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D Evain Brion

Publications and source records attributed to D Evain Brion.

6 recordsLinked to original sources

Impaired response of growth hormone-releasing hormone (GHRH) measured in plasma after L-dopa stimulation in patients with idiopathic delayed puberty.

In order to investigate the regulation of GH secretion in patients with idiopathic delayed puberty (IDP), either prepubertal (stage P1) or early pubertal (P2), GHRH levels in plasma were measured after stimulation with L-Dopa in a group of 16 patients with IDP. The results were compared to those obtained in 12 patients with constitutional short stature (CSS) at the same stages of puberty, who underwent L-Dopa test for insufficient height. Plasma GHRH levels were measured, after extraction and concentration on C18 Sep Pack columns, by radioimmunoassay using an antibody against 1-40 GHRH, which cross-reacts 100% with 1-44 GHRH. The sensitivity of the assay is 6-8 pg/ml. After L-Dopa intake, the peak of GH was mean +/- SEM 8.6 +/- 1.4 ng/ml in IDP and 12.0 +/- 0.8 ng/ml in CSS (NS). The peak of GHRH after L-Dopa was 41 +/- 10 pg/ml in IDP and 96 +/- 25 pg/ml in CSS (p less than 0.02). A significant (p less than 0.02) decrease of plasma GHRH peak values (mean +/- SEM 17.3 +/- 4.4 pg/ml) was noted in the five patients with IDP whose growth velocity was below -2 SD for their bone age compared to the patients with normal growth velocity (mean +/- SEM 75.0 +/- 14.5 pg/ml). These results suggest a hypothalamic dysfunction in patients with IDP, and a relationship between the well-known partial and transitory somatotropic deficiency found in some adolescents having a pubertal delay and their secretion of the releasing hormone GHRH.

Adolescent

Effect of bromocriptine treatment on circulating somatomedins in tall adolescents.

Somatomedin and bromocriptine levels were measured before and after 3 months of bromocriptine treatment (5 mg/day) in the sera of 16 tall adolescents with excessive adult height prediction. Somatomedins were measured by RIA for somatomedin C and IgFII and by measuring thymidine incorporation into human lectin-activated lymphocytes. Mean +/- SEM levels of bromocriptine after three months of treatment were 0.61 +/- 0.08 ng/ml. No changes in radioimmunoassayable somatomedin C were observed after bromocriptine intake respectively 1.34 +/- 0.17 U/ml before and 1.4 +/- 0.01 U/ml during treatment. On the opposite a significant decrease of thymidine activity (p less than 0.002) from 1.45 +/- 0.17 U/ml to 1.12 +/- 0.19 U/ml was observed. No changes of IgFII levels were observed in the sera of the 8 patients where they were measured. In order to test a possible direct effect of bromocriptine on peripheral tissues bromocriptine mesylate was added in somatomedin bioassays. Inhibitory effect of bromocriptine in vitro is seen at higher levels (1 microM) compared to the circulating one (1 nM). This study demonstrates that the major effect of bromocriptine which is the acceleration of bone maturation is not related to changes in somatomedin C.

Body Height

Negative correlation between peripheral plasma somatostatin levels and GH responses to GH-RH stimulation tests in children.

On forty-six fasting and resting children, aged 5-17 years, with short stature (below -2 SD) a growth hormone releasing hormone (GH-RH) stimulation test (2 micrograms/kg iv bolus, Sanofi) was performed. Twenty-two children were prepubertal, of which, 13 had a constitutional short stature (CSS), nine an idiopathic growth hormone deficiency (IGHD). Twenty-four subjects were pubertal, at the stage II or III of Tanner. Among them, six had a constitutional short stature (CSS) and 18 an idiopathic delayed puberty (IDP). Blood samples were taken for determination of plasma somatostatin-like immunoreactivity (SLI) in chilled test tubes containing EDTA + aprotinin. Plasma SLI levels were measured after extraction and concentration on C18 Sep Pack columns by radioimmunoassay using an antibody against 1-14 somatostatin. The sensitivity of this assay is around 3 pg/ml. After GH-RH stimulation the peak of GH (mean +/- SEM) was in prepubertal subjects: 25.3 +/- 9.1 micrograms/l in CSS, and 18.6 +/- 10.3 micrograms/l in IGHD. In pubertal subjects GH peaks were 17.6 +/- 8.4 micrograms/l in CSS and 15.6 +/- 3.8 micrograms/l in children with IDP. No significant differences was found between basal plasma SLI levels in the four groups of subjects, being respectively (mean +/- SEM) 11.9 +/- 1.8 pg/ml in prepubertal subjects with CSS, 9.6 +/- 2.6 pg/ml in IGHD, 7.6 +/- 1.7 pg/ml in pubertal children with CSS and 6.6 +/- 1.5 pg/ml in children with IDP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent

Studies in constitutionally tall adolescents: somatostatin decrease associated with growth hormone increase after TRH injection.

The paradoxical GH response to TRH observed in certain adolescents with constitutional tall stature is associated with a 60% fall in plasma levels of somatostatin. Conversely, those tall subjects who do not show a GH increase after TRH, or during a saline control infusion maintain steady levels of somatostatin in plasma. It is thus hypothesized that the GH release after TRH is due to a decreased inhibitory effect of somatostatin at the pituitary level and that this reduced effect may play an aetiological role in certain children with 'constitutional' tall stature.

Adolescent

[Benign unilateral testicular hypertrophy beginning at puberty].

Two normal boys, with no previous history, were referred at the onset of puberty for unilateral testicular hypertrophy. Radiological and biological investigations, and in one case testicular biopsy, ruled out cellular proliferation or tumor. Except for FSH level slightly above normal in one case, no endocrine abnormality was found. This is a rare, and probably non pathologic event.

Adolescent