ESPE Abstracts

Background: While reports of hypopituitarism resulting from traumatic brain injury are increasingly common in European countries, long-term clinical courses are scarcely documented. We here present Japanese 31-year-old case with hypopituitarism caused by traumatic brain injury at the age of 5 months.

Objective and hypotheses: To clarify the evolution of clinical and endocrinological data for 30 years in this patient. We hypothesize that the evolution progressed gradually.

Method: Retrospective analysis of the chart.

Results: He was born uneventfully by spontaneous cephalic delivery. He had no hypoglycemia or polyuria. Micropenis was not observed. Height velocity began to decrease around the age of 3 years, which was the initial symptom. Height was 107 cm (−3.4 S.D.), and he did not have micropenis at the age of 7 years. Endocrinological tests at this time were as follows: TSH 1.38 μU/ml, T₄ 3.91 μg/dl, LH <0.1 mIU/ml, FSH <0.1 mIU/ml, GH response to arginine 1.8 ng/ml, and cortisol peak to insulin 12.53 μg/dl. We diagnosed him as having GH, TSH, ACTH, and GN deficiencies. The pituitary stalk could not be identified on MRI, and ectopic posterior pituitary bright spot was noted. ACTH deficiency deteriorated with age. Cortisol peak to insulin was 3.0 μg/dl at the age of 10 years, when hydrocortisone therapy was started. Testosterone enanthate therapy was needed to induce pubertal development at the age of 14 years, when hypogonadotropic hypogonadism was confirmed (LH, FSH, testosterone; all below the detection limit). After starting GH injection, growth rate improved with his final height being 0.4 S.D. at the age of 31 years. The mutations for congenital hypopituitarism were not detected, such as POU1F1, LHX4, KAL1.

Conclusion: After the head trauma, GH, ACTH, and GN gradually worsened in this patient.