title: How should we treat tophaceous gout in patients with allopurinol hypersensitivity?
abstract: We studied purine metabolism in gouty patients from three categories: primary gout, familial juvenile hyperuricaemic nephropathy (FJHN) and partial HPRT deficiency.
authors.affiliation: Department of Rheumatology, Royal London Hospital, United Kingdom.
authors.forename: R
authors.initials: R
authors.lastname: Grahame
authors.forename: H A
authors.initials: HA
authors.lastname: Simmonds
authors.forename: M B
authors.initials: MB
authors.lastname: McBride
authors.forename: F P
authors.initials: FP
authors.lastname: Marsh
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000493:Allopurinol / Q000009:adverse effects*; D001553:Benzbromarone / Q000627:therapeutic use; D003404:Creatinine / Q000097:blood; D004342:Drug Hypersensitivity; D006073:Gout / Q000097:blood / Q000188:drug therapy / Q000628:therapy*; D006074:Gout Suppressants / Q000009:adverse effects / Q000627:therapeutic use*; D006801:Humans; D007041:Hypoxanthine Phosphoribosyltransferase / Q000172:deficiency; D007676:Kidney Failure, Chronic / Q000150:complications; D008297:Male; D008875:Middle Aged; D011686:Purine-Pyrimidine Metabolism, Inborn Errors / Q000628:therapy*; D014527:Uric Acid / Q000097:blood
chemical_list: D006074:Gout Suppressants; D014527:Uric Acid; D001553:Benzbromarone; D000493:Allopurinol; D003404:Creatinine; D007041:Hypoxanthine Phosphoribosyltransferase