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CENTRAL PRECOCIOUS PUBERTY and GONADOTROPIN RELEASING HORMONE AGONIST TREATMENT Cover Illustration: L'enfance Retrowee - Corneille (19941

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CENTRAL PRECOCIOUS PUBERTY and GONADOTROPIN RELEASING HORMONE AGONIST TREATMENT Cover Illustration: L'enfance Retrowee - Corneille (19941 CENTRAL PRECOCIOUS PUBERTY AND GONADOTROPIN RELEASING HORMONE AGONIST TREATMENT Cover illustration: L'enfance retrowee - Corneille (19941 Central precocious puberty and gonadotropin releasing hormone agonist treatment. Wilma Oostdijk. Thesis, Erasmus University Rotterdam. - With ref. With summary in Dutch. ISBN 90-9009946-8 NUGI 742 Keywords: child; central precocious puberty; GnRH agonist treatment; growth No parts of this thesis may be reproduced in any form or by any means without written permission by the author. Composition and lay-out: Editor Printed by Ridderprint, Ridderkerk Central precocious puberty and gonadotropin releasing hormone agonist treatment CENTRALE TE VROEGE PUBERTEIT EN DE BEHANDELING MET EEN GONADOTROPINEN RELEASING HORMOON AGONIST PROEFSCHRIFT ter verkrijging van de graad van doctor aan de Erasmus Universiteit Rotterdam op gezag van de Rector Magnificus Prof. dr P.W.C. Akkermans M.A. en volgens besluit van het College v~~r Promoties De openbare verdediging zal plaatsvinden op woensdag 18 december 1996 om 9.45 uur door Wilma Oostdijk geboren te 's-Gravenhage PROMOTIECOMMISSIE Promotor Prof. dr S.l.S. Drop Overige leden Prof. dr J.M. Wit Prof. dr F.H. de Jong Dr. B.C.J.M. Fauser 17le primil/g of this thesis was fil/al/cially supported by Ferril/g B. v.; Hoofddorp,17le Netherlal/ds. III gedachtellis aall miJlI ollders Dirk Hillebralld OostdiJk ell WillY Heuy vall del' Hoeven CONTENTS Chapter 1: General Introduction 10 1. Normal puberty 10 1.1. The control of the onset of puberty 12 1.2. Gonadotropins 12 1.2.1. Gonadotropins in the fetal and prepubertal period 13 1.2.2. Gonadotropins during puberty 13 1.2.2.1. Basal values 13 1.2.2.2. Stimulated values 13 1.3. Clinical presentation 14 1.4. Bone maturation 14 1.5. Pelvic ultrasonography 15 2. Central precocious puberty 16 2.1. History 16 2.2. Incidence 17 2.3. Etiology 17 2.4. Pathophysiology 18 2.5. Gonadotropins in central precocious puberty 19 2.5.1. Basal values 19 2.5.2. Stimulated values 19 2.6. Clinical presentation 20 2.7. Bone maturation and height prediction 21 2.8. Pelvic ultrasonography 22 2.9. Diagnosis 22 2.10. Differentiation between CPP and premature thelarche 23 2.11. Treatment 24 2.11.1. The goals of treatment 24 2.11. 2. Progestational agents 24 2.11.3. Gonadotropin releasing hormone agonists 24 2.11.3.1. Pituitary desensitization 24 2.11.3.2. Structure-related characteristics 25 2.11.3.3. Treatment in central precocious puberty 26 3. Structure of the thesis 26 References 27 Chapter 2: Treatment of children with central precocious puberty by a slow-release GnRH agonist. 39 Eur J Pediatr 1990; 149: 308-313 7 Chapter 3: Comparison of complete and incomplete suppression of pituitary gonadal activity in girls with central precocious puberty 53 Horl1l Res 1993;39: 111-117 Chapter 4: Long-term results with a slow-release GnRH agonist in central precocious puberty. 65 Acta Paediatr Scand 1991; 372{supplj: 39-45 Chapter 5: Growth and pubertal development during and after treatment with a slow-release GnRH agonist in central precocious puberty. 77 Hor", Res 1991;36: 121-125 Chapter 6: Hormonal evaluation during and after long-term treatment with a slow-release GnRH agonist of children with central precocious puberty. 87 In: Plam TM & Lee PA (Eds) The neurobiology of puberty. Bristol:] Endoennol Ltd 1995,pp 319-325 Chapter 7: Final height in central precocious puberty after long-term treatment with a slow-release GnRH agonist. 95 Arch Dis Child 1996; 75:292-297 ChapterS: Idiopathic isosexual central precocious puberty: magnetic resonance findings in 30 patients. 109 Brit] Radio11995; 68: 34-38 Chapter 9: Combined treatment with a depot GnRH agonist and GH in girls with central precocious puberty and low height velocity: Effects on growth and bone maturation. 121 Chapter 10: The impact of early puberty on final height in foreign-born, adopted children in the Netherlands. 135 Submitted Chapter 11: General discussion and conclusions 152 Chapter 12: Summary/Samenvatting 165 List of abbrevations 173 Dankwoord 174 Curriculum vitae 176 8 CHAPTER 1 INTRODUCTION In order to understand the processes occurring during precocious puberty, one needs to specify what is currently known about normal pubertal development. 1. NORMAL PUBERTY Puberty can be defined as a maturational process of the hypothalamic-pituitary­ gonadal axis, which results in the development of the gonads and, concomitantly, in the physical and physiological processes which constitute adulthood and the capacity to reproduce. The regulation of puberty is a very complex process, involving the hormonal interaction of the cells in the hypothalamus, pituitary and gonads. A central role in this process is played by the Gonadotropin Releasing Hormone (GnRH or LHRH: Luteinizing Hormone Releasing Hormone) which is produced and secreted by the hypothalamus. 