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Serum GH Concentrations (serum + gh_concentration)

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Medical Sciences	100%

Selected Abstracts

Impaired GH secretion to provocative stimuli in two families with hypocalciuric hypercalcaemia

CLINICAL ENDOCRINOLOGY, Issue 5 2003
Elisabetta Cecconi
Summary objective, To determine whether hypercalcemia per se might be responsible for an impairment in GH secretion. design, Prospective study. patients, Six subjects of two unrelated families with familial hypocalciuric hypercalcaemia (FHH), an autosomal dominant disorder due to inactivating mutations in the calcium receptor gene, leading to an increase in serum calcium levels and inappropriately normal serum PTH concentrations. Forty normal subjects, matched for sex and age served as controls. measurements, Serum GH concentrations were measured after GHRH-Arginine (GHRH-Arg) stimulation test; serum IGF-I, ACTH, cortisol, FT4, FT3, TSH, PRL, LH, FSH levels were measured under basal conditions. results, All subjects (two male, four female, age range 24,74 years) had increased serum ionized calcium levels (range 1·36,1·56 mmol/l) and five of six patients had normal PTH levels (range for all patients was 14,68 ng/l). Basal serum GH concentrations ranged from 0·1 to 7·0 µg/l. Mean serum GH secretory peak after GHRH-Arg stimulation test was reduced in five subjects (mean 9·3 ± 3·6 µg/l, P < 0·006 vs. Controls, mean 67·0 ± 44·0 µg/l, cut-off, 16·0 µg/l) and normal in one subject (38·7 µg/l). However, serum IGF-I levels were reduced only in two patients (29 and 57 µg/l) and normal in four subjects (range 127,208 µg/l). The basal secretion of the other anterior pituitary hormones was within their normal ranges. conclusions, The results of the present study support the concept that elevated serum calcium levels impair GH secretion. However, the clinical relevance of GH deficiency in FHH remains to be elucidated. [source]

The Inhibition of Inducible Nitric Oxide Synthase Reverts Arthritic-Induced Decrease in Pituitary Growth Hormone mRNA But Not in Liver Insulin-Like Growth Factor I mRNA Expression

JOURNAL OF NEUROENDOCRINOLOGY, Issue 12 2003
I. Ibáñez De Cáceres
Abstract Experimental arthritis induced by Freund-adjuvant administration is a model of chronic inflammation and rheumatoid arthritis associated with a decrease in pituitary growth hormone (GH) and hepatic insulin-like growth factor I (IGF-I) gene expression. Excessive nitric oxide (NO) synthesis by inducible NO synthase (iNOS) has been implicated in the pathogenesis of inflammatory illness. Moreover, NO participates in the regulation of GH secretion at both the hypothalamus and the pituitary. We have examined the role of iNOS activation in producing the changes in the GH-IGF-I axis in arthritic rats. Adult male Wistar rats received aminoguanidine or vehicle from day 20, after adjuvant or vehicle injection, until day 28. Two hours and 30 min after the last aminoguanidine injection, all rats were killed by decapitation. Arthritis increased hypothalamic expression of somatostatin mRNA while it decreased pituitary GH mRNA expression, and both effects were prevented by aminoguanidine administration. In arthritic rats, the parallel decrease in serum IGF-I, and in hepatic IGF-I content and mRNA expression, correlates with the decrease in circulating GH concentrations. Aminoguanidine administration to arthritic rats did not modify either serum GH or serum IGF-I concentrations, or hepatic IGF-I mRNA expression. However, aminoguanidine administration to control rats resulted in a decrease in serum GH concentrations and in a decrease in both hepatic IGF-I mRNA expression and serum IGF-I concentrations. These data suggest that NO mediates the arthritis-induced decrease in GH mRNA expression by acting at a hypothalamic level, but it is not involved in the decrease in hepatic IGF-I mRNA expression. [source]

Effects of Body Condition and Protein Supplementation on LH Secretion and Luteal Function in Sheep

