Abstract
Background: Traumatic brain injury (TBI) is a leading cause of secondary hypopituitarism in children and adults, and is responsible for impaired quality of life, disabilities and compromised development. Alterations of pituitary function can occur at any time after the traumatic event, presenting in various ways and evolving during time, so they require appropriate screening for early detection and treatment. Although the exact pathophysiology is unknown, several mechanisms have been hypothesized, including hypothalamic-pituitary autoimmunity (HP-A). The aim of this study was to systematically review literature on the association between HP-A and TBI-induced hypopituitarism. Major pitfalls related to the HP-A investigation were also discussed. Methods: The PubMed database was searched with a string developed for this purpose, without temporal or language limits, for original articles assessing the association of HP-A and TBI-induced hypopituitarism. Results: Three articles from the same group met the inclusion criteria. Anti-pituitary and anti-hypothalamic antibodies were detected using indirect immunofluorescence in a significant number of patients with acute and chronic TBI. Elevated antibody titer was associated with an increased risk of persistent hypopituitarism, especially somatotroph and gonadotroph deficiency, while no correlations were found with clinical parameters. Conclusion: HPA seems to contribute to TBI-induced pituitary damage, although major methodological issues need to be overcome and larger studies are warranted to confirm these preliminary data.
Highlights
Traumatic brain injury (TBI) is a major and increasing cause of morbidity and mortality in adult and pediatric population in Western Countries and is associated with a significant financial and social burden [1].According to the National Center for Injury Prevention and Control, in 2010 about 2.5 million emergency department visits, hospitalizations (280,000) or deaths were caused by TBI in United States, with an estimated economic cost of nearly $76.5 billions [2].Based on the Glasgow Coma Scale, the severity of TBI is categorized as mild (≥14), moderate (9–13) or severe (≤8) [3]
With the aim of reviewing literature assessing the association of pituitary autoimmunity and pituitary dysfunction in patients with TBI, we searched the PubMed database using a string developed for that purpose—(traumatic brain injury) AND (autoimmunity OR) AND (hypopituitarism OR)—with no language or time interval limits
(64% mild, 20% moderate and 16% severe based on Glasgow Coma Scale) for basal and stimulated pituitary function, and the presence of antipituitary antibodies (APA) and anti-hypothalamic antibodies (AHA)
Summary
Traumatic brain injury (TBI) is a major and increasing cause of morbidity and mortality in adult and pediatric population in Western Countries and is associated with a significant financial and social burden [1]. Millions; 435,000 in children under 14 years of age; 70% rate increase from 2001 to 2010), hospitalizations (280,000) or deaths (more than 50,000 total; about 2700 in children) were caused by TBI in United States, with an estimated economic cost of nearly $76.5 billions [2]. Severe and moderate traumas are often associated with long-term impairment of quality of life and disabilities in adults, and compromised development in children [1]. Falls are the leading cause of TBI (about 40% of the total, typical of children and older people), followed by blunt trauma (15%), road accidents (14%) and assaults/child abuse. Some recreational activities and sports—especially those involving contact/collision (i.e., boxing, football, soccer, ice hockey and the martial arts) or high speed (i.e., cycling, motor racing, equestrian sports, skiing and skating)—are often associated with mild and repetitive head trauma, secondary to concussion, with a cumulative effect on the development of pituitary dysfunction [4,5]
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