Date of Award

Summer 1992

Document Type


Degree Name

Master of Science (MS)


Chemistry & Biochemistry



Committee Director

James H. Yuan

Committee Member

Mark S. Elliot

Committee Member

Roy L. Williams

Call Number for Print

Special Collections LD4331.C45H78


Gout is a chronic metabolic disorder caused by deposition of uric acid on the joint. It is categorized into two types: primary and secondary. Primary gout is uric acid overproduction, caused by excessive synthesis of the purine precursors. Secondary gout occurs also as the result of overproduction or decreased renal excretion of uric acid resulting from other disease processes or medication.

The two purine bases, hypoxanthine and xanthine, liberated from ribosides by the action of nucleoside phosphorylase, are degraded to uric acid as the final excretory product in the purine degradation pathway. Hypoxanthine and xanthine are the physiological substrates of xanthine oxidase which in turn converts them into uric acid. Therefore, understanding of any of the alterations of hypoxanthine and xanthine metabolism of the primary gout pathogenesis.

It has been reported that gout could be polygenic or multifactorial inheritance and has high family incidence, but the possible genetic factors influencing gout occurrence are still not understood. In this study, in order to better understand the familial nature of gout, the possible relationship of uric acid, xanthine, hypoxanthine and xanthine oxidase in gout families was investigated. The hypoxanthine and xanthine levels were determined by HPLC analysis; uric acid levels were determined by automation analysis; xanthine oxidase levels were determined by photometric method.

The members of the patient's family included the gout patient and their relatives with or without gout problems. This study consisted of investigating 27 gout families which consist of 214 people. The data obtained was analyzed with the use of multi-variance statistics to study the relationship between the subjects and of gout families and the normal healthy subjects.

The results of this study indicate that hypoxanthine and xanthine are better indicators than uric acid for gout diagnosis, xanthine could be better than even hypoxanthine. Xanthine oxidase is not a relevant parameter in the diagnosis of gout shown in this study. The higher hypoxanthine and xanthine levels or family gout history were found to be related to high risk of gout. The annual family incidence from 1981 to 1991 yielded a rate ranging from 0.6% to 5 .5 % in this study, which is higher than the gout incidence of general population reported. The subjects of gout families shown to be with earlier gout onset than the subjects of normal population.

Consequently, gout has high familial incidence and is related to the hypoxanthine and xanthine plasma levels. In order to complete the familial study of the possible polygenic or multi-factorial inheritance in each family, more specimens should be drawn in each gout family in the future investigation.


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