With the objective of determining the optimal initial dose of benzbromarone, a comparative study was conducted on 40 patients with gout or hyperuricemia resulting from underexcretion of uric acid. The patients were divided into treatment groups receiving 12.5-mg and 25-mg initial doses. All patients treated with 12.5-mg initial dose were gouty patients who had gouty attack within one month before consulting our clinic. On the other hand, the 25-mg initial dose group consisted of 2 patients with asymptomatic hyperuricemiaa nd 18 patients with gout. There was no significant difference in serum urate level between the two groups prior to the start of administration. Two weeks after the start of administration, the serum urate level decreased by 1.7mg/dL (20.2%)from before the start to 6.7±1.2mg/dL in the 12.5-mg initial dose group, while a significantly greater decrease of 2.6 mg/dL (31.0%) from before the start to 5.8±1.2mg/dL was observed in the 25-mg initial dose group. One patient in each group developed gouty attacks during this period. Since patients who had developed attacks in the previous one month and those who were thus more susceptible to gouty attack induction were allocated to the 12.5-mg initial dose group, the risk of gouty attack induction may have been even higher had such patients been administered an initial dose of 25 mg. These findings suggest that the optimal initial dose of benzbromarone for preventing gouty attack induction is 12.5 mg.

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We established and implemented a computer-aided hyperuricemia management-support system, which makes a diagnosis on a complete medical checkup of ningen dock in accordance with the guidelines for the management of hyperuricemia and gout (issued in 2002), by simultaneously collecting and utilizing detailed medical information (obtained from the participants by sending them a questionnaire in advance), examination results, and laboratory data obtained through comprehensive screening. When 9diagnosing doctors, after a complete physical examination, made a diagnosis at their own discretion regarding the uric acid level, there was substantial variation among the doctors and participants, even though the diagnosis was made based on identical information obtained from interviews and identical examination results. On the other hand, utilization of this management-support system may yield the following benefits: 1. Consistent diagnoses can be obtained, generating less variation among the diagnosing doctors, and among participants. When the participants are on medication, the validity of the treatment can be judged automatically as a second opinion.2. By building the diagnostic logic in accordance with the guidelines issued by a specialist society, even doctors who are not familiar with the guidelines for the management of hyperuricemia and gout can offer evidencebased diagnosis.3. It provides an opportunity for doctors to learn about the guidelines.4. Automatic printing of the doctor' s comments avoids complaints about doctor' s poor handwriting.5. Automatic input of diagnosis and comments reduces the doctor' s administrative burden.

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Concentrations of purine bases in several Japanese foods and in some health care supplements were quantitatively determined using high-performance liquid chromatography (HPLC). After adenine, guanine, hypoxanthine and xanthine were determined, total purine bodies were calculated by the sum of each purine base. Concentrations of purine bases were as follows: Japanese vegetables: 35.1-129.6mg/100g; Japanese snacks: 31.4-138.3mg/100g; powdered soup: 37.6-180.0mg/100g; health care supplements: 40.2-21493.6mg/100g.
It is recommended that the amount of dietary purine bodies for a gouty or hyperuricemic patient be limited to less than 400mg per day. In this study, some health care supplements contained a large amount of purine bodies. Special attention should be paid to avoiding those health care supplements in the management of hyperuricemia.

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Inherited mutations of a purine salvage enzyme, hypoxanthine guanine phosphoribosyltransferase (HPRT), give rise to Lesch-Nyhan syndrome or HPRT-related gout. We have identified a number of HPRT mutations in Asian patients manifesting different clinical phenotypes, by analyzing all nine exons of the HPRT gene (HPRT1) from the genomic DNA and reverse transcribed mRNA using PCR technique coupled with direct sequencing. In this study, we update the spectrum of mutations with six novel mutations. Two missense mutations (T124P and D185G)were detected in patients with HRH (HPRT-related hyperuricemia). In a patient having a severe partial deficiency of HPRT with neurological dysfunction (HRND: HPRT-related neurological dysfunction), a single nucleotide substitution (27+5G>A) causing a splicing error was found in intron 1. The mutation resulted in a remarkably decreased level of normal mRNA, and production of an abnormal mRNA with a 49-bp insert at the 5'-end of intron 1, which caused the frame-shift of an amino acid codon (10fs27X). In three typical Lesch-Nyhan families, we found two single amino acid deletions (V8del and Y28del)responsible for 3-bp deletions, and a frame shift mutation (219fs250X) with a 1-bp deletion (635delG). Including these six mutations,42 HPRT1 mutations have been identified among 47 Asian families with deficiency of HPRT.

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