Biomedical subjects
Publications and source records attributed to P H Thomas.
Serum concentrations of follicle-stimulating hormone (FSH) were measured in a 33-year-old eumenorrhoeic woman with primary infertility. Postmenopausal levels were obtained. Using an alternative assay, the patient was found to have normal levels of FSH. The probable cause of the misleading result is discussed.
Fifty-nine short children 2-19 years, 25 females and 34 males, were studied for clinical and biochemical evidence of growth hormone deficiency (GHD). Group 1 (n = 32), mean height SDS -3.26 +/- 1.5, mean retardation of bone age 2 years, had a mean peak GH of 6.1 +/- 3.7 mIU/l during tests of GH release, and were classified as GHD. Group 2 (n = 27), had a mean height SDS of -2.65 +/- 1, mean bone age retardation of 1.7 years and had a mean peak GH during provocation tests of 24.3 +/- 11.1 mIU/l and were classified as non-GHD. Basal IGF-I concentrations were correlated with height and bone age, for both groups and for GHD children, with pubertal score. Neither peak GH values nor integrated GH concentrations in a provocative test were correlated with IGF-I values. The minimum IGF-I concentrations occurred at a bone age of 8 years, the reference point that was taken as the average expected time of maturational change. IGF-I concentrations rose in five GHD children when their bone age exceeded 8 years and when their free testosterone was greater than 10 pmol/l. Eighty-nine per cent of the GHD children with a bone age at or below 8 years were identified as GHD from their basal IGF-I values, but for all bone ages this fell to 62.5%. Basal IGF-I values appear to be less discriminatory for identification of GHD as sexual maturity and bone age advance.
SHBG concentrations in GHD and non GHD children of both sexes were studied in relation to their weight and androgen status. SHBG was inversely related to age in short and control children, but not for GHD. Correction for body weight restored the inverse relationship in these children and improved the correlation for the other groups. DHAS concentrations were similar in GHD and short children, suggesting GH per se does not influence adrenal androgen synthesis. The mean free testosterone in GHD children 12.7 pmol/L, was similar to that in short children, 14.3 pmol/L, and lower than controls 21.2 pmol/L, but consistent with their pubertal status. The linear regression of SHBG on IGF-1 was r = -0.605 (P less than 0.01). It was postulated that IGF-1 and free testosterone may regulate SHBG synthesis. Administration of native and synthetic GH to prepubertal GHD children lowered SHBG without a significant change in TBG, albumin or free testosterone. The fall in SHBG concentration after HGH in GHD children is suggested as a selective mechanism which may lead to improved pubertal development.