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At least 361 records · Page 20Linked to original sources
PubMed1991

National Cancer Institute study of luteinizing hormone-releasing hormone plus flutamide versus luteinizing hormone-releasing hormone plus placebo.

A randomized, double-blind trial in patients with disseminated, previously untreated prostate cancer (stage D2) was designed to test the hypothesis that maximal androgen blockade improves the effectiveness of the treatment of prostatic cancer. Six hundred three men received leuprolide in combination with either placebo or flutamide, and were followed for a minimum of 5 years. The 303 patients randomly assigned to receive leuprolide and flutamide had a longer progression-free survival and an increase in the median length of survival compared with the 300 patients receiving leuprolide plus placebo. Differences between the treatments were particularly evident for men with minimal disease and good performance status.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1992

Diagnostic value of growth hormone-releasing hormone test in children and adolescents with idiopathic growth hormone deficiency.

Average growth hormone (GH) peaks following an i.v. growth hormone releasing hormone (GHRH) 1-29 stimulation test were significantly lower in 48 children and adolescents with GH deficiency (GHD) than in 20 age-matched controls (15.2 + 12.7 vs 37.5 + 28.1 ng/ml, 2 P less than 0.001). Twelve patients exhibited a low GH peak (less than 5 ng/ml), 27 demonstrated a normal response (greater than 10 ng/ml) and 9 showed an intermediate rise in plasma GH (5-10 ng/ml). Six of the 12 patients with low GH response to the first GHRH stimulation failed to respond to two other tests immediately before and after a 1 week priming with s.c. GHRH. These subjects with subnormal GH increase at repeat testing had total GHD (TGHD) and multiple pituitary hormone deficiency (MPHD) and had suffered from perinatal distress. On the contrary, 26 of 27 patients with normal GH response to the first test had isolated GHD and only a minority (8/27) had signs of perinatal distress. It is concluded that perinatal injuries primarily damage pituitary structures and that a pituitary defect more probably underlies more severe forms (TGHD and MPHD) of GHD.

Adolescent↗
PubMed1985

Growth hormone secretion in anaesthetized fowl. 1. Refractoriness to repeated stimulation by human pancreatic growth hormone-releasing factor (hpGRF) or thyrotrophin releasing hormone (TRH).

The intravenous (iv) administration of thyrotrophin releasing hormone (TRH, at 1.0 or 10.0 micrograms/kg) or human pancreatic growth hormone-releasing factor (hpGRF(1-44)NH2, at 10 micrograms/kg) markedly increased the growth hormone (GH) concentration in the plasma of immature or adult cockerels anaesthetized by sodium pentabarbitone (30 mg/kg, iv). A second injection of either TRH or hpGRF failed to increase the GH concentration in immature chicks when administered 15, 30, or 60 min after the first injection. However, significant GH responses to TRH or hpGRF were observed when the interval between injections was either 120 or 240 min. The magnitude of the GH responses to TRH were, however, diminished by 83.3 and 26.7% when given 120 or 240 min after the initial TRH injection, and the responses to hpGRF were similarly reduced by 68.3 and 33.6%. A similar period of GH refractoriness to TRH or hpGRF stimulation was also observed in adult birds, although the recovery of GH responsiveness occurred earlier. While a second injection of hpGRF was ineffective in increasing the plasma GH concentration if given within 30 min of the first, it was fully effective when the interval between injections was greater than 60 min. In response to a second injection of TRH, the GH concentration was elevated when the interval between injections was greater than 120 min, after which the magnitude of the response evoked was greater than that induced by the initial injection. Growth hormone secretion secretion in immature and adult fowl is therefore refractory to repeated provocative stimuli, although the mechanism involved is unknown.

Anesthesia↗
PubMed1989

Triiodothyronine inhibition of thyrotropin-releasing hormone- and growth hormone-releasing factor-induced growth hormone secretion in anesthetized chickens.

The ability of triiodothyronine (T3) to reduce basal and secretagogue-induced growth hormone (GH) release was examined in anesthetized young and adult male chickens. Infusion of T3 had no effect on basal plasma concentrations of GH in either young or adult chickens. However, GH secretion following challenge with either thyrotropin-releasing hormone (TRH) or growth hormone-releasing hormone (GRF) was reduced, in a dose-dependent manner, by the infusion of T3. In vivo sensitivity to T3 inhibition was greater with TRH- than GRF-stimulated GH release in either young (ED50 for TRH-induced GH release, 0.34 microgram T3/kg/min; ED50 for GRF-induced GH release, 0.49 microgram T3/kg/min) or adult chickens (ED50 for TRH-induced GH release, 0.11 microgram T3/kg/min; ED50 for GRF-induced GH release 1.89, micrograms T3/kg/min). Moreover, there was an increase in sensitivity of TRH-induced GH release to T3 with age.

