Serum thyroxine and thyroid stimulating hormone values in unreferred children with short stature.

Of 449 children aged 6-9 years with heights below the first centile in a total population of 48 221, only 1 had previously undiagnosed hypothyroidism. In a community with well developed health services hypothyroidism is unlikely to be the cause of short stature among primary school children.

Differences in physical characteristics, perinatal histories, and social backgrounds between children with growth hormone deficiency and constitutional short stature.

Four hundred and forty-nine children with heights below -2.5 SD were identified by screening for height a total population of 48221 in three Scottish cities. Children participating in the study could be classified into 5 groups: severe growth hormone deficiency (n = 13), partial growth hormone deficiency (n = 25), low birthweight short stature (n = 34), constitutional short stature (n = 178), and short stature associated with some underlying disease (n = 106). Children with growth hormone deficiency tended to be shorter, were more likely to be obese, were growing more slowly, more often were the products of an abnormal pregnancy, and were less socially disadvantaged than constitutionally short children. Their parents were also more likely to have sought medical advice about the short stature. These findings have important implications for improved case-finding of children suffering from growth-hormone deficiency, who in this study accounted for about 10% of all short but otherwise normal children who came from non-disadvantaged communities.

Indices of serum androgens in normal puberty: correlations of two indices with chronological age, bone age and pubertal development in boys and girls.

Two indices of free serum androgenic activity, the normalized androgen ration (NAR) and the free androgen index (FAI) were determined in 218 normal children aged 8-17.9 years. Before the onset of puberty and between chronological age 8 and 11.9 years, NAR and FAI were similar in both sexes, the NAR being less than 0.8 and FAI less than 0.1. In boys mean NAR value increased from 0.87 to 1.39 between 12.5 and 17.5 years, and mean FAI from 0.14 to 1.85 between 12.5 and 17.5 years. In girls mean NAR increased from 0.79 to 0.85 between 12.5 and 15.5 years, and mean FAI from 0.11 to 0.23, between 12.5 and 15.5 years. Both indices did not change significantly between 15.5 and 17.5 years in girls. A rapid increase in NAR and FAI occurred in boys from a mean testicular volume of 4.1 to greater than 20 ml and from genital stage G2+ to 5+. In girls a gradual increase in NAR and FAI occurred from breast stage B2+ to 5+ . Although the androgen indices increased in both sexes between pubic hair stages PH2+ and 6+, the values in girls were always less than in boys at corresponding stages suggesting an increased androgen sensitivity of the female pubic hair follicle during adolescence. The peak rise in NAR and FAI in boys between 13 and 15 years correlated closely with the timing of the pubertal growth spurt in this sex. A similar rise was not seen in girls at the time of their peak growth velocity between 11 and 13 years and suggested that androgens play only a minor or complementary part in the female growth spurt.

Prevalence of severe growth hormone deficiency.

Four hundred and forty-nine short children, who were all over 2-5 standard deviations below the mean height for age, were identified by screening the heights of 48 221 6- to 9-year-old children in three Scottish cities. Most were screened for growth hormone deficiency (GHD). The prevalence of severe GHD in this sample may have been as high as 1 in 4018, much higher than reported. The findings suggest that present referral patterns may account for the delayed or missed diagnosis of the condition in girls or children with less severe short stature.