Endocrinological Complications of Traumatic Brain Injury: A Comprehensive Narrative Review

INTRODUCTION Traumatic brain injury (TBI) is a major cause of neuroendocrine dysfunction, primarily affecting the hypothalamic-pituitary axis. Hypopituitarism, particularly involving growth hormone, gonadotropins, ACTH, and TSH deficiencies, is frequently observed in TBI survivors. The underlying pathophysiology includes direct mechanical damage, vascular compromise, and neuroinflammatory processes that impair hormone secretion. Despite its significant impact on metabolism, cognition, and overall recovery, endocrine dysfunction remains underdiagnosed due to its nonspecific presentation and overlap with other post-TBI sequelae. OBJETIVE To comprehensively analyze the prevalence, pathophysiology, clinical manifestations, diagnostic challenges, and management strategies of endocrine dysfunction in patients with traumatic brain injury. METHODS This is a narrative review which included studies in the MEDLINE – PubMed (National Library of Medicine, National Institutes of Health), COCHRANE, EMBASE and Google Scholar databases, using as descriptors: “Traumatic Brain Injury” OR “Endocrine Dysfunction” OR “Hypopituitarism” OR “Neuroinflammation” OR “Hormonal Deficiencies” in the last years. RESULTS AND DISCUSSION Neuroimaging studies have revealed structural pituitary abnormalities in some patients, although functional impairments may occur even in the absence of detectable changes. Laboratory testing remains essential for diagnosis, with dynamic hormone stimulation tests playing a crucial role in detecting deficiencies. Growth hormone deficiency is one of the most common post-TBI endocrinopathies, contributing to metabolic disturbances, muscle wasting, and reduced quality of life. Hypogonadism, adrenal insufficiency, and thyroid dysfunction further complicate the clinical course, necessitating early detection and appropriate management. Emerging research suggests that neuroinflammatory mechanisms, genetic predispositions, and autoimmunity may play roles in the pathogenesis of post-TBI endocrine dysfunction. CONCLUSION Long-term follow-up and endocrine screening are essential for optimizing patient outcomes, as some deficiencies manifest years after the initial injury. Hormonal replacement therapy has shown benefits in restoring metabolic balance and improving neurocognitive function. Future research should focus on refining diagnostic protocols, identifying predictive biomarkers, and developing targeted neuroprotective strategies. A multidisciplinary approach, integrating neurology, endocrinology, and rehabilitation medicine, is critical for improving the long-term prognosis of TBI survivors with endocrine dysfunction.