Animals↗
PubMed1992

Neuroendocrine regulation of growth hormone secretion in sheep. V. Growth hormone releasing factor and thyrotrophin releasing hormone.

The effects of intravenous (IV) and intracerebroventricular (ICV) administration of either bovine growth hormone releasing hormone (GRF) or thyrotrophin releasing hormone (TRH) on plasma growth hormone (GH) and glucose levels have been examined in sheep. Intravenous GRF 1-29NH2 at 3 and 30 micrograms stimulated an increase in GH levels in a dose-dependent fashion; administration of GRF into a lateral cerebral ventricle, however, produced a smaller GH response which was similar at these two doses. Evaluation of somatostatin levels in petrosal sinus blood (which collects pituitary effluent blood) showed that ICV administration of GRF stimulated a release of somatostatin into the blood. Furthermore, concurrent administration of GRF and a potent anti-somatostatin serum ICV resulted in a much enhanced release of GH which was similar to that obtained with a comparable dose of GRF given IV. TRH (as another putative GH-secretagogue) was also administered both IV and ICV. When given IV, 200 micrograms (but not 100 micrograms) TRH produced an elevation in GH levels. By contrast, when 5 micrograms TRH was given ICV there was a decrease in circulating GH levels, but no change in plasma somatostatin concentrations. These results indicate that the smaller GH response to ICV- compared with IV-administered GRF is due to the release of somatostatin within the brain. In addition, it would seem that TRH is not a physiological GH-secretagogue in sheep.

Animals↗
PubMed1996

Growth hormone-releasing hormone and somatostatin concentrations in the hypophysial portal blood of conscious sheep during the infusion of growth hormone-releasing peptide-6.

The effects of growth hormone-releasing peptide-6 (GHRP-6) on peripheral plasma concentrations of growth hormone (GH) and hypophysial portal plasma concentrations of growth hormone-releasing hormone (GHRH) and somatostatin (SRIF) were investigated in conscious ewes. Paired blood samples were collected from the hypophysial portal vessels and from the jugular vein of nine ewes for at least 2 hr. The sheep were then given a bolus injection of 10 micrograms of GHRP-6 per kg followed by a 2-hr infusion of GHRP-6 (0.1 microgram/kg.hr). Blood sampling continued throughout the infusion and for 2 hr afterwards. An increase in plasma GH concentration was observed in the jugular samples of six of the nine ewes (1.4 +/- 0.3 vs 7.4 +/- 2.0 ng/ml, P < 0.05) 5-10 min after the GHRP-6 bolus injection, but in no case did we observe a significant coincident release of GHRH. During the infusion period, mean plasma GHRH levels were not significantly increased but there was a 50% increase (P < 0.05) in GHRH pulse frequency; GHRH pulse amplitude was not changed. Mean SRIF concentration, pulse frequency, and pulse amplitude were unchanged by GHRP-6 treatment. These data indicate that GHRP-6 causes a small, but significant effect on the pulsatile secretion of GHRH, indicating action at the hypothalamus or higher centers of the brain. The large initial GH secretory response to GHRP-6 injection does not appear to be the result of GHRP-6 action on GHRH or SRIF secretion.

Animals↗
PubMed2005

Tissue responses to thyroid hormone in a kindred with resistance to thyroid hormone harboring a commonly occurring mutation in the thyroid hormone receptor beta gene (P453T).

Resistance to thyroid hormone (RTH) is a dominantly inherited syndrome of reduced tissue responsiveness to thyroid hormone (TH) usually due to mutations in the TH receptor beta gene (TRbeta). We studied pituitary and peripheral tissue responses to graded doses of liothyronine (L-T3) in 5 affected members (2 children and 3 adults) of a family with RTH due to the common TRbeta mutation P453T. Overall, the 5 subjects studied exhibited suppressed thyrotropin response to thyrotropin-releasing hormone of 51% +/- 8%, 12.1% +/- 1.5%, and 6.3% +/- 3% of the 100% baseline on 50, 100, and 200 microg/dL L-T3, respectively. This degree of suppression was greater than that observed in subjects with RTH due to other TRbeta mutations, indicating less resistance. Compared with normal subjects, however, the family described here demonstrated less suppression by L-T3, compatible with their RTH, although of a mild magnitude. The 2 children with RTH demonstrated less L-T3-mediated suppression of prolactin and cholesterol than the adults. Patients often receive thyroid ablative therapy before the diagnosis of RTH and are left with variable degrees of hypothyroidism. Our results demonstrate that graded doses of L-T3 can be used to evaluate RTH patients, even under the condition of limited thyroid reserve, when results are compared with their baseline. We demonstrate that RTH patients can be evaluated either on or off thyroid hormone and still be distinguished from hypothyroid subjects without RTH.

Adult↗