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Urodynamics and hypercalciuria
838
E d i t o r i a l correspondence
Reply To the Editor." The conclusions of our study were not altered by additional data analysis. Two-way analysis of variance with repeated measures, with treatment as the repeated factor and sequence of treatment as the other factor, was carried out as suggested by Drs. Pons and Dewailly. Treatment sequence had no statistically significant effect (p = 0.07) on the percentage of time that esophageal pH was <4.0, whereas the difference between treatments (placebo vs metoclopramide) was significant at p <0.001, as stated in our article. This is not suprising, because the protocol was designed to negate treatment sequence bias by randomizing sequence assignment. Furthermore, the total duration of study in each patient was only 14 days, a length of time within which gastroesophageal reflux would not be expected to change spontaneously with maturation. Vasundhara Tolia, MD Director, Pediatric Gastroenterology and Nutrition Ralph E. Kauffman, MD Director, Clinical Pharmacology & Toxicology Children's Hospital o f Michigan Detroit, M1 48201
Urodynamics and hypercalciuria To the Editor: Alon et al. (J PEDIATR1990; l 16:103-5) reported their experience with reference to the onset of idiopathic hypercalciuria (1H) with dysuria and frequency. Their data confirm those of Moore 1 and of other, later studies2, 3 that noted that IH may be associated not only with dysuria and frequency but also with incontinence, urgency, and nocturnal enuresis, thus presenting a clinical picture similar to those described for bladder instability (BI), a clinical condition in which urodynamic studies show uninhibited bladder contractions after progressive filling of the bladder.4 Recently we have studied urodynamics in three girls with a diagnosis of IH. They had diurnal incontinence, urgency, and other symptoms of BI. Two of the girls had normal urodynamic values, but the third had BI; at the time of thestudy, this child's calciuria was normal after dietary restriction of salt and dairy products. We conclude that there was no causal relation between the original hypercalciuria and BI. In short, IH may produce a clinical condition like that of BI, but with normal urodynamics. Detrusor contractions may be triggered by urine with a high calcium content, and not when the bladder is filled with distilled water, as is normally the case during urodynamic studies. V. Garcia Nieto, MD D. Castro Diaz, MD J. L. Gbmez de la Rosa, MD Centro de Especialidades Pediittricas Seccibn de Urodinamia del Hospital Universitario de Canarias Tenerife. Canary Islands. Spain
The Journal o f Pediatrics November 1990
REFERENCES
1. Moore ES. Hypercalciuria in children. In" Berlyne GM, Giovannetti S, Thomas S, eds. Contributions to nephrology. New York: Karger, 1981:20-32. 2. Cervera A, Corral M J, G6mez Campdera F J, De Lecea AM, Luque A, L6pez Gomez JM. Idiopathic hypercalciuria in children: classification, clinical manifestations and outcome. Acta Paediatr Scand 1987;76:271-8. 3. Garcla Nieto V, Garcia J, Le6n C, M6ndez ML, G6mez J, Higueras LM. Etiologia y clinica de presentaci6n de la hiperealciuria en la infancia. Nefrologia 1989;9:224. 4. Mundy AR. The unstable bladder. Urol Clin North Am 1985;12:317-28.
Reply To the Editor." We agree with the comment by Garcla Nieto et al. that hypercalciuria in children can be manifested by a variety of symptoms, some of them identical with those observed in children with bladder instability. The speculation that detrusor contractions might be triggered by the high calcium content in the urine is intriguing; however, the fact that the urodynamic values were found to be normal when the patients had hypercalciuria does not support the speculation. Further investigations are required to identify the pathophysiologic mechanisms kinking hypercalciuria and the symptoms associated with it. Uri Alon, MD Bradley A. Warady, MD Stanley Hellerstein, MD Division o f Pediatric Nephrology Children's Mercy Hospital Kansas City, MO 64108
Uridine diphosphate glucose and uridine diphosphate galactose in
galactosemia To the Editor." In an article on galactosemia, Drs. Kaufman, Xu, Ng, and Donnell (J PED1ATR1988;112:754-6) (1) offered evidence that children with galactosemia are deficient in uridine diphosphate galactose (UDPGal), a product of the enzyme that is defective in the disorder, (2) suggested that this deficiency may account for the late-onset abnormalities of galactosemia, and (3) proposed that such children be given uridine, which raises the levels of UDPGal and uridine diphosphate glucose (UDPG)/,2 On the basis of this information from the authors, parents are asking that their galactosemic children be treated with uridine. UDPGal, however, can be made readily by UDPGal-4-epimerase, which is unaffected in galactosemia. Thus there is biochemical reason to doubt that a deficiency of UDPGal would occur in galactosemia. One of my technicians and I, with more than 20 years of experience with enzymatic
