Influence of estrogen administration on growth hormone response to GHRH and L-Dopa in patients with Turner's syndrome

1989 ◽  
Vol 120 (4) ◽  
pp. 442-446 ◽  
Author(s):  
E. Schober ◽  
H Frisch ◽  
F. Waldhauser ◽  
Ch. Bieglmayr
Keyword(s):  
Growth Hormone ◽  
Priming Effect ◽  
Ovarian Failure ◽  
Estrogen Deficiency ◽  
Growth Hormone Response ◽  
Turner's Syndrome ◽  
Hormone Response ◽  
Turner’S Syndrome ◽  
Gh Secretion ◽  
Estrogen Administration

Abstract. The modulating effect of estrogen on GH secretion was studied in 22 patients with Turner's syndrome. Estrogen administration (0.5 μg/kg ethinylestradiol) for a period of 4 weeks resulted in a significant increase in basal GH concentrations (2.6 vs 4.8 μg/l, P< 0.01). The L-Dopa-stimulated GH concentrations were also significantly increased (P< 0.01), whereas no effect of estrogen substitution on GH responses to GHRH (1–44) and Sm-C levels was seen. Our findings demonstrate a priming effect of estrogen on GH secretion in patients with Turner's syndrome. These patients generally lack the puberty-associated rise in GH secretion, which might be due to ovarian failure and the concomitant estrogen deficiency.

Turner's Syndrome Associated with Growth Hormone Deficiency

1981 ◽  
Vol 26 (3) ◽  
pp. 240-244 ◽  
Author(s):  
Eileen M. C. Duke ◽  
Dia M. Hussein ◽  
W. Hamilton
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Normal Population ◽  
Normal Growth ◽  
Growth Hormone Response ◽  
Hormone Deficiency ◽  
Turner's Syndrome ◽  
Hormone Response ◽  
Turner’S Syndrome ◽  
Hormone Responses

11 out of the 13 children with Turner's syndrome currently attending our endocrine clinic were investigated for possible growth hormone deficiency. The parents of two of the 13 children refused permission for these studies. One child had inadequate hypoglycaemia and the test was not repeated. Six of the ten children with adequate hypoglycaemia had an adequate growth hormone response to hypoglycaemia, while 4 children did not. This contradicts several previous studies on children with Turner's syndrome, which have reported normal growth hormone responses to provocative tests. In the normal population approximately one in 15 has an inadequate growth hormone response to hypoglycaemia.

Growth hormone response to growth hormone-releasing hormone (GHRH), insulin, clonidine and arginine after GHRH pretreatment in obese children: evidence of somatostatin increase?

1995 ◽  
Vol 132 (6) ◽  
pp. 716-721 ◽  
Author(s):  
Cecilia Volta ◽  
Sergio Bernasconi ◽  
Lorenzo lughetti ◽  
Lucia Ghizzoni ◽  
Maurizio Rossi ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Normal Weight ◽  
Growth Hormone Response ◽  
Growth Hormone Releasing Hormone ◽  
Hormone Response ◽  
Obese Children ◽  
Normal Children ◽  
Insulin Hypoglycemia ◽  
Releasing Hormone ◽  
Gh Secretion

Volta C. Bernasconi S, lughetti L, Ghizzoni L, Rossi M, Costa M, Cozzini A. Growth hormone response to growth hormone-releasing hormone (GHRH), insulin, clonidine and arginine after GHRH pretreatment in obese children: evidence of somatostatin increase? Eur J Endocrinol 1995; 132:716–21. ISSN 0804–4643 To clarify the possible neuroendocrine mechanisms underlying the impairment in growth hormone (GH) secretion present in obesity, the GH response to GH-releasing hormone (GHRH, N = 6), insulin hypoglycemia (N = 6), clonidine (N = 7) and arginine (N = 8) after GHRH pretreatment (1 μg/kg iv 2 h before the tests) was evaluated in 27 obese peripubertal children and in a group of normal-weight short-normal children (N = 26). Growth hormone-releasing hormone pretreatment and all further stimuli elicited a statistically significant GH response in both obese and short-normal children; in the latter group arginine did not induce a significant GH response. No differences were found among the GH responses after the second stimuli in obese children, while in short-normal children the arginine peak and area values were lower than after GHRH and clonidine. Comparison between the two groups showed similar baseline but higher stimulated GH levels in normal-weight children after all tests except ariginine, after which no difference was present. In conclusion, the neuroregulation of GH release seems to be similar qualitatively in normal-weight and obese youngsters; the different behavior observed after arginine, which is supposed to act through somatostatin inhibition, might be due to a chronic increase in somatostatinergic tone responsible for the lower stimulated GH levels in obesity. Sergio Bernasconi, Clinica Pediatrica, Via Gransci 14, 43100 Parma, Italy

