Oral dexamethasone administration: new pharmacological test for the assessment of growth hormone secretion

Pineda, J; Martul, P.; Casanueva, Felipe F.; Diéguez, Carlos; Rica, Itxaso; Loridan, Liliane

doi:10.1530/eje.0.1310598

Cited by 7 publications

(7 citation statements)

References 10 publications

(14 reference statements)

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“…The positive e ect of the exogenous corticosterone on the secretion of GH reported here accords with data from a number of clinical studies which have demonstrated prompt increases in serum GH following acute administration of glucocorticoids by mouth or parenterally (Buguera et al, 1990;Casanueva et al, 1990;Muruais et al, 1991;Pineda et al, 1994;Pinto et al, 1997;Pellini et al, 1998) and advocated a role for GCs in the diagnosis of GH de®ciency (Pineda et al, 1994;Pellini et al, 1998). Our ®nding that the hypersecretion of GH provoked by a single injection of corticosterone in the rat is (a) blocked speci®cally by central but not peripheral administration of anti-annexin 1 pAb and (b) mimicked by a central injection of annexin 1 Ac2 ± 26 suggests that the steroid exerts its positive in¯uence on the GH axis via an annexin 1-dependent mechanism within the hypothalamus.…”

Section: Discussionsupporting

confidence: 88%

“…This is due largely to actions of the steroids at the hypothalamic level which increase the expression and release of somatostatin (Papachristou et al, 1994;Fife et al, 1996;Lam & Srivastava, 1997) and decrease the production of GH releasing hormone (GHRH, Fernandez-Vazquez et al, 1995;Fife et al, 1996;Lam & Srivastava, 1997). Paradoxically, the impact of the consequent change in the hypothalamic drive to the somatotrophs is attenuated by concomitant actions of the steroids at the pituitary level which increase GHRH receptor (Tamaki et al, 1996;Miller & Mayo, 1997) and GH (Oosterom et al, 1983;Evans et al, 1992;Nogami et al,complicated by ®ndings in man that acute administration of GCs causes a transient (3 ± 4 h), but marked, increase in serum GH (Buguera et al, 1990;Casanueva et al, 1990;Muruais et al, 1991;Pineda et al, 1994;Pinto et al, 1997;Pellini et al, 1998). The mechanism by which the GCs evoke this secretory response is unclear.…”

Section: Introductionmentioning

confidence: 99%

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Opposing influences of glucocorticoids and interleukin‐1β on the secretion of growth hormone and ACTH in the rat in vivo: role of hypothalamic annexin 1

Philip

John

Cover

et al. 2001

British J Pharmacology

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This study exploited established immunoneutralization protocols and an N‐terminal annexin 1 peptide (annexin 1Ac2 – 26) to advance our knowledge of the role of annexin 1 as a mediator of acute glucocorticoid action in the rat neuroendocrine system in vivo. Rats were treated with corticosterone (500 μg kg−1, i.p.) or annexin 1Ac2 – 26 (0.1 – 10 ng rat−1, i.c.v.) and 75 min later with interleukin 1β (IL‐1β, 10 ng rat−1, i.c.v. or 500 μg kg−1, i.p). Blood was collected 1 h later for hormone immunoassay. Where appropriate, anti‐annexin 1 polyclonal antiserum (pAb) was administered subcutaneously or centrally prior to the steroid challenge. Corticosterone did not affect the resting plasma corticotrophin (ACTH) concentration but suppressed the hypersecretion of ACTH induced by IL‐1β (i.p. or i.c.v.). Its actions were quenched by anti‐annexin 1 pAb (s.c. or i.c.v) and mimicked by annexin 1Ac2 – 26. By contrast, corticosterone provoked an increase in serum growth hormone (GH) which was ablated by central but not peripheral administration of anti‐annexin 1 pAb. IL‐1β (i.c.v. or i.p.) did not affect basal GH but, when given centrally but not peripherally, it abolished the corticosterone‐induced hypersecretion of GH. Annexin 1Ac2 – 26 (i.c.v.) also produced an increase in serum GH which was prevented by central injection of IL‐1β. The results support the hypothesis that the acute regulatory actions of glucocorticoids on hypothalamo‐pituitary‐adrenocortical function require annexin 1. They also provide novel evidence that the positive influence of the steroids on GH secretion evident within this timeframe is effected centrally via an annexin 1‐dependent mechanism which is antagonized by IL‐1β. British Journal of Pharmacology (2001) 134, 887–895; doi:10.1038/sj.bjp.0704324

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Opposing influences of glucocorticoids and interleukin‐1β on the secretion of growth hormone and ACTH in the rat in vivo: role of hypothalamic annexin 1

Philip

John

Cover

et al. 2001

British J Pharmacology

View full text Add to dashboard Cite

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“…Maxi mal values were observed after 120 and 150 min in the majority of the subjects. In adults, maximal GH eleva tions occur between 120 and 240 min, with predomi nance at 180 min [20], Pineda et al [25] have demon strated that children are more responsive to dexametha sone in terms of peak values, although no differences were observed in the AUC. This could suggest that children tend to have an earlier onset and a shorter duration of action associated with a higher amplitude of response.…”