E d i t o r i a l correspondence
Reply To the Editor." The conclusions of our study were not altered by additional data analysis. Two-way analysis of variance with repeated measures, with treatment as the repeated factor and sequence of treatment as the other factor, was carried out as suggested by Drs. Pons and Dewailly. Treatment sequence had no statistically significant effect (p = 0.07) on the percentage of time that esophageal pH was <4.0, whereas the difference between treatments (placebo vs metoclopramide) was significant at p <0.001, as stated in our article. This is not suprising, because the protocol was designed to negate treatment sequence bias by randomizing sequence assignment. Furthermore, the total duration of study in each patient was only 14 days, a length of time within which gastroesophageal reflux would not be expected to change spontaneously with maturation. Vasundhara Tolia, MD Director, Pediatric Gastroenterology and Nutrition Ralph E. Kauffman, MD Director, Clinical Pharmacology & Toxicology Children's Hospital o f Michigan Detroit, M1 48201
Urodynamics and hypercalciuria To the Editor: Alon et al. (J PEDIATR1990; l 16:103-5) reported their experience with reference to the onset of idiopathic hypercalciuria (1H) with dysuria and frequency. Their data confirm those of Moore 1 and of other, later studies2, 3 that noted that IH may be associated not only with dysuria and frequency but also with incontinence, urgency, and nocturnal enuresis, thus presenting a clinical picture similar to those described for bladder instability (BI), a clinical condition in which urodynamic studies show uninhibited bladder contractions after progressive filling of the bladder.4 Recently we have studied urodynamics in three girls with a diagnosis of IH. They had diurnal incontinence, urgency, and other symptoms of BI. Two of the girls had normal urodynamic values, but the third had BI; at the time of thestudy, this child's calciuria was normal after dietary restriction of salt and dairy products. We conclude that there was no causal relation between the original hypercalciuria and BI. In short, IH may produce a clinical condition like that of BI, but with normal urodynamics. Detrusor contractions may be triggered by urine with a high calcium content, and not when the bladder is filled with distilled water, as is normally the case during urodynamic studies. V. Garcia Nieto, MD D. Castro Diaz, MD J. L. Gbmez de la Rosa, MD Centro de Especialidades Pediittricas Seccibn de Urodinamia del Hospital Universitario de Canarias Tenerife. Canary Islands. Spain
The Journal o f Pediatrics November 1990
REFERENCES
1. Moore ES. Hypercalciuria in children. In" Berlyne GM, Giovannetti S, Thomas S, eds. Contributions to nephrology. New York: Karger, 1981:20-32. 2. Cervera A, Corral M J, G6mez Campdera F J, De Lecea AM, Luque A, L6pez Gomez JM. Idiopathic hypercalciuria in children: classification, clinical manifestations and outcome. Acta Paediatr Scand 1987;76:271-8. 3. Garcla Nieto V, Garcia J, Le6n C, M6ndez ML, G6mez J, Higueras LM. Etiologia y clinica de presentaci6n de la hiperealciuria en la infancia. Nefrologia 1989;9:224. 4. Mundy AR. The unstable bladder. Urol Clin North Am 1985;12:317-28.
Reply To the Editor." We agree with the comment by Garcla Nieto et al. that hypercalciuria in children can be manifested by a variety of symptoms, some of them identical with those observed in children with bladder instability. The speculation that detrusor contractions might be triggered by the high calcium content in the urine is intriguing; however, the fact that the urodynamic values were found to be normal when the patients had hypercalciuria does not support the speculation. Further investigations are required to identify the pathophysiologic mechanisms kinking hypercalciuria and the symptoms associated with it. Uri Alon, MD Bradley A. Warady, MD Stanley Hellerstein, MD Division o f Pediatric Nephrology Children's Mercy Hospital Kansas City, MO 64108
Uridine diphosphate glucose and uridine diphosphate galactose in
galactosemia To the Editor." In an article on galactosemia, Drs. Kaufman, Xu, Ng, and Donnell (J PED1ATR1988;112:754-6) (1) offered evidence that children with galactosemia are deficient in uridine diphosphate galactose (UDPGal), a product of the enzyme that is defective in the disorder, (2) suggested that this deficiency may account for the late-onset abnormalities of galactosemia, and (3) proposed that such children be given uridine, which raises the levels of UDPGal and uridine diphosphate glucose (UDPG)/,2 On the basis of this information from the authors, parents are asking that their galactosemic children be treated with uridine. UDPGal, however, can be made readily by UDPGal-4-epimerase, which is unaffected in galactosemia. Thus there is biochemical reason to doubt that a deficiency of UDPGal would occur in galactosemia. One of my technicians and I, with more than 20 years of experience with enzymatic