ESPE Abstracts (2015) 84 P-3-1149

Idiopathic Central Precocious Puberty - Treatment Criteria

Joana Serra-Caetanoa, Rita Coutinhoc, Maria Miguel Almirod, Daniela Guelhob, Rosa Dantase, Rita Cardosoa, Isabel Dinisa & Alice Mirantea


aEndocrinology, Diabetes and Growth Unit, Pediatric Hospital, Coimbra Hospital and University Centre, Coimbra, Portugal; bEndocrinology, Diabetes and Metabolism Department, Coimbra Hospital and University Centre, Coimbra, Portugal; cPediatric Department, Santo Andre Hospital, Leiria, Portugal, dPediatric Department, Baixo Vouga Hospital Centre, Aveiro, Portugal; eEndocrinology, Diabetes and Nutrition Department, Baixo Vouga Hospital Centre, Aveiro, Portugal


Background: Central precocious puberty is due to premature activation of the hypothalamo–pituitary–ovarian axis. In girls it is idiopathic in up to 95%. Children with clinical rapid progression are treated with prolonged activity GnRH agonist.

Objective and hypotheses: Characterise cases of idiopathic central precocious puberty (ICPP) followed at our hospital comparing the group treated with GnRH agonist (group A) with the group not treated (group B) at 6–12 months of follow-up.

Method: Retrospective study including children ICPP diagnosed between January/2006 and January/2014, with minimum 6 months’ follow-up. Data collected: age, auxologic data and Tanner stage, at admission and along follow-up; target family height (TFH), parental pubertal age, growth velocity (GV), hormonal levels, bone age, predicted adult height (PAH), and treatment. Statistical analysis with SPSS21th (P<0.05).

Results: We included 42 children with ICPP, without treatment criteria at first visit. All were females, with a mean follow-up time of 11months. Clinical progression was slow in 17 children (group A) and rapid in 25 children (group B). Group B was treated with LHRH, started 12,8 months after the first visit. TFH was 158.3±1.3 cm in group A and 159.3±1.1 cm in group B (P=NS). Mothers’ menarche age was under 10 year in 12.5% in group A and 32% in group B. At first visit, there was no significant difference in both groups in analysed variables. At about 12 months of follow-up, group B had significantly higher GV (8.8±1.9 vs 6.8±2.3; P=0.004), FSH (3.3±1.6 vs 1.8±1.0 UI/ml; P=0.001), IGF1 (410±125 vs 331±116 ng/ml; P=0.05) and IGF1 SDS (2.5±1.4 vs 1.3±1.1; P=0.005) than group A. Comparing data from first visit to 12 months follow-up visit, there was significant difference only for group B. This had a significantly increase of height-sds (P<0.0001), LH (P=0.004), FSH (P=0.006), IGF1 (P=0.003), bone age (P<0.0001) and a significantly decrease in PAH (P=0.019).

Conclusion: Our data confirmed the need to monitor puberty evolution along time, including height, growth velocity, bone age, gonadotropic hormones and IGF1. Children with rapid progressive puberty should be treated in order to avoid compromising final adult height.

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