The effects of treatment combining an agonist of gonadotropin-releasing hormone with growth hormone in pubertal patients with isolated growth hormone deficiency

1989 ◽  
Vol 120 (6) ◽  
pp. 795-799 ◽  
Author(s):  
Jean Edmond Toublanc ◽  
Claire Couprie ◽  
Philippe Garnier ◽  
Jean-Claude Job

Abstract. The final height of patients treated with growth hormone for isolated growth hormone deficiency has, up to now, been subnormal, with a mean below −2 sd in the series reported, an insufficient height at the onset of puberty and a more or less accelerated bone maturation during puberty being two important factors of the poor results. A long-acting analogue of gonadoliberin, Trp6-GnRH, has been given to GH-treated patients with isolated growth hormone deficiency at the time they reached pubertal stage 2, in combination with unchanged doses of GH, for one year in 11 and for two years in 7 of them. It resulted in an increase in the height age/bone age ratio and a reduction of the height insufficiency for bone age. The increase was slight but significant after one year, and fair after two years, in spite of a reduced annual growth rate. Post-analogue follow-up in 5 patients with continued GH treatment showed a good development of growth and of puberty. It is concluded that combination of the long-acting Trp6-GnRH analogue and GH for 1–2 years in patients with isolated growth hormone deficiency whose puberty starts with a very insufficient height may be an appropriate way to improve their growth parameters. Studies with increased doses of GH or increased frequency of injections could help to optimize the results. Several years of follow-up are needed for demonstrating the results on final height.

Neurosurgery ◽  
1990 ◽  
Vol 27 (2) ◽  
pp. 295-299 ◽  
Author(s):  
Neil A. Martin ◽  
Carol Lynn Macagba-Crain ◽  
Mitchell Geffner ◽  
Warwick Peacock

Abstract A 6.5-year-old girl with short stature (height age, 3 years; bone age, 1.75 years) had isolated growth hormone deficiency. Preoperative computed tomography and magnetic resonance imaging demonstrated a large, well-demarcated, homogeneous mass above the dorsum sellae with a density consistent with flowing blood. Vertebral angiography showed a giant intracranial varix caused by an arteriovenous fistula that originated at the apex of the basilar artery. At operation, an aneurysm clip was placed at the origin of the fistula, and occlusion of the fistula was confirmed by intraoperative digital subtraction angiography. There were no permanent neurological sequelae. Despite shrinkage of the varix, demonstrated by follow-up computed tomography, growth hormone deficiency persisted postoperatively. Biosynthetic growth hormone therapy was initiated 6.5 months after surgery and resulted in a height increment of 8.2 cm after 9 months of treatment.


1999 ◽  
Vol 9 ◽  
pp. 139
Author(s):  
X. Badia ◽  
A. Lucas ◽  
A. Sanmarti ◽  
M. Roset ◽  
A. Ulied

1998 ◽  
Vol 49 (6) ◽  
pp. 765-771 ◽  
Author(s):  
X. Badia ◽  
A. Lucas ◽  
A. Sanmartí ◽  
M. Roset ◽  
A. Ulied

2016 ◽  
Vol 174 (5) ◽  
pp. 669-679 ◽  
Author(s):  
Christopher J Child ◽  
Werner F Blum ◽  
Cheri Deal ◽  
Alan G Zimmermann ◽  
Charmian A Quigley ◽  
...  

ObjectiveTo determine characteristics of children initially diagnosed with isolated growth hormone deficiency (IGHD) of organic aetiology, who later developed multiple pituitary hormone deficiencies (MPHD).DesignData were analysed for 716 growth hormone-treated children with organic IGHD, who were growth hormone-naïve at baseline in the multinational, observational Genetics and Neuroendocrinology of Short Stature International Study.MethodsDevelopment of MPHD was ascertained from investigator-provided diagnoses, adverse events and concomitant medications. Analyses were performed for all patients and separately for those who developed MPHD within 4.5 years or had >3.5 years follow-up and continued to have IGHD (4-year cohort).ResultsMPHD developed in 71/716 (9.9%) children overall, and in 60/290 (20.7%) in the 4-year cohort. The most frequent additional deficiencies were thyroid-stimulating hormone (47 patients) and gonadotropins (23 patients). Compared with those who remained with IGHD, children who developed MPHD had more severe GHD at study entry, significantly lower baseline insulin-like growth factor1, peak stimulated growth hormone, and more frequent diagnosis of intracranial tumour or mutation of gene(s) controlling hypothalamic–pituitary development and/or function. Multivariate logistic regression analyses identified female gender, longer follow-up, higher baseline age and lower peak stimulated growth hormone as predictors of MPHD development.ConclusionsMPHD is more likely to develop in patients with severe organic IGHD, especially those with history of intracranial tumour or mutation of gene(s) controlling hypothalamic–pituitary development and/or function. Older baseline age, female gender and longer follow-up duration were also associated with higher incidence of MPHD. Long-term monitoring of pituitary function is recommended, irrespective of the aetiology of GHD.


1994 ◽  
Vol 130 (1) ◽  
pp. 65-69 ◽  
Author(s):  
A Albanese ◽  
R Stanhope

Albanese A, Stanhope R. Treatment of growth delay in boys with isolated growth hormone deficiency. Eur J Endocrinol 1994;130:65–9. ISSN 0804–4643 We report our experience in treating growth delay in boys with isolated growth hormone deficiency (IGHD) receiving biosynthetic human growth hormone. The study was performed in 15 boys with IGHD receiving GH. At the chronological age of 13.1 (1.1) years (sd), 13 were prepubertal, two were in early puberty and there was a mean bone age delay of 2.5 (1.4) years. A growth spurt was induced by either depot testosterone or oxandrolone. There was an increase in growth rate from 5.7 (1.6) cm/year, occurring the year before anabolic or sex steroid therapy, to 8.1 (1.2) cm/year during treatment (p<0.05), followed by 7.3 (1.9) cm/year the year after the cessation of treatment (p< 0.05), There was no significant change in height sd score for bone age, which was −0.69 (0.97) at the commencement of anabolic or sex steroid therapy and −0.53 (0.84) at the end of treatment. Before the induced growth spurt, there was equal body proportion between sitting height and subischial leg length, which had no significant change following androgen treatment. Spontaneous progress in pubertal development was achieved by all patients with an increase in testicular volume from a mean of 2.9 (2–8) to 6.1 (4–10) ml. The pattern of growth presented by patients treated with oxandrolone or those with testosterone was similar. Our data suggest that growth delay and delayed puberty, in patients with IGHD during concomitant growth hormone therapy, can be treated without deterioration in height prognosis. Bringing forward the timing of pubertal growth into the normal range, which is usually delayed in boys with IGHD, may prevent prolonged growth deceleration and psychological distress, which are common sequelae. Intervention should be offered to patients thought to have "isolated" GHD if their puberty is delayed. Normal progression of testicular volumes through puberty will confirm the diagnosis of "isolated" GHD. Our data also have implications for the mechanism of the growth spurt of puberty, especially the relative importance of GH and androgens. R Stanhope, Medical Unit, Institute of Child Health, 30 Guildford Street, London WC1N 1EH, UK


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