Proyecto FOLTRA

Déficits hipofisarios tras TCE

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Déficits hipofisarios tras TCE

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Correo electrónico
Martes 25 de Octubre de 2011 00:00

Publicado el 12 de octubre en J ournal of Neurotrauma.  Los autores, de la Universidad de Lille, analizan una población de 55 pacientes que al menos un año antes habían sufrido traumatismo cráneo-encefálico y cuyas secuelas eran persistentes alteraciones cognitivas y/o de conducta. Entre las muchas variables estudiadas encuentran que el déficit de GH ocurrido tras el trauma era la afectación hormonal con mayor prevalencia (40%) a la vez que se asociaba con alteraciones de la atención y memoria y disminución de la capacidad del desarrollo de actividades de la vida diaria. 

J Neurotrauma. 2011 Oct 12. [Epub ahead of print]

Lasting pituitary hormone deficiency after traumatic brain injury.

Abstract

Pituitary deficiencies have been reported after traumatic brain injury (TBI) and may contribute to lasting cognitive disorders in this context. In a population of TBI patients with persistent cognitive and/or behavioural disorders, we sought to determine the prevalence of lasting pituitary deficiency and relationships with TBI severity, cognitive disorders and impairments in activities of daily living (ADL). Fifty-five patients were included (mean age: 36.1; 46 men) at least one year after TBI. They underwent a comprehensive evaluation of pituitary function (basic tests and stimulation), initial TBI severity and long-term outcomes (Cognitive performance, Glasgow Outcome Scale score, impact on ADL and Quality of Life). We used chi-2 and Mann-Whitney tests to probe for significant (p ≤ 0.05) relationships between pituitary disorders and other parameters. Thirty-eight (69%) patients had at least one pituitary hormonedeficiency. Growth hormone deficiency was more prevalent (severe: 40.0%; partial: 23.6%) than corticotropin (27.3%) or thyrotropin (21.8%) deficiencies. Other deficiencies were rare. Growth hormone deficiency was associated with attention and verbal memory disorders and reduced involvement in ADL. We did not find any relationship between pituitary deficiency and the TBI's initial severity. In a multivariate analysis, the TBI severity was introduced as a first factor, and pituitary deficits in a secondary factor for explaining the late outcome (ADL, QoL). In conclusion, TBI patients with cognitive sequelae must undergo pituitary screening because growth hormone, corticotropin and thyrotropin deficits are particularly frequent and can participate in the dependency in ADL and reduced QoL. 

 

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