Pulsatile growth hormone (GH) secretion plays a central role in human growth during the prepubertal period of life. In order to investigate whether or not short stature in prepubertal children with normal variants of short stature (NVSS) may be explained, at least in part, by the presence of abnormalities in the pulsatile pattern of GH secretion, we have studied the spontaneous secretion of GH/24 h in 139 prepubertal children with short stature (< or = -2 SD) and normal growth velocity (> -1 SD) and in 37 prepubertal children with normal height and growth velocity. All of the subjects included in this study exhibited a body mass index (BMI) lower than 1 SD. The patients with short stature were divided into three groups according to their bone age and the existence of familial antecedents of short stature. These groups were: (1) familial short stature without bone age retardation (FSS-1); (2) constitutional, nonfamilial short stature, with bone age retardation suggesting further delay of puberty (possible constitutional delay of growth and puberty), and (3) familial short stature with bone age retardation (FSS-2). Spontaneous GH secretion was analyzed by using a computerized mathematical algorithm of pulsatility (Cluster). In addition, in all of the patients with short stature, the GH secretory response to three different pharmacological stimuli was evaluated, including: clonidine, growth hormone-releasing hormone (GHRH) and hypoglycemia after insulin administration. The mean values of GH/24 h exhibited a wide range of distribution (1.4-7.8ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)