Section: Discussionmentioning

confidence: 99%

“…This effect is apparently independent of the type of steroid used [22]. Moreover, in adults, different doses of dexamethasone (8, 4 and 2 mg) have been employed with equal effectiveness [20,23,24], The GH-stimulatory effect is observed when corticoids are used by both intravenous or oral routes of administration [20,25], In obesity and acromegaly the GH-releasing action of intravenous dexamethasone ad ministration has not been verified [21,22,26,27],…”

Section: Introductionmentioning

confidence: 99%

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Effect of Low-Dose Oral and Intravenous Dexamethasone Administration on Growth Hormone Secretion in Children

Pinto

Ninno²,

Lengyel³

1997

Horm Res

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Acute dexamethasone administration (2 mg/m² i.v. and 4 mg orally) increases growth hormone (GH) release in children. We evaluated the effect of a low intravenous dose (1 mg/m²) of dexamethasone on GH secretion in 8 short normal children and in 6 GH-deficient children. There was a significant GH increase at 120, 150 and 180min in short normal children (maximal value: 18.9 ± 2.1 μg/l; X ± EP), compared to placebo administration. In contrast, no significant GH elevation was seen in GH-deficient children (1.3 ± 0.4 μg/l). There was no difference in the GH response after intravenous dexamethasone and oral clonidine in these same 8 short normal children and 6 GH-deficient children. Although no significant GH release was observed after dexamethasone or clonidine in GH deficiency, an increase in GH after GH-releasing hormone was seen (6.1 ± 1.9 μg/l). There was a significant GH increase (18.5 ± 3.3 μg/l) after low-dose (2-mg) oral dexamethasone administration in another 8 short normal children, which was similar to values after intravenous injection. No side effects were noted after intravenous or oral dexamethasone. In conclusion, low-dose intravenous or oral dexamethasone administration causes a marked GH release in short normal children, probably mediated by hypothalamic structures.

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Abnormalities of GH secretion in a young girl with Floating-Harbor syndrome

Cannavò

Bartolone

Lapa

et al. 2002

J Endocrinol Invest

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We present a 9.1-year-old girl of Calabrian (Italy) ancestry, with clinical features (cranio-facial dysmorphism, short stature with delayed bone age and speech delay) suggesting the diagnosis of Floating-Harbor syndrome (FHS). Physical examination showed: height 113.9 cm (-2.9 SD), with a parent's target of 156.2 cm (+1.0 SD), weight 20.7 kg, BMI 16.0 (-0.04 SD), and many phenotypic abnormalities: long eyelashes, large bulbous nose with broad nasal bridge, short philtrum, moderately broad mouth, tooth folding and malocclusion, posteriorly rotated ears, low posterior hair line, short neck, clinodactyly of the 5th finger and hyperextensible finger joints. Diffused hyperpigmentation and hypertrichosis with sporadic pubic terminal hairs, but neither clitoromegaly nor other signs of hyperandrogenism and/or precocious puberty, were observed (T1, P1). Carpal bone evaluation showed a delayed bone age (TW2: 5-5/10, - 3.6 yr) and the statural age/bone age ratio was 1.1. Other dysmorphic syndromes were excluded on the basis of clinical evidence, also evaluated by a computer-assisted search (P.O.S.S.U.M. version 3.5, 1992). Analysis of chromosome 22 by the FISH method, using specific probes Cos29 and Tuple1, excluded microdeletions in the region 22q11.2, typical of Velo-cardio-facial syndrome. In this case, we report the impairment of serum GH responsiveness (GH baseline values: 0.2-1.9 ng/ml) to the administration of oral 150 microg clonidine [peak 4.7 ng/ml, normal values (nv)>10 ng/ml] and oral 4 mg dexamethasone (8.1 ng/ml, nv>10 ng/ml). Moreover, the evaluation of spontaneous 24-h GH secretion (Carmeda AB, Stockholm, Sweden) showed low mean GH levels (1.75 ng/ml, nv>3.0 ng/ml), with a maximum sleep-related peak of 2.8 ng/ml. Serum IGF-1 values were in the low-normal range (80-176 ng/ml, nv 133-626 ng/ml). While in FHS the cranio-facial features minimize with advancement of age, the impairment of growth velocity is permanent and results in severe dwarfism. In our case, treatment with recombinant GH (0.10 U/kg/day), administered by a needle-free device, induced a dramatic increase of growth velocity, increasing the height from -2.8 to -1.9 SD after 18 months, thus indirectly confirming a role of GH deficiency in the pathogenesis of FHS dwarfism.

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Oral dexamethasone administration: new pharmacological test for the assessment of growth hormone secretion

Cited by 7 publications

References 10 publications

Opposing influences of glucocorticoids and interleukin‐1β on the secretion of growth hormone and ACTH in the rat in vivo: role of hypothalamic annexin 1

Opposing influences of glucocorticoids and interleukin‐1β on the secretion of growth hormone and ACTH in the rat in vivo: role of hypothalamic annexin 1

Effect of Low-Dose Oral and Intravenous Dexamethasone Administration on Growth Hormone Secretion in Children

Abnormalities of GH secretion in a young girl with Floating-Harbor syndrome

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