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

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.

PEDIATRICS ◽  
1999 ◽  
Vol 104 (Supplement_5) ◽  
pp. 1021-1024
Author(s):  
Kirt E. Simmons

Normal craniofacial and dental growth and development is dependent on growth hormone (GH) and insulin-like growth factor I (IGF-I). Deficiencies of either during childhood cause diminished growth of the maxilla and (to a greater degree) the mandible. Dental development/eruption also is compromised. Conversely, excessive GH/insulin-like growth factor I causes overgrowth, with the mandible again more affected than the maxilla. Replacement therapy in deficiency conditions generally normalizes craniofacial growth. Systemic GH also has been used in other disorders for which overt deficiency of GH has not been demonstrated. One such condition, Turner's syndrome, is now widely treated with GH. Although systemic GH in Turner's syndrome has been shown to positively affect stature, the effects on craniofacial growth and dental development/eruption are largely unknown. To explore these issues, standardized lateral radiographs of seven untreated patients with Turner's syndrome were analyzed and revealed hypoplasias of the cranial base, maxilla, and mandible. Dental development/eruption of patients with Turner's syndrome was found to be significantly advanced (by 0.63 years), relative to control subjects, in a separate study. Annual radiocephalometric measurements of 19 patients with Turner's syndrome treated with GH were compared with nonaffected control subjects over 1 year of treatment. Compared with age-matched historic control subjects, all maxillary—and most mandibular—growth measures were within 2 standard deviations of control. However, in our patients with Turner's syndrome, we found two measures of mandibular growth that deviated by more than 3 standard deviations from control. These data, although preliminary and only encompassing a short period, indicate that mandibular growth may be more affected than is maxillary growth by GH treatment and should be monitored over long-term-therapy.


2016 ◽  
Vol 101 (Suppl 1) ◽  
pp. A262.2-A262 ◽  
Author(s):  
V Price ◽  
D Hawcutt ◽  
S Fryer ◽  
J Bellis ◽  
J Blair

1981 ◽  
Vol 26 (3) ◽  
pp. 240-244 ◽  
Author(s):  
Eileen M. C. Duke ◽  
Dia M. Hussein ◽  
W. Hamilton

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.


1989 ◽  
Vol 121 (2) ◽  
pp. 290-296 ◽  
Author(s):  
Izumi Sukegawa ◽  
Naomi Hizuka ◽  
Kazue Takano ◽  
Kumiko Asakawa ◽  
Reiko Horikawa ◽  
...  

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.


1989 ◽  
Vol 120 (4) ◽  
pp. 442-446 ◽  
Author(s):  
E. Schober ◽  
H Frisch ◽  
F. Waldhauser ◽  
Ch. Bieglmayr

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.


1983 ◽  
Vol 40 (10) ◽  
pp. 1622-1627 ◽  
Author(s):  
Alan W. Hopefl ◽  
Donald R. Miller ◽  
James D. Carlson ◽  
Beverly J. Lloyd ◽  
Brian Jack Day ◽  
...  

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