Methotrexate inhibits purine synthesis by targeting formation of:
N10-formyl-tetrahydrofolate from tetrahydrofolate and formate.
Folic acid from PABA and pteridine precursor.
Tetrahydrofolate from dihydrofolate.
S-adenosylmethionine from methionine.
The sulfa drugs, e.g., sulfanilamide, act:
To overcome feedback control of purine nucleotide biosynthesis.
To inhibit the production of FH4 from dietary folate.
As pseudo-feedback inhibitors of purine nucleotide biosynthesis.
To inhibit FH4 synthesis de novo in certain bacteria.
To inhibit single-carbon transfers from tetrahydrofolic acid (FH4).
Which of the following is not known to be a cause of gout?
Enhanced AMP levels due to drinking ethanol
Congenitally high PRPP levels
Decreased xanthine oxidase levels
Enhanced lactate levels due to drinking ethanol
A patient who has Lesch-Nyhan syndrome is given allopurinol by his physician to treat symptoms the physician attributes to gout. In this patient,
The drug would have no effect on hypoxanthine-guanine phosphoribosyl-transferase (HGPRT), since it would be converted into the riboside.
The drug should help in the control of his increased excretion of uric acid.
The drug would have no effect, since the target-enzyme for the action of allopurinol is missing or deficient in this syndrome.
The symptoms could not be attributed to gout, so this is clearly an example of misdiagnosis.
Allopurinol would be a true wonder drug, reversing the physiologic effects of this syndrome.
