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Growth Hormone Deficiency During the Transition Phase

Published Online: September 12th 2012 European Endocrinology, 2012;8(2):112-115 DOI: http://doi.org/10.17925/EE.2012.08.02.112
Authors: Antonio F Radicioni, Matteo Spaziani, Gilda Ruga, Simona Granato, Natascia Tahani, Giorgio Papi, Andrea M Isidori, Andrea Lenzi
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Abstract:
Overview

The growth hormone (GH)-insulin-like growth factor-1 (IGF-1) axis has several roles. While achievement of a satisfactory height is probably the most important and well-known, it is now clear that it also affects body composition, metabolism, muscle mass and bone density during the transition period. Recombinant-growth hormone (Rec-GH) therapy is normally administered to GH-deficient children to achieve a reasonable final height. Retesting with a provocative test (insulin tolerance test or growth-hormone-releasing hormone + arginine test) is necessary during the transition period, after measuring IGF-1 levels. If the patient is still GH-deficient, rec-GH therapy should be restarted at 0.2–0.5 mg/day up to a final dosage of 0.8–1.0 mg/day (albeit there is no general consensus on the dosage). In fact, there is widespread literature evidence of the negative impact of GH-deficiency during the transition period, which provokes increased visceral fat and waist/hip ratio, decreased muscle mass and bone density and increased cardiovascular morbidity and mortality.

Keywords

Growth hormone, growth hormone deficiency, transition period, bone mineral density, peak bone mass, body composition, dysmetabolism, fertility, quality of life, retesting

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The transition period is the span of time in which people complete their somatic and psychological development after reaching their full stature (also known as late teenage years, post-adolescence or young adulthood). It starts in late puberty and comes to an end at around 25 years of age, thus lasting from three to 10 years. It includes hormonal and many lifestyle changes that lead to a different perception of the self and one’s capacity to relate to others.

The transition period is the span of time in which people complete their somatic and psychological development after reaching their full stature (also known as late teenage years, post-adolescence or young adulthood). It starts in late puberty and comes to an end at around 25 years of age, thus lasting from three to 10 years. It includes hormonal and many lifestyle changes that lead to a different perception of the self and one’s capacity to relate to others. There is also a change in the mental and physical needs of patients with growth hormone deficiency (GHD) who are leaving childhood to become adolescents and then young adults.1,2

Peak bone mass and complete reproductive maturation (demonstrated, in males, by the refinement of semen parameters) are achieved in the transition period. As confirmed by the literature over the last decade, the growth hormone-insulin-like growth factor-1 (GH-IGF-1) axis is essential to achieve optimal body composition and bone density and maintain a safe metabolic profile (thereby decreasing cardiovascular risk). It also has a generally positive influence onquality of life. Normally, recombinant GH (rec-GH) therapy is administered to GH-deficient children to enable them to achieve a satisfactory height, the main target for this period of life. However its use is now accepted and recognised for patients entering the transition period who were GH-deficient during childhood and adolescence, given these other important effects.7,8 It should also be considered if there is a possibility of youth-onset GHD (e.g. following a road accident), which is presumably more difficult to diagnose and would generate less concern, especially if final height had already been reached. Given this, a retest during the transition period is essential, in order to evaluate if there is still a GH-deficiency and if a replacement therapy is still required. It is useful to comment briefly that GH is a polypeptide hormone produced by somatotrope cells of the adenohypophysis: its release is stimulated by growth hormone-releasing hormone (GHRH) produced by the hypothalamus, and inhibited by somatostatin. GH does not work alone, but has a peripheral effector known as IGF-1 due to its structural similarity with insulin. IGF-1 is produced by the liver under GH stimulation and is the substance that actually interacts with peripheral tissues.

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Disclosure

The authors have no conflicts of interest to declare.

Correspondence

Antonio F Radicioni, Section of Medical Pathophysiology, Food Science and Endocrinology, Department of Experimental Medicine, Sapienza University of Rome, Policlinico “Umberto I”, V.le del Policlinico, 00161 Roma, Italy. E: antonio.radicioni@uniroma1.it

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Antonio F Radicioni, Section of Medical Pathophysiology, Food Science and Endocrinology, Department of Experimental Medicine, Sapienza University of Rome, Policlinico “Umberto I”, V.le del Policlinico, 00161 Roma, Italy. E: antonio.radicioni@uniroma1.it

Received

2012-07-25T00:00:00

References

  1. Molitch ME, Growth hormone treatment in adults with growth hormone deficiency: the transition, J Endocrinol Invest, 2011;34:150–14.
  2. Clayton PE, Cuneo RC, Juul A, et al., Consensus statement on the management of the GH-treated adolescent in the transition to adult care, Eur J Endocrinol, 2005;152:165–70.
  3. Schneider HJ, Pagotto U, Stalla GK, Central effects of the somatotropic system, Eur J Endocrinol, 2003;149:377–92.
  4. Lackey BR, Gray SL, Henricks DM, The insulin-like growth factor (IGF) system and gonadotropin regulation: actions and interactions, Cytokine Growth Factor Rev, 1999;10:201–17.
  5. Andreassen TT, Oxlund H, The effects of growth hormone on cortical and cancellous bone, J Musculoskelet Neuronal Interact, 2001;2:49–58.
  6. Sartorio A, Ortolani S, Conti A, et al., Effects of recombinant growth hormone (GH) treatment on bone mineral density and body composition in adults with childhood onset growth hormone deficiency, J Endocrinol Invest, 1996;19:524–9.
  7. Nguyen VT, Misra M, Transitioning of children with GH deficiency to adult dosing: changes in body composition, Pituitary, 2009;12:125–35.
  8. Attanasio AF, Shavrikova E, Blum WF, et al., Continued growth hormone (GH) treatment after final height is necessary to complete somatic development in childhoodonset GH-deficient patients, J Clin Endocrinol Metab, 2004;89:4857–62.
  9. Johannsson G, Albertsson-Wikland K, Bengtsson BA, Discontinuation of growth hormone (GH) treatment: metabolic effects in GH-deficient and GH-sufficient adolescent patients compared with control subjects, Swedish Study Group for Growth Hormone Treatment in Children, J Clin Endocrinol Metab, 1999;84:4516–24.
  10. Carroll PV, Drake WM, Maher KT, et al., Comparison of continuation or cessation of growth hormone (GH) therapy on body composition and metabolic status in adolescents with severe GH deficiency at completion of linear growth, J Clin Endocrinol Metab, 2004;89:3890–5.
  11. Gotherstrom G, Bengtsson BA, Bosaeus I, et al., A 10-year, prospective study of the metabolic effects of growth hormone replacement in adults, J Clin Endocrinol Metab, 2007;92:1442–5.
  12. Fideleff HL, Jonsson B, Koltowska-Haggstrom M, et al., GH deficiency during the transition period: clinical characteristics before and after GH replacement therapy in two different subgroups of patients, J Pediatr Endocr Met, 2012;25(1–2):97–105.

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