Influence of estrogen administration on growth hormone stimulation in patients with Turner's syndrome

1987 ◽  
Vol 116 (3_Suppl) ◽  
pp. S175-S176 ◽  
Author(s):  
E. SCHOBER ◽  
H. FRISCH ◽  
F. WALDHAUSER ◽  
CH. BIEGELMAYER
Keyword(s):  
Growth Hormone ◽  
Turner's Syndrome ◽  
Turner’S Syndrome ◽  
Hormone Stimulation ◽  
Estrogen Administration

Lack of growth hormone response to acute administration of dexamethasone in anorexia nervosa

1995 ◽  
Vol 132 (2) ◽  
pp. 152-158 ◽  
Author(s):  
Massimo Scacchi ◽  
Cecilia Invitti ◽  
Angela I Pincelli ◽  
Claudio Pandolfi ◽  
Antonella Dubini ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Anorexia Nervosa ◽  
Normal Subjects ◽  
High Plasma ◽  
Normal Weight ◽  
Growth Hormone Response ◽  
Acute Administration ◽  
Hormone Response ◽  
Gh Secretion ◽  
Plasma Gh

Scacchi M, Invitti C, Pincelli AI, Pandolfi C, Dubini A, Cavagnini F. Lack of growth hormone response to acute administration of dexamethasone in anorexia nervosa. Eur J Endocrinol 1995;132:152–8. ISSN 0804–4643 High plasma growth hormone (GH) levels, associated with abnormal hormone responses to provocative stimuli, point to an altered GH secretion in anorexia nervosa. The GH-releasing effect of acutely administered glucocorticoids, firmly established in normal subjects, has not been reported in these patients. In this study, acute iv administration of 4 mg of dexamethasone, compared with saline, increased plasma GH in nine normal-weight women (AUC 848.2 ± 127.95 vs 242.8 ± 55.35 μg·l−1·min−1, p < 0.05, respectively) but was ineffective in 11 anorectic patients (AUC 3271.8 ± 1407.11 vs 2780.0 ± 1162.04 μg·l−1·min−1, NS). After dexamethasone, a significant lowering of plasma cortisol was observed in normal women (AUC 25367.0 ± 3128.43 vs 47347.1 ± 4456.61 nmol·l−1·min−1, after dexamethasone and saline, respectively, p < 0.05), but not in anorectic patients (AUC 77809.3 ± 8499.92 vs 78454.9 ± 7603.62 nmol·l−1·min−1, NS). In both groups, plasma adrenocorticotrophin (ACTH) displayed a significant decrease after dexamethasone (AUC 523.6 ± 92.08 vs 874.2 ± 115.03 pmol·l−1·min−1, p < 0.05, after dexamethasone and saline, respectively, in anorectic patients and 377.5 ± 38.41 vs 1004.9 ± 200.51 pmol·l−1·min−1, p < 0.05, in controls). However, when considering the hormonal decremental areas, a significant dexamethasone-induced ACTH inhibition, compared to saline, was evidenced in normal (ΔAUC –414.4 ± 65.75 vs 222.9 ± 42.40 pmol·l−1·min−1, p < 0.05) but not in anorectic women (ΔAUC –254.2 ± 96.92 vs 2.9 ± 132.32 pmol·l−1·min−1, NS). In conclusion, compared to normal subjects, anorectic patients do not display an increase of plasma GH levels and show a lower degree of inhibition of the hypothalamic–pituitary–adrenal axis following acute iv administration of dexamethasone. This observation broadens the array of the abnormal GH responses to provocative stimuli in anorexia nervosa and supports the existence, in these patients, of a decreased hypothalamic somatostatin secretion, although the possibility of a reduced tissue sensitivity to glucocorticoids cannot be excluded. Francesco Cavagnini, 2nd Chair of Endocrinology, University of Milan, Istituto Scientifico Ospedale San Luca, Centro Auxologico Italiano, via Spagnoletto 3, 20149 Milano, Italy

