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Failure of folic acid (pteroylglutamic acid) to affect hyperuricemia | JoVE Visualize

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Failure of folic acid (pteroylglutamic acid) to affect hyperuricemia

G R Boss, R A Ragsdale, A Zettner

The Journal of Laboratory and Clinical Medicine|November 1, 1980

View abstract on PubMed

Summary

High doses of pteroylglutamic acid (PGA) did not reduce serum urate in hyperuricemic subjects. However, folate was well absorbed with no toxicity observed, indicating PGA is not an effective urate-lowering agent.

Area of Science:

Biochemistry
Pharmacology
Clinical Nutrition

Background:

Hyperuricemia is associated with gout and kidney stones.
Xanthine oxidase is a key enzyme in uric acid production.
Pteroylglutamic acid (PGA) is a form of folate.

Purpose of the Study:

To investigate the efficacy of PGA in lowering serum urate concentration.
To assess the absorption, excretion, and toxicity of high-dose PGA.
To evaluate PGA's inhibitory effect on human liver xanthine oxidase.

Main Methods:

Five hyperuricemic subjects received oral doses of PGA up to 1000 mg/day.
Serum urate, urinary urate, and total oxypurine excretion were measured.
Serum and erythrocyte folate concentrations were monitored.
In vitro assays assessed PGA's inhibition of human liver xanthine oxidase.

Main Results:

PGA administration did not significantly lower serum urate or alter urate/oxypurine excretion.
Folate was well absorbed, with significant increases in serum and erythrocyte levels.
Up to 50% of administered folate was recovered in urine, with no observed toxicity.
PGA showed weak in vitro inhibition of xanthine oxidase, largely due to pterin-6-aldehyde contamination.

Conclusions:

PGA is not an effective therapeutic agent for lowering serum urate in hyperuricemic individuals.
High-dose PGA is well-absorbed and tolerated, but does not impact uric acid metabolism.
The observed weak inhibition of xanthine oxidase by PGA is likely artifactual.

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Failure Of Folic Acid (pteroylglutamic Acid) To Affect Hyperuricemia