Serum and Urinary Amino Acids in Normouricemic and Hyperuricemic Subjects

Article1 April 1965Serum and Urinary Amino Acids in Normouricemic and Hyperuricemic SubjectsDAVID KAPLAN, M.D., DAVID BERNSTEIN, M.D., STANLEY L. WALLACE, M.D., F.A.C.P., DAVID HALBERSTAM, M.S.DAVID KAPLAN, M.D.Search for more papers by this author, DAVID BERNSTEIN, M.D.Search for more papers by this author, STANLEY L. WALLACE, M.D., F.A.C.P.Search for more papers by this author, DAVID HALBERSTAM, M.S.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-62-4-658 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThere are potentially two main causes of the hyperuricemia in gout—underexcretion of uric acid and overproduction of uric acid. Underexcretion can occur either in the gastrointestinal tract or in the kidney. Sorensen (1) has shown that uric acid destruction by bacterial flora of the gastrointestinal tract is not decreased and may even be increased in gouty subjects. Underexcretion of uric acid in the kidney, however, has been demonstrated in some gouty individuals (2, 3). These patients had decreased clearance of endogenous uric acid when all other parameters of renal function were normal. Inability of the gouty patient to excrete normal...References1. SORENSEN JB: Degradation of uric acid in man. Metabolism 8: 687, 1959. MedlineGoogle Scholar2. SEEGMILLERGRAYZELLASTERLIDDLE JEAILL: Uric acid production in gout. J. Clin. Invest. 40: 1304, 1961. CrossrefMedlineGoogle Scholar3. WYNGAARDEN JB: On the dual etiology of hyperuricemia in primary gout. Arthritis Rheum. 3: 414, 1960. CrossrefMedlineGoogle Scholar4. NUGENTTYLER CAFH: The renal excretion of uric acid in patients with gout and in nongouty subjects. J. Clin. Invest. 38: 1890, 1959. CrossrefMedlineGoogle Scholar5. 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YUWASSERMANBENEDICTBIENGUTMANSTETTEN TFLRJDEJABD: A simultaneous study of glycine-N15 incorporation into uric acid and heme, and of Fe59 utilization in a case of gout associated with polycythemia secondary to congenital heart disease. Amer. J. Med. 15: 845, 1953. CrossrefMedlineGoogle Scholar30. YUWEISSMANNSHARNEYKUPFERGUTMAN TFBLSAB: On the biosynthesis of uric acid from glycine-N15 in primary and secondary polycythemia. Amer. J. Med. 21: 901, 1956. CrossrefMedlineGoogle Scholar31. LASTERMULLER LAF: Uric acid production in a case of myeloid metaplasia associated with gouty arthritis, studied with N15 labelled glycine. Amer. J. Med. 15: 859, 1953. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Brooklyn, New YorkFrom the Department of Medicine, State University of New York, Downstate Medical Center, and the Department of Medicine, the Jewish Hospital of Brooklyn, Brooklyn, N. Y.This study was supported in part by grant AM-06671 from the U. S. Public Health Service, Bethesda, Md., and in part by a grant from the New York Chapter of the Arthritis and Rheumatism Foundation.This paper was read at the Forty-fifth Annual Session of the American College of Physicians, April 6-10, 1964, in Atlantic City, N. J.Requests for reprints should be addressed to David Kaplan, M.D., State University of New York, Downstate Medical Center, 450 Clarkson Ave., Brooklyn, N. Y. 11203. 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SILBERMAN, M.D.Renal Handling of Glycine in Primary HyperuricaemiaUric Acid in Human Plasma: V. Isolation and Identification of Plasma Proteins Interacting with UrateGout 1 April 1965Volume 62, Issue 4Page: 658-666KeywordsAmino acidsArthritisExcretionGastrointestinal tractHospital medicineKidneysMedical servicesUric acid Issue Published: 1 April 1965 PDF downloadLoading ...