EFFECT OF RESERPINE ON GROWTH HORMONE RESPONSE TO INSULIN HYPOGLYCAEMIA AND TO ARGININE INFUSION IN NORMAL SUBJECTS AND HYPERTHYROID PATIENTS

1971 ◽  
Vol 51 (4) ◽  
pp. 651-656 ◽  
Author(s):  
F. CAVAGNINI ◽  
M. PERACCHI
Keyword(s):  
Growth Hormone ◽  
Normal Subjects ◽  
Growth Hormone Response ◽  
Hormone Response ◽  
Arginine Infusion ◽  
Gh Secretion ◽  
Adrenergic Control ◽  
Significant Change ◽  
Hyperthyroid Patients

SUMMARY The effect of reserpine on growth hormone (GH) secretion induced by insulin hypoglycaemia and by arginine infusion was studied in ten normal subjects and ten hyperthyroid patients. In both groups of subjects, oral reserpine administration resulted in a reduction of GH response to hypoglycaemia, but caused no significant change of GH release after arginine infusion. These results strongly support the theory of an adrenergic control of GH secretion and indicate that arginine stimulates GH secretion in a different way from insulin and independently of catecholamines.

Growth hormone secretion in patients with Turner's syndrome as determined by time series analysis

1992 ◽  
Vol 127 (1) ◽  
pp. 7-12 ◽  
Author(s):  
Jan M Wit ◽  
Albert A Massarano ◽  
Gerdine A Kamp ◽  
Peter C Hindmarsh ◽  
An van Es ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Ethinyl Estradiol ◽  
Height Velocity ◽  
Breast Development ◽  
Turner's Syndrome ◽  
Turner’S Syndrome ◽  
Estradiol Treatment ◽  
Gh Secretion ◽  
Short Children ◽  
Significant Difference

Twenty-four-hour growth hormone (GH) profiles in 26 girls with Turner's syndrome were compared with those of 26 normally growing short children and 24 slowly growing short children. All children were prepubertal and below 12 years of age. A subgroup of 13 girls was treated with ethinyl estradiol and a 24-h GH profile was reassessed. In an additional group of 45 girls with Turner's syndrome (aged 6.7–18.9 years) the effect of age, spontaneous breast development and ethinyl estradiol treatment was studied. The profiles were assessed by Fourier analysis. The oscillatory activity and the mean 24-h GH concentration were similar in children with Turner's syndrome and the normally growing short children, in contrast to lower levels in the slowly growing short children. The periodicity of GH secretion was similar in all groups. In the longitudinal study, ethinyl estradiol treatment resulted in a significant increase in pulse amplitude, but not in periodicity. In the cross-sectional study there was no significant difference between the subgroups of girls with either presence or absence of breast development or ethinyl estradiol treatment. GH secretion was not significantly related to age, height in standard deviation score or height velocity. These data imply that there is no abnormality in GH secretion in girls with Turner's syndrome.

Measurement of nocturnal urinary growth hormone values

1989 ◽  
Vol 121 (2) ◽  
pp. 290-296 ◽  
Author(s):  
Izumi Sukegawa ◽  
Naomi Hizuka ◽  
Kazue Takano ◽  
Kumiko Asakawa ◽  
Reiko Horikawa ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Gh Deficiency ◽  
Turner's Syndrome ◽  
Turner’S Syndrome ◽  
Gh Secretion ◽  
Short Children ◽  
The Mean ◽  
Plasma Gh ◽  
Normal Adults ◽  
Collection Time

Abstract. Nocturnal urinary growth hormone values were measured by a sensitive enzyme immunoassay in normal adults, patients with GH deficiency, patients with Turner's syndrome, normal but short children who had normal plasma GH responses to provocative tests, and patients with acromegaly. The mean nocturnal urinary GH values in patients with acromegaly were significantly greater than those in normal adults (1582.3 ± 579.8 vs 53.5 ± 8.6 pmol/mmol creatinine (± sem); p < 0.05). In the normal but short children and patients with Turner's syndrome, the mean nocturnal urinary GH values were 83.1 ± 5.2 and 79.8 ± 29.5 pmol/mmol creatinine, respectively. In patients with GH deficiency, the nocturnal urinary GH values were undetectable (< 5.3 pmol/mmol creatinine) except in one patient where the value was 6.3 pmol/mmol creatinine. The nocturnal urinary GH values of the patients with GH deficiency were significantly lower than those of the other groups (p < 0.05). In normal but short children, the nocturnal urinary GH values correlated significantly with mean plasma nocturnal GH concentrations (r = 0.76, p < 0.001), and 24-hour urinary GH values (r = 0.84, p < 0.001), respectively. In 4 patients with GH deficiency who had circulating anti-hGH antibody, the urinary GH values were also undectable. These data indicate that nocturnal urinary GH value reflects endogenous GH secretion during collection time, and that measurement of the nocturnal urinary GH values is a useful method for screening of patients with GH deficiency and acromegaly.

