XDH and Lesch-Nyhan syndrome: The primary triggers include abnormalities in key enzyme function (e.g., hyperactivity of xanthine oxidase (XO), which accelerates the conversion of hypoxanthine to uric acid (Maesaka and Fishbane, 1998), overactivation of phosphoribosylpyrophosphate synthase (PRPS), or a deficiency in hypoxanthine-guanine phosphoribosyltransferase (HGPRT), as occurs in Lesch–Nyhan syndrome).