We assessed the effect of zinc supplementation on growth velocity in 79 children and adolescents (48 males, 38 females) with idiopathic short stature. Their height-for-age was < 5th percentile (NCHS standards) and their weight-for-age was normal. Patients were assigned randomly to a supplemented group (S) to receive Zn 10 mg/day or to a placebo (P) group, according to gender and age, and were followed-up for 12 months using a double-blind design. Weight, height, armspan, length of lower segment and plasma and hair concentrations of Zn were measured at 0, 3, 6 and 12 months. On admission and at 6 months, energy, protein, dietary fiber and zinc intakes were similar for groups S and P; mean zinc intake was < 6.5 mg/day. No differences were found in plasma zinc, hair zinc, weight, armspan or lower segment increments. Pre-adolescent males in group S had a significantly greater increase in stature compared with group P (6.2 +/- 2.1 versus 4.5 +/- 1.2 cm/year p < 0.025); z score improved from -2.42 to -2.24 in group S and from -2.63 to -2.61 in group P. For adolescent males, the difference was also significant (8.3 +/- 1.5 versus 6.2 +/- 2.1 cm/year; p < 0.025). No differences were noted in females. In Chilean male schoolchildren and adolescents with idiopathic short stature, zinc supplementation increases growth velocity over a 12-month period.
To determine whether delay of puberty alters adult height, we retrospectively evaluated the adult height of 41 patients who met rigorous criteria for the diagnosis of isolated hypogonadotropic hypogonadism. The adult height of these patients was compared with the mean height of normal American men at age 18 in the 1979 National Center for Health Statistics survey and with the mean adult height of 50 male normal volunteers who had been studied on the same wards as the patients with hypogonadotropic hypogonadism. The mean adult height of the men with isolated hypogonadotropic hypogonadism was 179.7 cm, which exceeded the height of the 50 control subjects and the normal American men (both 176.8 cm) by 2.9 cm (P less than 0.05 and P less than 0.006, respectively). The mean age at treatment to induce puberty was 20.0 yr, which corresponded to a mean delay in the onset of puberty of more than 8 yr relative to normal males. The final height of the men with hypogonadotropic hypogonadism correlated significantly with the duration of pubertal delay (r = 0.32, P = 0.04). Most of the enhanced mean adult height of the patients with isolated hypogonadotropic hypogonadism was attributable to those patients in whom treatment to induce puberty had been delayed to age 18 or greater. The mean adult height of these patients was 182.4 cm, or 5.6 cm greater than the mean height of the 50 controls or of normal American men (P less than 0.001). The mean adult height of patients whose treatment began between 10 and 17 yr of age was 175.0 cm, which did not differ significantly from that of normal men. We conclude that prolonged delay of puberty (6 or more yr) in men with isolated hypogonadotropic hypogonadism is associated with a modest increase (approximately 5 cm) of adult height.
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