Changes in intracellular folate metabolism during high-dose methotrexate and Leucovorin rescue therapy in children with acute lymphoblastic leukemia.


Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2019
Historique:
received: 08 04 2019
accepted: 09 08 2019
entrez: 19 9 2019
pubmed: 19 9 2019
medline: 17 3 2020
Statut: epublish

Résumé

Methotrexate (MTX) is an important anti-folate agent in pediatric acute lymphoblastic leukemia (ALL) treatment. Folinic acid rescue therapy (Leucovorin) is administered after MTX to reduce toxicity. Previous studies hypothesized that Leucovorin could 'rescue' both normal healthy cells and leukemic blasts from cell death. We assessed whether Leucovorin is able to restore red blood cell folate levels after MTX. We prospectively determined erythrocyte folate levels (5-methyltetrahydrofolate (THF) and non-methyl THF) and serum folate levels in 67 children with ALL before start (T0) and after stop (T1) of HD-MTX and Leucovorin courses. Erythrocyte folate levels increased between T0 and T1 (mean ± SD: 416.7 ± 145.5 nmol/L and 641.2 ± 196.3 nmol/L respectively, p<0.001). This was due to an increase in 5-methyl THF levels (mean increase: 217.7 ± 209.5 nmol/L, p<0.001), whereas non-methyl THF levels did not change (median increase: 0.6 nmol/L [-9.9-11.1], p = 0.676). Serum folate levels increased between T0 and T1 (median increase: 29.2 nmol/L [32.9-74.0], p<0.001). Results were not significantly affected by age, sex, ALL immunophenotype and MTHFR c.677C>T genotype. Intracellular folate levels accumulate after HD-MTX and Leucovorin therapy in children with ALL, suggesting that Leucovorin restores the intracellular folate pool. Future studies are necessary to assess concomitant lower uptake of MTX.

Sections du résumé

BACKGROUND
Methotrexate (MTX) is an important anti-folate agent in pediatric acute lymphoblastic leukemia (ALL) treatment. Folinic acid rescue therapy (Leucovorin) is administered after MTX to reduce toxicity. Previous studies hypothesized that Leucovorin could 'rescue' both normal healthy cells and leukemic blasts from cell death. We assessed whether Leucovorin is able to restore red blood cell folate levels after MTX.
METHODS
We prospectively determined erythrocyte folate levels (5-methyltetrahydrofolate (THF) and non-methyl THF) and serum folate levels in 67 children with ALL before start (T0) and after stop (T1) of HD-MTX and Leucovorin courses.
RESULTS
Erythrocyte folate levels increased between T0 and T1 (mean ± SD: 416.7 ± 145.5 nmol/L and 641.2 ± 196.3 nmol/L respectively, p<0.001). This was due to an increase in 5-methyl THF levels (mean increase: 217.7 ± 209.5 nmol/L, p<0.001), whereas non-methyl THF levels did not change (median increase: 0.6 nmol/L [-9.9-11.1], p = 0.676). Serum folate levels increased between T0 and T1 (median increase: 29.2 nmol/L [32.9-74.0], p<0.001). Results were not significantly affected by age, sex, ALL immunophenotype and MTHFR c.677C>T genotype.
CONCLUSION
Intracellular folate levels accumulate after HD-MTX and Leucovorin therapy in children with ALL, suggesting that Leucovorin restores the intracellular folate pool. Future studies are necessary to assess concomitant lower uptake of MTX.

Identifiants

pubmed: 31527879
doi: 10.1371/journal.pone.0221591
pii: PONE-D-19-10004
pmc: PMC6748431
doi:

Substances chimiques

Antidotes 0
Folic Acid Antagonists 0
Homocysteine 0LVT1QZ0BA
Folic Acid 935E97BOY8
Vitamin B 12 P6YC3EG204
Leucovorin Q573I9DVLP
Methotrexate YL5FZ2Y5U1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0221591

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Natanja Oosterom (N)

Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands.
Erasmus MC, University Medical Center Rotterdam, Department of Clinical Chemistry, Rotterdam, The Netherlands.

Robert de Jonge (R)

VU Medical Center, Department of Clinical Chemistry, Amsterdam, The Netherlands.
Academic Medical Center, Department of Clinical Chemistry, Amsterdam, The Netherlands.

Desiree E C Smith (DEC)

VU Medical Center, Department of Clinical Chemistry, Amsterdam, The Netherlands.

Rob Pieters (R)

Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands.

Wim J E Tissing (WJE)

Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands.
Department of Pediatric Oncology, University of Groningen, Beatrix Children's Hospital, University Medical Center Groningen, Groningen, The Netherlands.

Marta Fiocco (M)

Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands.
Mathematical Institute, Leiden University, Leiden, The Netherlands.
Leiden University Medical Center, Department of Biomedical Data Sciences, Leiden, The Netherlands.

Bertrand D van Zelst (BD)

Erasmus MC, University Medical Center Rotterdam, Department of Clinical Chemistry, Rotterdam, The Netherlands.

Marry M van den Heuvel-Eibrink (MM)

Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands.

Sandra G Heil (SG)

Erasmus MC, University Medical Center Rotterdam, Department of Clinical Chemistry, Rotterdam, The Netherlands.

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Classifications MeSH