Endocrine Abstracts

Introduction: Male hypogonadotropic hypogonadism (HH) is a consequence of congenital or acquired diseases that affect the hypothalamus or the pituitary gland. In HH, secretion of gonadotropin releasing hormone (GnRH) is absent or inadequate. Diagnosis during adulthood (after normal puberty) suggests an acquired etiology. Acquired hypogonadotropic hypogonadism can be caused by drugs, infectious or infiltrative lesions, systemic diseases, radiation and TBI. Post-TBI neuroendocrine disorders have been increasingly acknowledged in recent years, especially related to road accidents, sports or falls. The frequency of hypopituitarism after TBI varies between 15-50% among different studies. Hypopituitarism can be complete (panhypopituitarism) or parcial (isolated deficiency). GH is the most common hormone lost after TBI, followed by ACTH, gonadotropins (FSH and LH), and TSH.

Case study: Man, 38, a member of the Air Force Rescue Squadrons, single, with a 7-year-old son, presents with asthenia, insomnia, decreased libido and difficulty in erection in early 2015. Blood tests revealed a low testosterone level, with gonadotropins in the normal range, suggestive of central hypogonadism. An evaluation of the pituitary axis was performed and cleared and an imaging study with MRI-CE did not report space occupying lesions (SOL). In the etiological evaluation for hypogonadism there is a history of orchidopexy, with a decrease in testis at the age of 8. Also, a work accident in late 2014 with electrocussion without apparent sequels. He is currently being medicated with testosterone IM 3/3 months with strong clinical and analytical improvement.

Discussion: The causes of acquired hypogonadotropic hypogonadism are multiple. In our patient we could not find any obvious etiology. There was no history of trauma, infection, systemic illnesses and he denied drug abuse. The MRI excluded the presence of any SOL. The only apparent insult to our patient’s pituitary was therefore electrical brain injury. Several authors have found similarities between victims of electrical injuries and of head trauma, although the mechanism of lesion is still uncertain. Given the temporal relationship between the work accident and the beginning of the symptoms (about 6 months), it was hypothesized that HH could be a deficit resulting from high-voltage electrical brain injury. We found no similar cases reported in the literature, therefore only time will tell if the condition may be reversible. Hormonal replacement therapy may reduce morbidity, optimize rehabilitation and improve the quality of life of the patients.