Growth hormone, somatomedin levels and growth regulation in Turner's syndrome

1987 ◽  
Vol 116 (2) ◽  
pp. 305-313 ◽  
Author(s):  
Michael B. Ranke ◽  
Werner F. Blum ◽  
Frank Haug ◽  
Werner Rosendahl ◽  
Andrea Attanasio ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Regulation ◽  
Bone Age ◽  
Serum Levels ◽  
Turner's Syndrome ◽  
Turner’S Syndrome ◽  
Normal Range ◽  
Cross Sectional ◽  
Gh Secretion ◽  
Igf I

Abstract. In a total of 56 children and adolescents with Turner's syndrome (41 with karyotype 45,X) basal serum levels of somatomedin bioactivity, Sm-C/IGF-I (RIA), IGF II (RIA), GH response to arginine and GHRH (GRF(1-29)NH2), and spontaneous GH secretion during 5.5 h of deep sleep were determined in a cross-sectional manner. GH responses to GRF and arginine as well as IGF-II levels were found to be in the normal range. Levels of somatomedin bioactivity were higher than normal before a bone age of 10 years, in the low-normal range thereafter, and below normal in some patients. Levels of Sm-C/IGF-I were found normal before and low-normal after a bone age of ten years. There was a trend towards increasing Sm-C/IGF-I levels with age. In contrast to the normal pattern, spontaneous sleep-related GH secretion was declining with age and did not show the puberty-associated rise. These findings suggest a normally functioning growth hormone-somatomedin axis in Turner's syndrome with alterations of its functioning level occurring secondarily as a result of absent gonadal activation. In single patients abnormally low growth hormone and/or somatomedin secretion may be present.

Decreased growth hormone response to growth hormone-releasing hormone in Turner's syndrome: Relation to body weight and adiposity

1991 ◽  
Vol 125 (1) ◽  
pp. 38-42 ◽  
Author(s):  
Jean-Claude Reiter ◽  
Margareta Craen ◽  
Guy Van Vliet
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Ideal Body Weight ◽  
Turner's Syndrome ◽  
Hormone Response ◽  
Turner’S Syndrome ◽  
Factor I ◽  
Ideal Body ◽  
Plasma Gh ◽  
Lean Children

Abstract. A decreased growth hormone response to various secretagogues has been described in Turner's syndrome, but the mechanisms responsible for this decrease are unknown. Seventeen prepubertal girls with Turner's syndrome (age 6.4 to 15.7 years; height −0.2 to −5.4 sd, bone age −3.7 to −0.3 sd; weight 93 to 169% of ideal body weight) underwent a stimulation test with GHRH (0.5 μg/kg). Plasma GH and prolactin were measured by radioimmunoassay from −30 to +120 min and insulin-like growth factor-I at time 0. These values were compared with those observed in lean children with constitutional short stature. Peak plasma GH after GHRH was 17.0±3.6 μg/l (mean±sem), significantly lower (p<0.001) than in the short lean children (39.2±5.1 μg/l. In Turner's syndrome patients, the peak GH value was negatively correlated with the percentage of ideal body weight (r=−0.58, p<0.02) and of body fat (r=−0.59, p<0.02). Plasma prolactin levels in Turner's syndrome did not rise after GHRH and showed a normal circadian variation, from 8.0±1.0 μg/l at 08.30 h to 5.0±0.7 μg/l at 11.00 h (mean ±sem). Mean (±sem) baseline plasma insulin-like growth factor-I concentrations was 0.88±0.14 kU/l, higher than in the short lean children (0.49±0.08 kU/l, p<0.05). We conclude that the decreased GH response to GHRH of girls with Turner's syndrome is related, at least in part, to their excess body weight and fat and is associated with higher IGF-I levels than in short lean children.

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