ESPE Abstracts (2015) 84 P-3-1109

Acute Phase Proteins and Endocrine Dysfunction after Traumatic Brain Injury in Childhood

Olga Verigakia, Ioannis Papassotirioub, Neofytos Prodromouc, George Sfakianosc, George Chrousosa & Christina Kanaka-Gantenbeina


aFirst Department of Pediatrics, University of Athens, Medical School, Agia Sophia Children’s Hospital, Athens, Greece; bDepartment of Clinical Biochemistry, Aghia Sophia Children’s Hospital, Athens, Greece; cDepartment of Neurosurgery, Aghia Sophia Children’s Hospital, Athens, Greece.


Background: Endocrine impairments, such as diabetes insipidus (DI), growth hormone deficiency (GHD) and, to a lesser degree, thyroid or cortisol deficiencies, have been reported after traumatic brain injury (TBI) in adults and much less in children both at the acute post-traumatic phase and after a lag period of time. However, no prospective data exist on the endocrine and acute phase protein response to TBI in childhood.

Aim/objective: To unravel possible endocrine impairment and acute phase protein response after TBI in children hospitalized in a single pediatric Neurosurgery department.

Methods: Twenty-one children (11 girls), age range 1.3–12.6 years, with TBI were prospectively enrolled and studied at three phases: at the acute phase and at 6 and 12–18 months following the injury. Five out of the 21 patients dropped-out at 6 months and three more patients at 12–18 months. The endocrine and acute phase protein assessment was performed at all time-points.

Results: At the acute phase, GHD, as assessed by low IGF-1 levels, was found in 24% of cases, DI in 19% and subclinical hypothyroidism in 5%. Permanent endocrine dysfunctions 12–18 months after TBI were hypothyroidism and DI in 15% and low IGF1 levels in 6%. Contrary to literature data, prolactin levels were normal during the 1st and 2nd phase, with an increase observed in 12% of the cases 12–18 months after TBI. Moreover, S100b, a biomarker of brain damage was increased in all children at all phases, indicating a persisting neuronal damage 12–18 months after TBI. All children demonstrated a good spontaneous recovery with no clinically relevant permanent neurological deficits.

Conclusions: Our results reveal a significant percentage of endocrine dysfunction in children after TBI, both at the acute phase and long after the incident. A subclinical persistent neuronal damage observed in all children calls for long-term surveillance of children post TBI.

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