Acute and chronic effects of subcutaneous growth hormone (GH) injections on plasma levels of GH binding protein in short children.

1995 ◽  
Vol 80 (9) ◽  
pp. 2756-2760
Author(s):  
R Bjarnason ◽  
K Albertsson-Wikland ◽  
L M Carlsson
1987 ◽  
Vol 17 (3) ◽  
pp. 601-607 ◽  
Author(s):  
D. J. Nutt ◽  
P. J. Cowen

SynopsisThe effect of diazepam on brain 5-HT-mediated neuroendocrine responses was studied in healthy male volunteers. An acute dose of diazepam (15 mg) significantly attenuated the prolactin and growth hormone responses to intravenous L-tryptophan. After 3 weeks administration of diazepam (25 mg/d) these responses had returned to normal despite much higher plasma diazepam concentrations, suggesting that tolerance had occurred. A reduction in brain 5-HT function may underlie some of the acute therapeutic actions of benzodiazepines. It is possible that excessive ‘rebound’ 5-HT activity may contribute to the abstinence syndrome seen on benzodiazepine withdrawal.


1981 ◽  
Vol 59 (11) ◽  
pp. 1139-1145 ◽  
Author(s):  
Patricia N. Prinz ◽  
Michael V. Vitiello ◽  
Timothy A. Roehrs ◽  
Markku Linnoila ◽  
Elliott D. Weitzman

The acute and chronic effects of phenobarbital and phenobarbital withdrawal on sleep patterns and on plasma growth hormone (GH) and Cortisol fluctuations occurring during sleep were studied. Before bed, five healthy men, aged 21 to 25, were given a placebo on three baseline nights, phenobarbital (100 mg p.o.) for nine nights, and a placebo on a final withdrawal night. Beginning on the third of three consecutive nights in the laboratory, all-night polygraphic sleep recordings and blood samples (obtained every 20 min through indwelling venous cannulae) were collected for the placebo, acute phenobarbital, chronic phenobarbital, and phenobarbital withdrawal conditions.Blood phenobarbital levels ranged between 5 to 9 μg/100 mL across all hours of the chronic drug night. At this low sedative dose, latency to sleep onset and stage 4 sleep were significantly reduced in the chronic drug condition, but REM sleep was not significantly reduced. No significant sleep change was observed on the withdrawal night. Both peak GH level and total integrated GH across the night were unaffected by the acute, chronic, and withdrawal conditions. The pattern of GH release appeared to be altered on the phenobarbital and phenobarbital withdrawal nights as compared with placebo. Nighttime plasma cortisol levels were not significantly altered by any experimental condition.


1995 ◽  
Vol 133 (2) ◽  
pp. 189-194 ◽  
Author(s):  
Annamaria Colao ◽  
Bartolomeo Merola ◽  
Diego Ferone ◽  
Paolo Marzullo ◽  
Gaetana Cerbone ◽  
...  

Colao A, Merola B, Ferone D, Marzullo P, Cerbone G, Longobardi S, Di Somma C, Lombardi G. Acute and chronic effects of octreotide on thyroid axis in growth hormone-secreting and clinically non-functioning pituitary adenomas. Eur J Endocrinol 1995;133:189–94. ISSN 0804–4643 The effect of somatostatin on thyroid function was studied in 12 patients with growth hormone (GH)-secreting and eight patients with clinically non-functioning adenomas (NFA) and normal pituitary/ thyroid axis; the patients were subjected to the administration of octreotide (OCT), which is a longacting somatostatin analog. All the patients received an acute test with 100 μg of OCT, both short term (1 month) and long term (6 months), with doses ranging from 300 to 600 μg/day, Serum thyroxine (T4). triiodothyronine (T3), free T4, free T3, thyroglobulin and basal and thyrotropin (TSH)-releasing hormone (TRH)-stimulated TSH were evaluated before and after 1 and 6 months of therapy. Circulating GH and insulin-like growth-factor I (IGF-I) in acromegalics and GH, IGF-I and α-subunit in NFA were assessed at baseline and every month. The acute administration of 100 μg of OCT significantly reduced the TSH response to TRH (p < 0.01) in both acromegalics and NFA. In all the patients OCT administration caused a significant decrease of GH, IGF-I and α-subunit levels (p < 0.01). In addition, after 1 month of therapy both baseline and TRH-induced TSH secretion were decreased significantly in acromegalics and NFA. After 6 months of therapy, baseline and TRH-induced TSH was still reduced in NFA. Conversely, in acromegalics, baseline TSH levels were increased while TSH response to TRH was inhibited. No change of T4, T3, free T4 and free T3 was observed in NFA, whereas a slight but significant increase of T4 and decrease of T3 was recorded in acromegalics. In conclusion, OCT does seem to possess long-term suppressive effects on TSH response to TRH, both in acromegalics and NFA. The lack of basal TSH level inhibition in acromegalics could depend on the restored peripheral conversion of T4 into T3 due to the normalized GH levels during long-term OCT administration. Annamaria Colao, Corso Europa 63, 80127 Napoli, Italy


Sign in / Sign up

Export Citation Format

Share Document