200 [1500, 2700] mg of thiamine. Blood lactate over the entire 7 days of treatment was similar between groups (mean difference = -0.1 (95 % CI -0.2 to 0.1) mmol/L; P = 0.55). The percentage change from lactate pre-randomization to T = 24 h was not statistically different (thiamine: -32 (-39, -26) vs. control: -24 (-31, -16) percent, P = 0.09). Clinical outcomes were not statistically different (days of vasopressor administration: thiamine 2 [1, 4] vs. control 2 [0, 5.5] days; P = 0.37, and deaths 9 (21 %) vs. 5 (11 %); P = 0.25). In critically ill enterally-fed patients who developed hypophosphatemia, intravenous thiamine did not cause measurable differences in blood lactate or clinical outcomes. Australian and New Zealand Clinical Trials Registry (ACTRN12619000121167).

Sections du résumé

BACKGROUND
Hypophosphatemia may be a useful biomarker to identify thiamine deficiency in critically ill enterally-fed patients. The objective was to determine whether intravenous thiamine affects blood lactate, biochemical and clinical outcomes in this group.
METHOD
This randomized clinical trial was conducted across 5 Intensive Care Units. Ninety critically ill adult patients with a serum phosphate ≤0.65 mmol/L within 72 h of commencing enteral nutrition were randomized to intravenous thiamine (200 mg every 12 h for up to 14 doses) or usual care (control). The primary outcome was blood lactate over time and data are median [IQR] unless specified.
RESULTS
Baseline variables were well balanced (thiamine: lactate 1.2 [1.0, 1.6] mmol/L, phosphate 0.56 [0.44, 0.64] mmol/L vs. control: lactate 1.0 [0.8, 1.3], phosphate 0.54 [0.44, 0.61]). Patients randomized to the intervention received a median of 11 [7.5, 13.5] doses for a total of 2200 [1500, 2700] mg of thiamine. Blood lactate over the entire 7 days of treatment was similar between groups (mean difference = -0.1 (95 % CI -0.2 to 0.1) mmol/L; P = 0.55). The percentage change from lactate pre-randomization to T = 24 h was not statistically different (thiamine: -32 (-39, -26) vs. control: -24 (-31, -16) percent, P = 0.09). Clinical outcomes were not statistically different (days of vasopressor administration: thiamine 2 [1, 4] vs. control 2 [0, 5.5] days; P = 0.37, and deaths 9 (21 %) vs. 5 (11 %); P = 0.25).
CONCLUSIONS
In critically ill enterally-fed patients who developed hypophosphatemia, intravenous thiamine did not cause measurable differences in blood lactate or clinical outcomes.
TRIAL REGISTRATION
Australian and New Zealand Clinical Trials Registry (ACTRN12619000121167).

Identifiants

pubmed: 34388414
pii: S0261-5614(21)00358-7
doi: 10.1016/j.clnu.2021.07.024
pii:
doi:

Substances chimiques

Biomarkers 0
Phosphates 0
Lactic Acid 33X04XA5AT
Thiamine X66NSO3N35

Types de publication

Journal Article Multicenter Study Randomized Controlled Trial Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

5047-5052

Informations de copyright

Copyright © 2021 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.

Auteurs

Adam M Deane (AM)

The University of Melbourne, Department of Critical Care, Melbourne Medical School, Melbourne, Australia; Intensive Care Unit, Royal Melbourne Hospital, Melbourne, Australia. Electronic address: adam.deane@mh.org.au.

Alice Jiang (A)

Monash University, Department of Epidemiology and Preventive Medicine, Australian and New Zealand Intensive Care Research Centre, Melbourne, Australia.

Brianna Tascone (B)

Intensive Care Unit, Royal Melbourne Hospital, Melbourne, Australia.

Annabelle Clancy (A)

Intensive Care Unit, Royal Melbourne Hospital, Melbourne, Australia.

Mark E Finnis (ME)

The University of Melbourne, Department of Critical Care, Melbourne Medical School, Melbourne, Australia; Monash University, Department of Epidemiology and Preventive Medicine, Australian and New Zealand Intensive Care Research Centre, Melbourne, Australia; The University of Adelaide, Discipline of Acute Care Medicine, Adelaide, Australia.

Jake T Collie (JT)

RMIT University, School of Health and Biomedical Sciences, Melbourne, Australia.

Ronda Greaves (R)

RMIT University, School of Health and Biomedical Sciences, Melbourne, Australia; Victorian Clinical Genetics Services, Murdoch Children's Research Institute, Melbourne, Australia.

Kathleen M Byrne (KM)

Intensive Care Unit, Royal Melbourne Hospital, Melbourne, Australia.

Tomoko Fujii (T)

Monash University, Department of Epidemiology and Preventive Medicine, Australian and New Zealand Intensive Care Research Centre, Melbourne, Australia; Intensive Care Unit, Jikei University Hospital, Tokyo, Japan.

James S Douglas (JS)

Department of Intensive Care, Western Health, Melbourne, Australia.

Alistair Nichol (A)

Monash University, Department of Epidemiology and Preventive Medicine, Australian and New Zealand Intensive Care Research Centre, Melbourne, Australia; School of Medicine and Medical Sciences, University College Dublin, Dublin, Ireland; Department of Intensive Care and Hyperbaric Medicine, The Alfred, Melbourne, Australia.

Andrew A Udy (AA)

Monash University, Department of Epidemiology and Preventive Medicine, Australian and New Zealand Intensive Care Research Centre, Melbourne, Australia; Department of Intensive Care and Hyperbaric Medicine, The Alfred, Melbourne, Australia.

Meredith Young (M)

Department of Intensive Care and Hyperbaric Medicine, The Alfred, Melbourne, Australia.

Giovanni Russo (G)

Intensive Care Unit, Royal Melbourne Hospital, Melbourne, Australia.

Kate Fetterplace (K)

The University of Melbourne, Department of Critical Care, Melbourne Medical School, Melbourne, Australia; Intensive Care Unit, Royal Melbourne Hospital, Melbourne, Australia.

Matthew J Maiden (MJ)

The University of Adelaide, Discipline of Acute Care Medicine, Adelaide, Australia; Intensive Care Unit, Barwon Health, Geelong, Australia.

Mark P Plummer (MP)

The University of Melbourne, Department of Critical Care, Melbourne Medical School, Melbourne, Australia; Intensive Care Unit, Royal Melbourne Hospital, Melbourne, Australia.

Fumitaka Yanase (F)

Department of Intensive Care, Austin Hospital, Melbourne, Australia.

Rinaldo Bellomo (R)

The University of Melbourne, Department of Critical Care, Melbourne Medical School, Melbourne, Australia; Department of Intensive Care, Austin Hospital, Melbourne, Australia.

Yasmine Ali Abdelhamid (Y)

The University of Melbourne, Department of Critical Care, Melbourne Medical School, Melbourne, Australia; Intensive Care Unit, Royal Melbourne Hospital, Melbourne, Australia.

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Classifications MeSH