Kinetics of plasma total homocysteine in patients receiving high-dose methotrexate therapy.

@article{Guttormsen1998KineticsOP,
  title={Kinetics of plasma total homocysteine in patients receiving high-dose methotrexate therapy.},
  author={Anne Berit Guttormsen and Per Magne Ueland and Per Eystein L{\o}nning and Olav Mella and Helga Refsum},
  journal={Clinical chemistry},
  year={1998},
  volume={44 9},
  pages={
          1987-9
        }
}
Homocysteine (Hcy) is a sulfur amino acid formed from methionine during transmethylation. Once formed, it is either remethylated to methionine or irreversibly catabolized to cystathionine. The remethylation is catalyzed by methionine synthase (EC 2.1.1.13), which requires cobalamin as cofactor and 5-methyltetrahydrofolate as substrate (1) . This explains why the fasting total homocysteine (tHcy) concentration is related to overall folate or cobalamin status and that increased tHcy has been used… Expand
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References

SHOWING 1-10 OF 20 REFERENCES
Changes in plasma methionine and total homocysteine levels in patients receiving methotrexate infusions.
TLDR
Investigation of the effects of moderate dose to very high dose methotrexate on methionine and total homocysteine as reflections of metotrexate induced intracellular events found changes in homocy steine and methionines may reflect biological effects of methot Rexate that may predict cytotoxicity of metHotrexate. Expand
Acute and long-term effects of high-dose methotrexate treatment on homocysteine in plasma and urine.
TLDR
It is suggested that the homocysteine response is not caused by an imbalance in methionine metabolism due to malignant disease or chemotherapy, and that the amount of homocy steine in plasma and urine decreased as a function of the number of MTX infusions. Expand
Kinetics of total plasma homocysteine in subjects with hyperhomocysteinemia due to folate or cobalamin deficiency.
TLDR
The kinetics of total Hcy in plasma after peroral Hcy administration in 19 volunteers with hyperhomocysteinemia suggest that mean plasma tHcy clearance is normal and that massive export of Hcy from tissues into plasma is the major cause of hyper homocysteine in cobalamin or folate deficiency. Expand
Folate depletion induced by methotrexate affects methionine synthase activity and its susceptibility to inactivation by nitrous oxide.
TLDR
The data show that MTX through depletion of 5-methyl-THF reduces both the Met synthase activity and the cellular CH3Cbl level, and the effect of MTX on the Hcy remethylation is more pronounced than the inhibition caused by nitrous oxide. Expand
Kinetic basis of hyperhomocysteinemia in patients with chronic renal failure.
TLDR
Patients with renal failure had markedly reduced clearance of tHcy from plasma, which probably accounts for their hyperhomocysteinemia. Expand
Plasma concentrations of homocysteine and other aminothiol compounds are related to food intake in healthy human subjects.
TLDR
Dietary changes in plasma homocysteine will probably not affect the evaluation of vitamin deficiency states associated with moderate to severe hyperhomocysteinemia but may be of concern in the risk assessment of cardiovascular disease in patients with mild hyperHomocysteemia. Expand
Interaction between methotrexate, "rescue" agents and cell proliferation as modulators of homocysteine export from cells in culture.
TLDR
Clinical data indicate that the burden of proliferating cells, cytotoxicity and the folate status are also determinants of extracellular Hcy, and the modulation of cellular Hcy egress by MTX, rescue agents, cell proliferation and cytot toxicity is investigated. Expand
Fasting plasma homocysteine as a sensitive parameter of antifolate effect: A study of psoriasis patients receiving low‐dose methotrexate treatment
TLDR
The level of fasting plasma homocysteine was shown to be a sensitive and responsive parameter of antifolate drug treatment and did not affect the plasma profile for homocy steine after methionine loading. Expand
Kinetics of plasma homocysteine in healthy subjects after peroral homocysteine loading.
TLDR
The kinetics of plasma homocysteine were determined in 13 healthy subjects after peroral administration and in one person after intravenous injection, and the transient hyperhomocysteinemia was associated with an increase in plasma methionine, which probably reflects intracellular remethylation of homocy steine. Expand
Determinants and vitamin responsiveness of intermediate hyperhomocysteinemia (> or = 40 micromol/liter). The Hordaland Homocysteine Study.
TLDR
It is concluded that most subjects with hyperhomocysteinemia in the general population have the C677T mutation combined with low folate status, and daily supplement of low dose folic acid will reduce and often normalize their tHcy level. Expand
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