Serum proteins selectively adsorbed on synthetic monosodium urate crystals were analyzed in quest of a major crystallization inhibitor. Low density lipoprotein (LDL) was found to be the main component adsorbed on the crystals. Protein (s) adsorbed on the crystals, but not LDL, at the travel range of alpha-2globulins by agarose-gel electrophoresis inhibited monosodium urate crystallization.
Pyrimidinea ppea rst o be especiallyi mportanti n the neonatal period, but the reference ranges for urinary pyrimidines have not been reported. We measured urinary pyrimidines in 23 healthy newborns on 6 successive days after birth (from day 0 to day 6) and at 1month of age. We also analyzed newborns with urea cycle disorders including ornithine transcarbamylase (OTC) deficiency. We measured urine samples using high-performancel iquid chromatographyw ith column switching. The reference ranges for urinary orotic acid, uracil and pseudouridine were determined. Orotic acid was greatly increased in OTC deficiency cases, but not in carbamoyl phosphate synthetas I deficiency. We speculate that urinary pyrimidine comcentrations is a useful index for diagnosis in the neonatal period.
The patient was a 26-year-old man who had been diagnosed with gout at the age of 24 years and had recurrent episodes of arthritis at the age of 26 years. The patient first consulted the Teikyo University Hospital in June 2002. He did not drink alcohol. Obesity (BMI: 27.2), hyperuricemia, and hepatic dysfunction(ALT: 123IU/l, and γ-GTP: 62IU/l)were confirmed, and abdominal ultrasound confirmed severe fatty liver. After five months of an 1800kcal/day diet, the patient's BMI had dropped to 24.6, and liver dysfunction had improved (ALT: 21IU/l), though hyperuricemia persisted (8.6-9.5 mg/dl). Benzbromarone (25 mg/day) was initiated in March 2003. However, after three months, ALT increased to 60 IU/l and thereafter increased rapidly to 120 and 210IU/l. Benzbromarone was therefore discontinued after six months; however, liver dysfunction did not improve, and the level of ALT increased to 581 IU/l two months after the end of therapy. Liver biopsy showed moderate-to-large fatty deposits in the parenchyma, edematous changes of hepatocytes, centrilobular fibrosis, and fibrosis accompanying focal necrosis of the portal region, confirming nonalcoholic steatohepatitis (NASH). The patient was instructed to refrain from eating large quantities of snacks and junk food. BMI decreased to 23.1 and liver function normalized. Since hyperuricemia did not improve even though BMI normalized, allopurinol was started. To the best of our knowledge, no previous reports have documented gout coexisting with NASH, and the present patient could therefore provide valuable information.