REPRODUCTION IN DOMESTIC ANIMALS, Issue 5 2007
CA Meza-Herrera
Contents In ruminants, nutrition is one of the exogenous inputs affecting reproductive function at different levels of the hypothalamic,hypophyseal,gonadal axis. However, the exact mechanisms or even the identification of the signalling metabolic compounds by which nutrition affects reproductive function still need further clarification. The role of static body condition (BC) and its interaction with a short-term protein supplementation (PL), on secretion of metabolic hormones [growth hormone (GH), insulin and insulin-like growth factor-1 (IGF-1)], as well as on secretion of LH and progesterone (P4) was evaluated in sheep. Twenty-four Rambouillet ewes divided into two groups, with lower (LBC) and higher body condition (HBC), were randomly assigned within BC to one of two PL levels: low (LPL, 24% of crude protein; 14 g/animal/day), and high (HPL, 44% of crude protein; 30 g/animal/day). The secretion of GH, insulin, IGF-1 and LH was evaluated on day 10 of the oestrous cycle; appearance and timing of oestrous behaviour were previously detected using rams. Progesterone secretion was evaluated on day 13 of the same cycle. No differences were found (p > 0.05) between PL groups on serum GH concentrations during the sampling period (overall mean of 4.0 ± 0.3 ng/ml), but a trend for lower values in HBC sheep was found (3.6 ± 0.4 vs 4.4 ± 0.4 ng/ml, p = 0.06). A BC effect was observed (p < 0.05) on serum IGF-1 level, with higher values in HBC sheep (p < 0.05). Neither BC nor PL affected (p > 0.05) secretion of LH and the number of corpora lutea, nor serum P4 and insulin concentrations. Results indicate a predominance of the static component of nutrition on sheep metabolic hormone responses, GH and IGF-1, with no effect of short-term PL on secretion of pituitary and ovarian hormones as well as luteal number and activity. [source]

Impaired GH secretion to provocative stimuli in two families with hypocalciuric hypercalcaemia

Confirmation of severe GH deficiency after final height in patients diagnosed as GH deficient during childhood

CLINICAL ENDOCRINOLOGY, Issue 4 2002
Andrea F. Attanasio
Summary objective Human GH treatment of patients with childhood-onset (CO) growth hormone deficiency (GHD) ceases when they reach final height; this provides an opportunity to retest GH status in all patients before determining whether GH therapy will be required in adult life. At present, the diagnostic approach to these patients is not fully standardized. This study aimed to characterize a large group of previously GH-treated CO GHD patients and establish their GH status. patients and methods The multinational study included 167 patients diagnosed as GH deficient and treated with hGH to final height during childhood. Mean age was 19·2 years and mean height standard deviation score (SDS) was ,1·08. Peak serum GH concentrations were determined in standard GH stimulation tests. IGF-I and IGFBP-3 concentrations were determined at a central laboratory and converted to SDS values by reference to a normal population. results Using only a peak GH value of less than 3 µg/l (1 mg = 3 U) in stimulation tests as the cut-off, 133 (79·6%) patients would be classed as GH deficient. Using only an IGF-I value less than ,2 SDS as the cut-off, 134 (80·2%) patients would be classed as GH deficient. However, by using both criteria there were 120 (71·9%) patients who were definitely severely GH deficient (group 1) and 20 (12·0%) who were not GH deficient (group 2), leaving 14 (8·4%) classed as GH deficient from IGF-I SDS only (group 3) and 13 (7·8%) classed as GH deficient from stimulation test only (group 4). There was no difference between the groups in height SDS or body mass index (BMI), but the GH-deficient patients tended to have been diagnosed at a younger age (group 1, 8·2 ± 3·9; group 2, 10·0 ± 4·0; P = 0·052). For patients classed as GH deficient compared with those not GH deficient, the percentage of males was lower (group 1, 64·2%; group 2, 90·0%; P = 0·022) and the percentage with multiple pituitary hormone deficiencies was higher (group 1, 81·7%; group 2, 20·0%; P < 0·001), with the other two groups being intermediate in each case. Only the group classed as GH deficient by both criteria had a mean IGFBP-3 less than ,2 SDS and both IGF-I SDS and IGFBP-3 SDS increased steadily across the four groups. conclusions A high percentage (71·9%) of these childhood-onset GH-deficient patients were still GH deficient in adult life and are likely to require further hGH treatment. While 12·0% could be classed as definitely no longer GH deficient, there are some patients who are intermediate (16·2%) and may be classed as GH deficient by one criterion but not the other. When GH stimulation test results and IGF-I concentration are discordant, the IGFBP-3 level does not establish diagnosis and the hGH treatment requirement of such patients remains a dilemma. [source]