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Pediatric Endocrinology Unit and INSERM U.30, Hôpital des Enfants-Mahdes (R.B., R.R., C.P., P.C.) Paris (J.M.Z., P.B.)
The Pediatric Oncology Unit, Institut Curie Paris (J.M.Z., P.B.)
The Pediatric Oncology Unit, Institut Gustave Roussy (J.L., D.S.) Villejuif, France
The Department of Pediatrics, McGill University, Montreal Childrens Hôpital (H.J.G.) Montreal, Canada
Address requests for reprints to: Dr. R. Brauner, Pediatric Endocrinology Unit, Hopital des Enfants-Malades, 149 rue de Sevres, 75743 Paris Cedex 15, France.
Although GH deficiency (GHD) is the most frequent hormonal abnormality that occurs after cranial radiation, the natural course of this complication and its relationship to growth in children are not known. Therefore, we undertook a 2-yr prospective study of 16 children, aged 1.7–15 yr at the time of treatment, who received cranial [31–42 Gy (1 Gy = 100 rads)] and spinal radiation for medulloblastoma or ependymoma (group I). Their growth was compared to that of 11 children given similar doses of cranial radiation only (group II). The mean plasma GH response to arginine-insulin test (AITT) was 9.1 ± 1.5 (±SE) µg/L in group I and 8.5 ±1.8 µg/L in group II (P = NS). After 2 yr, 16 of the 27 children had a peak plasma GH value below 8 µg/L after AITT, and 10 children had a peak response less than 5 µg/L. In addition, in group I, AITT and sleep-related GH secretion were compared; at the 2 yr follow-up only 3 of 13 children had discrepant results.
At the 2 yr follow-up children treated by cranial and spinal radiation had a mean height of –1.46 ± 0.40 SD below the normal mean. In contrast, the children given only cranial radiation had a mean height of –0.15 ± 0.18 SD; P < 0.02. Therefore, most of the growth retardation appeared to be due to lack of spinal growth.
GHD is thus an early complication of cranial radiation in these children, and no significant growth retardation can be attributed to GHD during the first 2 yr. These data contribute to the organization of follow-up in irradiated children in order to decide when human GH treatment is necessary
* This work was supported by a grant from INSERM (PRC 1982–1984). Presented in part at the Joint Meeting of the European Society for Pediatric Endocrinology and the Lawson Wilkins Pediatric Endocrinology Society, Baltimore, 1985 (Pediatr Res 19:57A, 1985).
Received June 6, 1988.
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