Volume 121 Number 1
2. Johnson CF, Peterson RM, Koch R, Friedman EG. Congenital and neurological abnormalities in infants with phenylketonuria. Am J Ment Def 1978;82:375-9. 3. Pitt D. The natural history of untreated phenylketonuria. Med J Aust 1971;1:378-83. 4. Kirby ML, Miyagawa ST. The effects of high phenylalanine concentration on chick embryonic development. J Inher Metab Dis 1990;13:634-40.
Urinary calcium excretion and nonsteroidal antiinflammatory treatment To the Editor." Szer et al.l recently reported the paucity of renal complications associated with nonsteroidal antiinflammatory treatment in children with juvenile rheumatoid arthritis (JRA). Of their 226 patients receiving such therapy for 6 months or longer, only one child receiving acetylsalicylic acid had persistent proteinuria; 21 patients had transitory proteinuria or hematuria or both, but these abnormalities resolved, usually without discontinuation of the drug. Calcium excretion was not measured in this study, although Stapleton et al. 2 had previously shown a higher-than-normal frequency of hypercalciuria in children with JRA. The latter investigators claimed that hypercalciuria might be related to the pathogenesis of hematuria in JRA. In our department, 20 children with JRA have been treated during the past 4 years. All received naproxen for at least 2 months (mean 13 months; range 2 to 46 months). In addition to routine studies, renal function and urinary calcium and phosphate excretion tests were performed monthly. The pretreatment values showed hypercalciuria (calcium output >0.1 mmol/kg per 24 hours) in five children, whereas 15 patients had normocalciuria. Calcium excretion was measured weekly during naproxen therapy, and no changes were observed. None of the patients had proteinuira or hematuria. The five children with hypercalciuria had normal serum calcium and phosphate levels; no relationship between calcium excretion and either drug therapy or onset type of JRA was observed. Our findings confirm the conclusion of Szer et a l / t h a t children with JRA receiving nonsteroidal antiinflammatory drugs are at no significant risk of renal damage. At the same time, our data indicate that hypercalciuria (and consequent hematuria or urolithiasis or both) in such patients is probably independent of JRA and drug administration. Ferenc Harangi, MD Department of Pediatrics University Medical School 7623 Pbcs, Hungary REFERENCES
1. Szer IS, Goldenstein-Schainberg C, Kurtin PS. Paucity of renal complications associated with nonsteroidal antiinflamma-
tory drugs in children with chronic arthritis. J PEDIATR 1991;119:815-7. 2. Stapleton FB, Hanissian AS, Miller LA. Hypercalciuria in children with juvenile rheumatoid arthritis: association with haematuria. J PEDIATR 1985;107:235-9.
Reply To the Editor: Dr. Harangi's findings strengthen and corroborate our observations, and further emphasize the benign nature of long-term administration of nonsteroidal antiinflammatory drugs regarding renal sequelae in children with JRA. Because we did not measure calcium excretion during our study, we cannot comment on the causal relationship between JRA and hypercalciuria. Ilona S. Szer, MD Associate Head, Pediatric Rheumatology Paul S. Kurtin, MD Director, End-Stage Renal Program Childrens Hospital Los Angeles Los Angeles, CA 90027
Screening for glucose-6-phosphate
dehydrogenase deficiency To the Editor: We read the report of the Greek glueose-6-phosphate dehydrogenase (G6PD) deficiency screening program (J PEDIATR 1991;119:293-9) with great interest, and commend the authors on successfully surveying as much as 97% of their newborn population. Severe neonatal jaundice is a major concern in G6PD-deficient infants, even when all known triggers of hemolysis have been eliminated. The condition is especially prevalent in Greece and has been associated in that country with an incidence of kernicterus of as much as 30% in enzyme-deficient infants. The results of any screening test done concurrently with screening for phenylketonuria will not be available to detect those infants at high risk for the development of severe hyperbilirubinemia in the first week of life. It is unfortunate, therefore, that immediate postnatal screening was not aimed for, and that the mean age at the time of the laboratory procedure was as much as 14 or 15 days. In Israel, G6PD deficiency is prevalent among some subsets of Sephardic Jews (Oriental ancestry). In this hospital, G6PD screening is performed, within 48 hours of delivery, on all infants born to mothers whose families stem from known high-risk geographic areas. Results are therefore available soon after birth and can guide the physician regarding delay of discharge, in the case of a jaundiced baby, or inviting the baby back for a follow-up serum bilirubin determination. Parents receive counseling regarding both neonatal hyperbilirubinemia and the avoidance of hemolytic triggering agents. It is paradoxical, considering the magnitude of G6PD-deficiency-associated neonatal hyperbilirubinemia in Greece, that a major