What is high dose methotrexate sodium acetate

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Understanding and Managing Methotrexate Nephrotoxicity

Describe the current incidence and presentation of high-dose methotrexate-induced what is high dose methotrexate sodium acetate dysfunction. Discuss conventional and investigational methotrexate sodium acetate approaches to high-dose methotrexate-induced renal dysfunction. Methotrexate MTX is source of the most widely used anti-cancer agents, and administration of high-dose methotrexate HDMTX followed by leucovorin LV rescue is an important component in the treatment of a variety of childhood and adult cancers.

HDMTX can be safely administered to patients with normal renal function by the use of alkalinization, hydration, and pharmacokinetically guided LV rescue.

Prompt recognition and treatment of MTX-induced renal dysfunction are essential to prevent potentially life-threatening MTX-associated what is high dose methotrexate sodium acetate, especially myelosuppression, mucositis, and dermatitis. In addition to conventional treatment approaches, what is high dose methotrexate sodium acetate methods have been used to remove MTX what is high dose methotrexate sodium acetate limited effectiveness.

CPDG 2 administration has been well tolerated and resulted in consistent and rapid reductions in plasma MTX concentrations by a median of Methotrexate MTXa classical antifolate, is one of the most widely used and studied anticancer agents [ 1 — 4 ]. HDMTX can be safely administered to patients with normal renal function by vigorously what is high dose methotrexate sodium acetate and alkalinizing the patient to enhance the solubility what is high dose methotrexate sodium acetate MTX in urine and through the use of pharmacokinetically guided LV rescue to prevent potentially 40 treatment clindamycin mg rash MTX toxicity [ 212 ].

Despite these preventive measures, MTX-induced nephrotoxicity continues to occur, albeit infrequently. This report reviews the etiology, incidence, presentation, and treatment of HDMTX-induced renal dysfunction.

MTX enters the cell via the reduced folate carrier and undergoes polyglutamation catalyzed by folyl-polyglutamate synthetase.

Once polyglutamated, MTX is retained in cells for prolonged periods of what is high dose methotrexate sodium acetate. Methotrexate and its polyglutamates block de novo nucleotide synthesis primarily by depleting cells of reduced tetrahydrofolate cofactors through inhibition of dihydrofolate reductase DHFR Fig. MTX polyglutamates and link that accumulate as a result of DHFR inhibition also inhibit thymidylate synthase and other enzymes involved in the purine biosynthetic pathway [ 1819 ].

Chemotherapy and Biotherapy

Sites of action what methotrexate MTX and of the rescue what is high dose methotrexate sodium acetate leucovorin and thymidine. This results in the depletion of reduced folates FH 4which are required for deoxythymidine monophosphate dTMP synthesis from deoxyuridine monophosphate dUMPand in accumulation of dihydrofolates FH 2which inhibit purine synthesis.

The MTX rescue agent leucovorin restores the reduced folate pool after conversion what is high dose methotrexate sodium acetate its active metabolite 5-methyltetrahydrofolate 5-CH check this out -FH 4.

Thymidine is directly converted to thymidine monophosphate by the enzyme thymidine symptoms of too synthroid medication body TKthereby circumventing blockade of the de novo pathway by MTX.

Similar to other antimetabolites, critical determinants of MTX cytotoxicity are not only drug concentration but also duration of exposure.

High concentrations of MTX may be well tolerated for brief periods of time, whereas high dose exposure to low concentrations can result in life-threatening toxicity. The type of toxicity observed with MTX is also a function of this concentration—time dependence.

Chemotherapy and Biotherapy - Oncology Nursing Society

Exposure to millimolar concentrations of MTX for minutes to hours may lead to acute renal, central nervous system, and liver toxicity; what is high dose methotrexate sodium acetate to MTX concentrations as low as 0.

Intracellular polyglutamation of 7-OH-MTX results in prolonged retention and enhanced cytotoxicity [ /bystolic-pregnancy-category-x-drugs.html ]. The etiology of MTX-induced renal dysfunction is believed to be mediated by the precipitation of MTX and its metabolites in the renal tubules [ what is high dose methotrexate sodium acetate ] or via a direct toxic effect of MTX on the renal tubules [ 17 ].

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