Standard Gonadotropin-Suppressive Therapy in Japanese Girls with Idiopathic Central Precocious or Early Puberty Does Not Adversely Affect Body Composition

Abstract

Estrogen deprivation, for instance after ovariectomy or natural menopause, is associated with significant bone loss in adult women. (Lindsay, 1995) Gonadotropin-releasing hormone agonist (GnRHa) inhibits hypothalamo-pituitary-gonadal hormone secretion and gradually reduces the estrogen level. (Wacharawsindhu et al., 2006) Consequently, decreases in bone mineral density, which are also observed after ovariectomy and natural menopause, have been observed during GnRHa therapy in women with endometriosis and men with benign prostatic hyperplasia. (Goldray et al., 1993) Moreover, women who were treated with this analog showed body composition changes, including a decrease in lean mass and an increase in fat mass, which resemble the body changes that occur during the menopause. (Revila et al., 1998) Meanwhile, GnRHa has also been the treatment of choice for central precocious puberty (CPP) since the mid-1980s. (Crowley et al., 1981) Many of the previous studies on the auxological effects of GnRHa treatment on CPP have focused on assessing the patient’s final height, whereas much less attention has been paid to changes in their weight and body composition. (Arrigo et al., 2004) However, concern has been expressed that CPP might be associated with increases in body mass index (BMI) both at the initial presentation and during GnRHa treatment (Boot et al., 1998) and that individuals with the condition are prone to developing obesity. This concern is supported by adult cases that were treated with GnRHa, as described above. On the other hand, it is well known that BMI and percentage body fat increase during puberty. Consequently, gonadotropin-suppressive therapy can theoretically halt the progression to obesity by inhibiting pubertal development. Recently, there have been many reports about the changes in body composition that occur in children with CPP who are treated with GnRHa (Wacharsindhu et al., 2006, Arrigo et al., 2004, Boot et al., 1998, Feuillan et al.,1999, Palmert et al., 1999, Chiumello et al., 2000, van der Sluis et al., 2002, Paterson et al., 2004, Oosdijk et al., 1996, Traggiai et al., 2005, Herger et al., 1999, Pasuquino et al., 2008). Some reports have shown that obesity occurs at a high frequency among children with CPP (Arrigo et al., 2004, Feuillan et al., 1999, Palmert et al.,