Long-term morbidity after traumatic brain injury (TBI) in childhood: Endocrine dysfunction, fatigue, impact on cognition and health related quality of life (HRQL). [KHINES (Kid's Head Injury NeuroEndocrine Study)]

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 130-162-Neuroendocrinology
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-147
Nik Daskas1, Peta Sharples1, Wolf Woltersdorf2, Ute Leonards3, Stafford L Lightman3 and Elizabeth C Crowne*1
1Bristol Royal Hospital for Children, Bristol, United Kingdom, 2Bristol Royal Infirmary, Bristol, United Kingdom, 3University of Bristol, Bristol, United Kingdom
Although TBI is recognized as a cause of acquired hypopituitarism, the reported long-term prevalence of endocrine dysfunction varies due to differences in group selection (age at injury, trauma severity) and also by timing and method of hormonal evaluation.

Objective: To determine long-term endocrine and functional outcome after TBI in childhood.

Patients-Methods: 71 participants (48 male); 54 with TBI (24 mild, 30 moderate/severe) and 17 controls matched for age, gender and socioeconomic status. All participants had clinical review, quality of life and psychology assessments. Participants with mod/sev TBI had blood tests including overnight 12 hour GH and cortisol venous profiles (15 min sampling) followed by an insulin tolerance test (ITT).

Quality of life was assessed with the Paediatric Quality of Life Inventory (PedsQL 4.0), health status with the Health Utilities Index (HUI), fatigue with the Chalder Fatigue Scale and depression with the BDI-II (Beck Depression Inventory). The Achenbach System of Empirically Based Assessment (ASEBA) was used to assess adaptive functioning.

Results: None of the TBI participants had clinical problems with seizures, growth, onset of puberty or thyroid status. Median age 19.8 [range 11-26y], time post TBI 9[7-11y]; age at TBI 12[1-17y]. In 8/25 (33%) ITT’s the GH response was abnormal but spontaneous GH secretion was normal in 3 of them. In 7/17 participants with normal ITT results, spontaneous GH secretion was abnormal (reduced mean GH secretion and number of concentration peaks). Peak stimulated GH levels correlated with mean spontaneous GH secretion pulse mass but not with mean or maximum spontaneous GH secretion. Cortisol response was abnormal in one case. Fatigue scores correlated with measures of spontaneous GH secretion (r=-.47, p=0.032) but not with stimulated.

Overall Quality of Life assessment using the PedsQL and HUI3 was not different between groups but analysis of single-attribute utility functions was significantly different for cognition (p=0.005). Depression (p=0.03) and fatigue scores (p=0.01) were also higher in the mod/sev TBI group vs control group. Externalizing behavior (aggressive, rule breaking, intrusive) scores were significantly higher in the mod/sev TBI group (p=0.029).

Conclusions: Evidence of poor HRQL, cognition, behavior difficulties and fatigue are identifiable 8-10 years post TBI. Their aetiology is not explained by GH status in standard provocation tests and requires further investigation.

Nothing to Disclose: ND, PS, WW, UL, SLL, ECC

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm

Sources of Research Support: Merck-Serono UK;  Above & Beyond Charity, Bristol, UK