Why is de novo biosynthesis of purines markedly elevated in patients with adeficiency in hypoxanthine-guanine phosphoribosyl transferase (HGPRT)?5-Fluoruracil is converted to methotrexate by a DPD deficiency, leadingto increased purine biosynthesis.HGPRT deficiency prevents purine salvage, leading to increased purinebiosynthesis to make up for it.HGPRT increases pyrimidine salvage and thereby increases purinebiosynthesis as a result.Increased purine biosynthesis is the result of ATP hydrolysis during theproduction of cyclic AMP.

HGPRT is an important enzyme in the recycling of building blocks of nucleic acids like DNA or RNA. It catalyses the reaction that attches the modified bases of Adenine, like guanine and hypoxanthine to a PRPP ( Phospho ribosyl pyro phosphate) residue to form nucleotides , which are building blocks of nucleic acid synthesis . Deficiency of Hypoxanthine Guanine phospho ribosyl transferase is associated with increased synthesis of purines because HGPRT deficiency inhibits the purine salvage which results in increased biosynthesis of purines. Due to deficiency of HGPRT, the unused PRPP stimulates the synthesis of purines . So the combined effect is the blocked purine salvage and stimulation by PRPP, purine biosynthesis increases in patients with HGPRT deficiency. option b is correct . option A is incorrect because deficiency of DPD( Dihydronpyrimidine dehydrogenase) , causes increase in unmetabolised 5 fluoro uracil as DPD catalyses the conversion of 5 fluorouracil into FUH2. option c is incorrect because HGPRT is involved in preventing purine salvage only but in pyrimidine salvage. option d is incorrect because increased purine biosynthesis in HGPRT deficiency is not related to ATP hydrolysis.