ESPE Abstracts (2016) 86 P-P1-754

ESPE2016 Poster Presentations Pituitary and Neuroendocrinology P1 (36 abstracts)

The Metabolic Negative Effect of Gonadotropin-Releasing Hormone Agonist Therapy in Childhood: Is it Short-Term and Reversible?

Lorenzo Iughetti a , Patrizia Bruzzi a , Elena Bigi a , Lara Valeri b , Elena Manzotti a , Laura Lucaccioni a & Barbara Predieri a


aDepartment of Medical and Surgical Sciences of Mothers, Children and Adults, University of Modena & Reggio Emilia, Paediatric Unit, Modena, Italy; bSchool of Medicine, University of Modena & Reggio Emilia, Modena, Italy

Background: Data on metabolic effects of gonadotropin-releasing hormone agonist (GnRHa) therapy are still controversial.

Objective and hypotheses: To longitudinally evaluate the effect of GnRHa therapy on BMI, glycaemic metabolism and lipid profile in children affected by idiopathic central precocious puberty (CPP).

Method: This longitudinal retrospective study included data from 42 children (7.70±0.80 years, 2 males) affected by CPP and treated with GnRHa followed from January 1996 to December 2007 in a tertiary center of paediatric endocrinology. Medical history together with anthropometric (BMI-SDS) and biochemical data (fasting glycaemia (mg/dl) and insulin (uIU/ml), Homeostatic model assessment (HOMA) index, total cholesterol (TC), LDL-cholesterol (LDL-C), HDL-cholesterol (HDL-C), triglycerides (TG) (mg/dl), LDL-C/HDL-C and TC/HDL-C ratios) were collected before starting GnRHa therapy (T0), during the treatment (T1) and after GnRHa discontinuation (T2).

Results: At T0, 23 and 16.7% of patients were found overweight and obese, respectively. On GnRHa, BMI-SDS further increased (0.76±0.85 vs 0.98±0.92, P 0.03). At T2 (7.54±1.59 years after T0), even if the 29 and 14% of population was still overweight and obese, respectively, BMI-SDS (0.73±1.21) decreased from T1 (P 0.01). Similarly, insulin-sensibility and lipid profile got worse during GnRHa treatment (T0 vs T1: HOMA index 1.02±0.74 vs 1.87±1.17, P 0.03; LDL-C/HDL-C ratio 1.44±0.38 vs 1.68±0.50, P 0.04) although the same deterioration did not persist at T2 (T2: HOMA index 1.41±0.82, LDL-C/HDL-C ratio 1.41±0.41).

Conclusion: It is known that early sexual maturation contributes to an adverse metabolic programming. Our results support a direct and negative effect of GnRHa per se on BMI, glycaemic metabolism and lipid profile in children affected by CPP. Nevertheless, these consequences appear to be short-term and reversible.

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