ESPE2016 Rapid Free Communications Pituitary (8 abstracts)
Children and Adolescents with Severe TBI can Develop Late Pituitary Dysfunction Independently of the Results of the First Pituitary Evaluation
Yamina Dassa a , Personnier Claire d , Crosnier Helene d , Chevignard Mathilde b , Bourgeois Marie c , Viaud Magali a & Polak Michel a,
aUnité d’Endocrinologie, Gynécologie et Diabétologie Pédiatrique, Hôpitakl Necker Enfants Malades, APHP, Université Paris-Descartes, PARIS, France; bService de Rééducation neurologique, Hôpitaux de Saint-Maurice, Saint Maurice, France; cService de Neurochirurgie Pédiatrique, Hôpital Necker Necker Enfants Malades, APHP, Université Paris-Descartes, PARIS, France; dService de Pédiatrie, Centre Hospitalier Intercommunal de Poissy-St Germain-en-Laye, Poissy- Saint-Germain-en-Laye Hospital, France; eINSTITUT IMAGINE, Paris, France
Background: Traumatic brain injury (TBI) is common in childhood and can induce pituitary defects. Long-term endocrine consequences are missing.
Objective and hypotheses: To determine in a prospective way if pediatric patients with a personal history of TBI developed long term pituitary deficiency independently of the results of the early hormonal investigation.
Method: Prospective follow-up of an initial cohort of subjects (0–15 years old) with a personal history of severe TBI1. Clinical and hormonal evaluation at inclusion (first year after TBI) and at last visit.
Results: In total of 37 patients are actually included in the follow-up (29 boys, median age: 13.4 years (yrs), 5.3 to 20.9). Median duration of follow-up was 5.9 yrs (3.9 to 7.1). 20/37 had normal pituitary function at first evaluation (group 1) and 17/37 had GH deficiency (GHD) (group 2). In group 1, one patient developed GHD requiring substitution (10 yrs of age - 5.1 yrs post TBI) and one girl developed precocious puberty (PP) (7.8–5.8 yrs post TBI). In group 2, 2 patients with biological GHD but regular growth velocity developed growth failure and had to be treated (11.9 yrs and 12.3 yrs – 4.3 and 5.1 yrs post TBI) and one boy developed PP (10 yrs – 6.3 yrs post TBI). No new patients developed gonadotropic, thyreotropic or corticotrophic deficiency or insipidous diabetes during the follow-up in both groups.
Conclusion: Children with a personal history of TBI can developed a clinical expression of pituitary dysfunction even they had normal evaluation one year post-TBI. These results argue for a prolonged endocrine follow-up of those patients contrary to reports in adults. Supported in part by Pfizer SAS. 1Personnier and al, JCEM 2014.
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