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Editorial correspondence

Such a conference would be of obvious interest to workers in this field, but we believe also that its findings could be a guide for editors of journals and their referees. We would welcome wider collaboration.

The Journal of Pediatrics July 1990

ter day 60 of gestation began to return to a normal growth pattern, would be supported.

Ken Tokugawa, MD Kohji Ueda, MD Department of Pediatrics, Faculty of Medicine Kyushu University 3-1-1, Maidashi, Higashi-ku, Fukuoka 812, Japan

Lesley Mutch, MD Social Paediatric and Obstetric Research Unit University of Glasgow Glasgow, Scotland

REFERENCE

M. Ann Johnson, MD Oxford Region Child Development Project John Radcliffe Hospital Oxford, England Ruth Morley, MB,BChir Medical Research Council, Dunn Nutrition Unit Cambridge, England

1. Tokugawa K, Ueda K, Fukushige J, Koyanagi T, Hisanaga S. Congenital rubella syndrome and physical growth: a 17-year, prospective, longitudinal follow-up in the Ryukyu Islands. Rev Infect Dis 1986;8:874-83.

Reply

REFERENCES

1. Mutch LMM, Johnson MA, Morley R. Follow-up studies: design, organisation and analysis. Arch Dis Child 1989;64:1394402. 2. International classification of diseases. 9th revision. Geneva: World Health Organization, 1970. 3. International Committee for the Classification of Retinopathy of Prematurity. An international classification of retinopathy of prematurity. Pediatrics 1984;74:127-33. 4. Evans p, Johnson A, Mutch L, Alberman E. A standard form for recording clinical findings in children with a motor deficit of central origin. Dev Med Child Neurol 1989;31:119-27.

Growth in congenital rubella syndrome

To the Editor: We thank Drs. Tokugawa and Ueda for their letter. Our populations differ in a number of ways. First, we did not observe a difference in the mean time of maternal infection between any of our three patient groups with different growth patterns (Group 1, normal growth; group 2, growth consistently less than the 5th percentile channel for height; group 3, initially relatively normal growth followed by early cessation of growth that resulted in final heights less than the 5th percentile channel). Second, we observed cataracts, unilateral or bilateral, in all of our patient groups. Specifically, in group 1, eleven had none, and six had unilateral and two bilateral cataracts. In group 2, four had none, and one had unilateral and nine bilateral cataracts. In group 3, eight had none, and 10 had unilateral and 17 bilateral cataracts. Therefore we cannot confirm Drs. Tokugawa's and Ueda's contention that children with CRS and cataracts grow poorly, whereas those without cataracts show normal catch-up growth.

Sharon E. Oberfield, MD Lenore S. Levine, MD Pediatric Service St. Luke-Roosevelt Hospital Center New York, N Y 10025

To the Editor." We read with interest the article by Chiriboga-Klein et al. entitled "Growth in Congenital Rubella Syndrome and Correlation With Clinical Manifestations" (J PEDIATR 1989; 115:251-5). However, they did not note a similar article that we pub!ished, l We compared the physical growth of our patients with congenital rubella syndrome (CRS) (in the Ryukyu Islands of Japan), grouped according to their clinical manifestations (i.e., cataract, congenital heart diseases, and deafness). Those CRS children who had cataract also had poor physical growth in both height and weight (below the - 1 SD line for standard values); the other CRS children had catch-up growth after school age. Furthermore, all CRS children had microcephaly. We did not note any correlation between mental retardation and physical growth retardation, as ChiribogaKlein et al. pointed out. We wonder whether those children with CRS who had growth consistently below the 5th percentile in the Chiriboga-Klein series were patients who have had cataract? If so, then our postulate that children supposedly exposed to maternal rubella before day 60 of gestation grew most poorly, whereas those supposedly infected af-

Jaundice with hypertrophic pyloric stenosis To the Editor: The article by Labrune et al. (J PEDIATR 1989; 115:93-5) makes a strong case for ascribing the jaundice associated with hypertrophic pyloric stenosis to an early manifestation of Gilbert syndrome, and the reduced hepatic activity of bilirubin uridine diphosphate-glucuronyl transferase seems to strengthen the argument. It would be interesting to attain a further value of this enzyme's activity at a later age (could it mature later?) and to record whether patient 2 ever has unconjugated hyperbilirubinemla in fu-

Growth in congenital rubella syndrome.

16 8 Editorial correspondence Such a conference would be of obvious interest to workers in this field, but we believe also that its findings could b...
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