THERAPEUTICAL DOSES OF SALBUTAMOL INHIBIT THE SOMATOTROPIC RESPONSIVENESS TO GROWTH HORMONE-RELEASING HORMONE IN ASTHMATIC CHILDREN

Purpose of the Study. To determine the effects of therapeutic β2 agonists (specifically salbutamol) on growth hormone (GH) response to growth hormone releasing hormone (GHRH) in children with asthma. Study Population. Fifteen prepubertal children with asthma, ages 6-11 (average age of 9) with normal or normal short stature were studied. Those with an endocrine abnormality, nutritional deficiency, psychological deprivation, or other systemic disease were excluded. Only those children with known bronchial asthma, who showed a 15% decrease of the 1-second forced expiratory volume (FEV1) with methacholine challenge were included. All patients were asymptomatic, and had not experienced an asthma exacerbation, respiratory infection or allergen exposure in the month preceding the study. No child was on medications. Methods. Subjects were divided into two groups. Both groups had baseline GH response to GHRH determined. After an overnight fast, GH levels were obtained the following morning at -60, 0, and then every 15 minutes until 120 minutes after GHRH administration. Two days following this, Group A received salbutamol (0.125 mg/kg) orally at -60 minutes and GH response to GHRH was remeasured. Group B received aerosolized salbutamol (2 mg over 15 minutes) (details of administration were not specified by the authors). All serum GH levels were measured in duplicate by immunoradiometric assay (sensitivity of 0.1 µg/L). Findings. Basal GH levels were similar in both groups. Orally administered salbutamol (Group A) markedly inhibited GH response to GHRH (peak of 3.7 ± 0.6 vs. 18.6 ± 4.7 g/L). Inhaled salbutamol (Group B), although blunting the GHRH-induced GH response, did so to a lesser extent (peak of 20.0 ± 7.5 vs. 35.8 ± 9.4 g/L, P < .02).

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Effect of 15-day treatment with growth-hormone-releasing hormone alone or combined with different doses of arginine on the reduced somatotrope responsiveness to the neurohormone in normal aging

Acta Endocrinologica ◽

10.1530/eje.0.1320032 ◽

1995 ◽

Vol 132 (1) ◽

pp. 32-36 ◽

Cited By ~ 10

Author(s):

E Ghigo ◽

GP Ceda ◽

R Valcavi ◽

S Goffi ◽

M Zini ◽

...

Keyword(s):

Growth Hormone ◽

Day Treatment ◽

Normal Aging ◽

Prolonged Treatment ◽

Elderly Subjects ◽

Growth Hormone Releasing Hormone ◽

Releasing Hormone ◽

Group A ◽

Group B ◽

Different Doses

Ghigo E, Ceda GP, Valcavi R, Goffi S, Zini M, Mucci M, Valenti G, Muller EE, Camanni F. Effect of 15-day treatment with growth hormone-releasing hormone alone or combined with different doses of arginine on the reduced somatotrope responsiveness to the neurohormone in normal aging. Eur J Endocrinol 1995;132:32–6. ISSN 0804–4643 It is well known that both spontaneous and growth hormone-releasing hormone (GHRH)-stimulated GH secretion undergo an age-related decrease; in addition, there is supportive evidence that the GH hyposecretory state of aging is of hypothalamic origin. The aims of the study in 35 normal elderly subjects (20 males and 15 females aged 65–89 years) were to verify whether the low somatotrope responsiveness to GHRH (1 μg/kg) can be primed by a daily GHRH treatment and whether the potentiating effect of both high intravenous (0.5 g/kg) and low oral (8 g) doses of arginine (ARG) on GH response to GHRH is maintained with time. In group A (N = 14) the GH response to GHRH on day 1 (AUC: 373.5 ± 78.5 μg·1−1·h−1) was unchanged after 7 (3720 ± 38 μg·1−1·h−1) and 15 days (377.9 ± 63.8 μg·1−1·h−1) of daily GHRH administration. In group B (N = 6) the GH response to GHRH co-administered with iv ARG on day 1 (1614.2 ± 146.2 μg · 1−1 · h−1) was higher (p < 0.05) than that of GHRH alone (group A) and persisted unchanged after 7 (1514.7±366.5 μg·1−1·h−1) and 15 days (1631.7 ± 379.1 μg · 1−1 · h−1) of treatment. In group C (N = 15) the GH response to GHRH co-administered with oral ARG on day 1 (950.6 ± 219.4 μg·1−1 · h−1) was higher (p < 0.03) than that of GHRH alone (group A) but lower (p < 0.05) than that to GHRH plus iv ARG (group B). It was unchanged after 7 (816.2 ± 208.5 μg·1−1 · h−1) and 15 days (760.4 ± 165.0 μg · 1−1· h−1) of treatment; these responses were still higher (p < 0.05) than that to GHRH alone. Insulin-like growth factor I levels were not modified by any of the treatments. In conclusion, our results demonstrate that in normal aging the low somatotrope responsiveness to GHRH is not improved by prolonged treatment with the neurohormone but it is enhanced by the combined treatment with ARG and this effect does not vanish after a 15-day treatment period. The effect of ARG is present even after a low oral dose, although less markedly than after a high intravenous dose. F Camanni, Divisione di Endocrinologia, Ospedale Molinette, C. so Dogliotti 14, 10126 Torino, Italy

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Association of pituitary adenoma with neuronal christoma: A TEM study

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s042482010016889x ◽

1994 ◽

Vol 52 ◽

pp. 232-233

Author(s):

Eva Horvath ◽

Kalman Kovacs ◽

B. W. Scheithauer ◽

R. V. Lloyd ◽

H. S. Smyth

Keyword(s):

Growth Hormone ◽

Pituitary Adenoma ◽

Pituitary Tumor ◽

Nervous Tissue ◽

Alternative Explanation ◽

Growth Hormone Releasing Hormone ◽

Cell Hyperplasia ◽

Releasing Hormone ◽

Secretory Neurons

The association of a pituitary adenoma with nervous tissue consisting of neuron-like cells and neuropil is a rare abnormality. In the majority of cases, the pituitary tumor is a chromophobic adenoma, accompanied by acromegaly. Histology reveals widely variable proportions of endocrine and nervous tissue in alternating or intermingled patterns. The lesion is perceived as a composite one consisting of two histogenetically distinct parts. It has been suggested that the neuronal component, morphologically similar to secretory neurons of the hypothalamus, may initiate adenoma formation by releasing stimulatory substances. Immunoreactivity for growth hormone releasing hormone (GRH) in the neuronal component of some cases supported this view, whereas other findings such as consistent lack of growth hormone (GH) cell hyperplasia in the lesions called for alternative explanation.Fifteen tumors consisting of a pituitary adenoma and a neuronal component have been collected over a 20 yr. period. Acromegaly was present in 11 patients, was equivocal in one, and absent in 3.

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