Renal toxicity of ifosfamide in children with cancer: an exploratory study integrating aldehyde dehydrogenase enzymatic activity data and a wide-array urinary metabolomics approach.

Aldehyde dehydrogenase Chemotherapy Childhood cancer Ifosfamide Nephrotoxicity

Journal

BMC pediatrics
ISSN: 1471-2431
Titre abrégé: BMC Pediatr
Pays: England
ID NLM: 100967804

Informations de publication

Date de publication:
19 Mar 2024
Historique:
received: 29 09 2023
accepted: 08 02 2024
medline: 20 3 2024
pubmed: 20 3 2024
entrez: 20 3 2024
Statut: epublish

Résumé

Ifosfamide is a major anti-cancer drug in children with well-known renal toxicity. Understanding the mechanisms underlying this toxicity could help identify children at increased risk of toxicity. The IFOS01 study included children undergoing ifosfamide-based chemotherapy for Ewing sarcoma or rhabdomyosarcoma. A fully evaluation of renal function was performed during and after chemotherapy. Proton nuclear magnetic resonance (NMR) and conventional biochemistry were used to detect early signs of ifosfamide-induced tubulopathy. The enzymatic activity of aldehyde dehydrogenase (ALDH) was measured in the peripheral blood lymphocytes as a marker of ifosfamide-derived chloroacetaldehyde detoxification capacity. Plasma and urine concentrations of ifosfamide and dechloroethylated metabolites were quantified. The 15 participants received a median total ifosfamide dose of 59 g/m Acute renal toxicity was frequent during chemotherapy and did not allow identification of children at risk for long-term toxicity. A role of ALDH in late renal dysfunction is possible so further exploration of its enzymatic activity and polymorphism should be encouraged to improve the understanding of ifosfamide-induced nephrotoxicity.

Sections du résumé

BACKGROUND BACKGROUND
Ifosfamide is a major anti-cancer drug in children with well-known renal toxicity. Understanding the mechanisms underlying this toxicity could help identify children at increased risk of toxicity.
METHODS METHODS
The IFOS01 study included children undergoing ifosfamide-based chemotherapy for Ewing sarcoma or rhabdomyosarcoma. A fully evaluation of renal function was performed during and after chemotherapy. Proton nuclear magnetic resonance (NMR) and conventional biochemistry were used to detect early signs of ifosfamide-induced tubulopathy. The enzymatic activity of aldehyde dehydrogenase (ALDH) was measured in the peripheral blood lymphocytes as a marker of ifosfamide-derived chloroacetaldehyde detoxification capacity. Plasma and urine concentrations of ifosfamide and dechloroethylated metabolites were quantified.
RESULTS RESULTS
The 15 participants received a median total ifosfamide dose of 59 g/m
CONCLUSIONS CONCLUSIONS
Acute renal toxicity was frequent during chemotherapy and did not allow identification of children at risk for long-term toxicity. A role of ALDH in late renal dysfunction is possible so further exploration of its enzymatic activity and polymorphism should be encouraged to improve the understanding of ifosfamide-induced nephrotoxicity.

Identifiants

pubmed: 38504218
doi: 10.1186/s12887-024-04633-1
pii: 10.1186/s12887-024-04633-1
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

196

Subventions

Organisme : Ministère des Affaires Sociales et de la Santé
ID : PHRC 2008

Informations de copyright

© 2024. The Author(s).

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Auteurs

Olivia Febvey-Combes (O)

Centre Léon Bérard, Direction de la Recherche Clinique et de l'Innovation, Lyon, France.

Jérôme Guitton (J)

Laboratoire de Pharmacologie et Toxicologie, Hospices Civils de Lyon, Hôpital Lyon Sud, Pierre-Bénite, France.
Faculté de Pharmacie, Département de toxicologie, Université Claude Bernard Lyon 1, Lyon, France.

Perrine Marec-Berard (P)

Institut d'hématologie et d'oncologie pédiatrique - Centre Léon Bérard, Département d'oncologie pédiatrique, Lyon, France.

Cécile Faure-Conter (C)

Institut d'hématologie et d'oncologie pédiatrique - Centre Léon Bérard, Département d'oncologie pédiatrique, Lyon, France.

Ellen Blanc (E)

Centre Léon Bérard, Direction de la Recherche Clinique et de l'Innovation, Lyon, France.

Sylvie Chabaud (S)

Centre Léon Bérard, Direction de la Recherche Clinique et de l'Innovation, Lyon, France.

Agnès Conjard-Duplany (A)

Faculté de Médecine Lyon Est, Physiopathologie et Génétique du Neurone et du Muscle, Université Lyon1, CNRS UMR 5261, INSERM U1315, Lyon, France.

Matthias Schell (M)

Institut d'hématologie et d'oncologie pédiatrique - Centre Léon Bérard, Département d'oncologie pédiatrique, Lyon, France.

Laurence Derain Dubourg (L)

Service de Néphrologie, Hospices Civils de Lyon, Hôpital Edouard Herriot, Dialyse, Hypertension et Exploration Fonctionnelle Rénale 5, place d'Arsonval, Lyon cedex 03, 69437, France. laurence.derain@chu-lyon.fr.
Université Lyon 1, CNRS UMR 5305, Lyon, France. laurence.derain@chu-lyon.fr.

Classifications MeSH