ESPE Abstracts (2015) 84 P-3-1107

Pituitary

Between 3 to 4 Years after Severe Traumatism Brain Injury 22% at Least of Children and Adolescents do have Persistent Pituitary Dysfunction

Yamina Dassaa,e, Claire Personniera,d, Hélène Crosniera,e, Mathilde Chevignardb, Marie Bourgeoisc, Magali Viauda,e & Michel Polaka,e


aDepartment of Paediatric Endocrinology, Gynecology and Diabet, Department of Paediatricology, Hôpital Universitaire Necker-Enfants Malades, APHP, Université Paris-Descartes, Paris, France, bDepartment of Rehabilitation, Saint-Maurice Hospitals, Saint-Maurice, France, cDepartment of Paediatric Neurosurgery, Hôpital Universitaire Necker-Enfants Malades, APHP, Université Paris-Descartes, Paris, France, dDepartment of Paediatric, Poissy-St Germain-en-Laye Hospital, Poissy, France, eImagine Institute, Paris, France.


Background: Traumatic brain injury (TBI) is common in childhood but long-term endocrine consequences are yet to be documented by prospective data.

Objective and hypotheses: We have previously demonstrated in prospective study that, 1 year after severe accidental TBI (ATBI) or inflicted TBI (ITBI), children and adolescents may present pituitary and growth hormone (GH) dysfunction. We present here the follow-up of this population to determine whether or not early GH dysfunction may be persistent.

Method: Our initial study included 87 patients (0–15 years old). After 1 year post-TBI 27/87 had presented GH dysfunction (two stimulated GH peak <7 ng/ml); 5/27 had GH deficiency (GHD) (GH peak <5 ng/ml, IGF1 <−2DS). The patients with GH dysfunction were included in the present study; clinical evaluation and pituitary hormonal testing (basal levels and dynamic GH tests) were performed between 3 and 4 years after TBI.

Results: 27 children were included (22 ATBI, 5 ITBI), 18 underwent hormonal investigations (16 ATBI, 2 ITBI), two declined study, three were lost and four missed hormonal evaluation at that time. Among the 18 investigated patients, two GHD (14.7 and 6.4 years old) started GH treatment 14 and 18 months post-TBI respectively, seven had normal pituitary function (2/7 were GHD at 1 year post-TBI) and nine had low stimulated GH peak. Among these nine patients, four were overweight, two had normal IGF1 levels, and three had low IGF1 with conserved growth velocity (one developed thyreotropic deficiency 18 months post-TBI). The GH treated adolescent remained GHD at the end of treatment. One normal girl had precocious puberty.

Conclusion: 6/27 included patients had persistent pituitary dysfunction (5/27 somatotropic dysfunction) of whom four needed treatment. These results lead us to recommend a prolonged endocrine follow-up of children who presented GH dysfunction 1 year post-TBI.

Funding: Supported in part by Pfizer SAS.

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