1.1 The control of the onset of puberty The reproductive endocrine system is controlled by a hypothalamic GnRH pulse generator: a network of neurons including both ti,e GnRH cells that discharge their products in a coordinated synchronous fashion into hypophyseal portal blood and the inputs that regulate this episodic pattern of release (Goodman et ai, 1981).The GnRH neurons arise outside the brain in the olfactory placode. During the first trimester of gestation they migrate across the nasal septum into the septic-preoptic area and the hypothalamus (Schwanzel-Fukuda et ai, 1992). The GnRH cells are then located in the arcuate nucleus~ in the preoptic area and the medial basal hypothalamus. The axons of the GnRH cells terminate in the external layer of the anterior median eminence. GnRH, a decapeptide, first characterized by Schally et al (1971) and the group of Guillemin (Monahan et aI, 1971), is secreted intermittently or in a pulsatile way from these nerve terminals into the first plexus of the hypothalamic-pituitary portal system, and carried to the anterior part of the pituitary, where the gonadotropic cells are located. GnRH stimulates these cells to release and synthesize luteinizing hormone (LH) and follicle stimulating hormone (FSH) (Clayton et ai, 1989). Additionally, it influences the number of GnRH receptors (Katt et ai, 1985) .The gonadotropic cells of the anterior pituitary respond not only to the signal provided by GnRH, but also to other central and anterior-pituitary-derived factors, such as neuropeptide Y (NPY), oxytocin, endothelin, y-aminobutyric acid (GABA), galanine and pituitary adenylate cyclase-activating peptide, which potentially modulate the action of GnRH (Crowley et ai, 1995). In all species the functional organization of the hypothalamus is dependent on the parallel processes of neural migration and peptidergic differentiation (Wray et ai, 1986; Foster et ai, 1994; Ojeda & Urbanski, 1994; Plant, 1994). At the level 10 GENERAL INTRODUCTION Clreadlan Signals anAH NE neurons GABA neurons NPV neurons Glullmate neuron a onadO ' (aphs @ ~ ®® Sterol eedbaek / ~Gonads Prepubertal Period Pubertal Period Figur. 1. Schematic presentation of the mechanism controlling the onset of puberty. Although, before the onset of puberty, GnRH neurons are already mature enough to release GnRH, tonic inputs from GABA neurons inhibit GnRH release. Diminution of GABA inhibition and concurrent or subsequent increase in facilitatory inputs from glutamate, NE and NPY neurons to GnRH neurons results in the onset of puberty and a cascade of pubertal events. The importance of inhibitory and facilitatory inputs to the GnRH neuroterminal region is emphasized by heavy lines. From Terasawa (! 995). of the neuronal cytoskeleton there are processes which regulate axonal elongation, neuritic arborization and synaptogenesis (Ojeda et ai, 1989). In a some recent reviews about synaptic connections involved in the regulation of gonadotropin release) the different populations of transmitter- and neUfO­ peptide-containing systems and their interaction in various parts of the hypothalamus are described (Crowley et ai, 1995; Leranth et ai, 1995;Terasawa, 1995)(figure 1). GnRH neurons are under the stimulatory influence of at least three excitatory neurotransmitter systems. These include neuronal networks that utilize norepinephrine (NE), NPY and excitatory amino acids, especially glutamate, as neurotransmitters. The main inhibitOlY neurotransmitters affecting GnRH are opioid pep tides and GABA. Both neuronal networks are connected synaptically to GnRH neurons (Ojeda et ai, 1995). A network of regula tory neuritic projections surrounding the GnRH neurons permits each GnRH neuron to receive a large number of inputs and to be modulated by a 11 CHAPTER I battery of aminoacids, peptides, steroids and otber chemicals (Bourguignon et ai, 1994a; Bourguignon, 1995); this results in a pattern of neuronal circuiting which can sustain synchronized pulsatile release of GnRH. The synchronized, rhythmic, and intermittent activity of tbe network of GnRH neurons is inherent in tbe GnRH cell itself (\Veiner et ai, 1993; Bourguignon et ai, 1994b). Structural changes or neuronal plasticity within tbe medial basal hypothalamus may underlie tbe pubertal acceleration in pulsatile GnRH release (Perera et ai, 1995). Additionally, tbis functioning hypotbalamic oscillator can be modulated by extrinsic cues such as photoperiod, nutritional balance, stress and lactation (Cameron et ai, 1989; Ebling & Foster, 1989; Ferin, 1989; Foster, 1994; Reppert et ai, 1989; Smitb et ai, 1989). In primates this GnRH oscillator is clearly operative before birth, but is tben suppressed during a prolonged
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