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Tadashi Asami

Publications and source records attributed to Tadashi Asami.

3 recordsLinked to original sources

Asymptomatic primary hyper- N-acetyl-beta-D-glucosaminidaseuria: a new clinical entity?

Urinary N-acetyl-beta-D-glucosaminidase (NAG) is excreted from renal tubular cells and increased urinary excretion reflects renal tubular damage. There are many causes for the elevation of urinary NAG; however, primary elevation of urinary NAG (primary hyper-NAGuria) has never been reported. Recently, we encountered two siblings with continuously elevated urinary NAG levels that could not been explained by any known causes. Two brothers, aged 13 and 11 years, were found to have continuously elevated urinary NAG levels that were repeatedly confirmed by urinary NAG levels (both per liter and urinary NAG/creatinine ratios). However, simultaneously measured urinary beta(2)-microglobulin levels were always within normal ranges. The elder brother is a heterozygous carrier for familial hypercholesterolemia, although this was not attributable to the urinary NAG elevation. The two patients were receiving no drugs when they were first examined at our hospital, and no nephrotoxic substances were found to be the cause for the elevation. Renal biopsy revealed no abnormal findings attributable to the abnormally high excretion of urinary NAG. Our two patients are considered to have asymptomatic primary hyper-NAGuria, which has not been previously reported. Although more cases are needed, this asymptomatic primary hyper-NAGuria is probably a new clinical entity of renal tubular disorders.

Acetylglucosaminidase↗

Marginal decrease in mortality and marked increase in incidence as a result of neuroblastoma screening at 6 months of age: cohort study in seven prefectures in Japan.

PURPOSE: To determine the usefulness of 6-month screening for neuroblastoma. PATIENTS AND METHODS: The cumulative incidence rates (IRs) and cumulative mortality rates (MRs) of neuroblastoma in children younger than 60 months of age were analyzed for control (n = 713,025), qualitative screening (Qual Screen, n = 1,142,519), and quantitative screening (Quan Screen, n = 550,331) cohorts, and for Screened and Unscreened subgroups within screening cohorts. RESULTS: IRs (per 100,000) for infants aged 6 to 11 months were 1.12 in Control, 5.69 in Qual Screen (P <.0001), and 17.81 in Quan Screen (P <.0001); IRs for children aged 12 to 59 months were 7.29 in Control, 5.86 in Qual Screen (P =.28), and 6.36 in Quan Screen (P =.60). IRs for children aged 12 to 59 months in Unscreened or Screened subgroups remained at the same level. When patients diagnosed at younger than 6 months of age were excluded, the MR (per 100,000) under 60 months for Control was 4.21; those in Unscreened and Screened subgroups were 3.84 and 2.53 in Qual Screen (P =.30), and 3.20 and 1.97 in Quan Screen (P =.73), respectively; MRs between Control and Unscreened subgroups revealed no significant differences (P =.89 in Qual Screen, P =.85 in Quan Screen). CONCLUSION: Six-month screening resulted in a marked increase in incidence for infants with no significant decrease in incidence for children older than 1 year of age. A decrease in mortality was observed, but it was not significant. The usefulness of screening is questionable, because the decrease of mortality should be balanced against the adverse effect of overdiagnosis and the psychological burden on parents and children.

Age Factors↗