Abstract
Traumatic brain injury (TBI)-related hypopituitarism has been recognized as a clinical entity for more than a century, with the first case being reported in 1918. However, during the 20th century hypopituitarism was considered only a rare sequela of TBI. Since 2000 several studies strongly suggest that TBI-mediated pituitary hormones deficiency may be more frequent than previously thought. Growth hormone deficiency (GHD) is the most common abnormality, followed by hypogonadism, hypothyroidism, hypocortisolism, and diabetes insipidus. The pathophysiological mechanisms underlying pituitary damage in TBI patients include a primary injury that may lead to the direct trauma of the hypothalamus or pituitary gland; on the other hand, secondary injuries are mainly related to an interplay of a complex and ongoing cascade of specific molecular/biochemical events. The available data describe the importance of GHD after TBI and its influence in promoting neurocognitive and behavioral deficits. The poor outcomes that are seen with long standing GHD in post TBI patients could be improved by GH treatment, but to date literature data on the possible beneficial effects of GH replacement therapy in post-TBI GHD patients are currently scarce and fragmented. More studies are needed to further characterize this clinical syndrome with the purpose of establishing appropriate standards of care. The purpose of this review is to summarize the current state of knowledge about post-traumatic GH deficiency.
Highlights
Traumatic brain injury (TBI) is one of the leading causes of disability and mortality affecting many people each year and resulting in a serious burden of devastating health consequences [1,2,3]
The pathophysiologic mechanisms underlying pituitary damage in TBI patients include a primary injury that may lead to direct trauma to the hypothalamus or pituitary gland, or to compressive effect from surrounding structures; secondary injuries, on the other hand, are mainly related to an interplay of a complex and ongoing cascade of specific molecular/biochemical events
The purpose of this review is to summarize the current state of knowledge about posttraumatic hypopituitarism, and especially about post-traumatic Growth hormone deficiency (GHD)
Summary
Traumatic brain injury (TBI) is one of the leading causes of disability and mortality affecting many people each year and resulting in a serious burden of devastating health consequences [1,2,3]. Even if ADC reduction with respect to healthy controls was found to be significant in the whole cohort of TBI patients, this alteration resulted to be more prominent in those which subsequently developed pituitary deficits at the hormonal follow-up; this is a further proof of the plausible relation between the severity of microstructural ischemic abnormalities in the short-term and the final functional outcome in the long-term. Pituitary function evaluation could be challenging in the acute phase post-TBI In this stage patients have hormonal changes as part of the stress response and acute adaptive response to injury. Symptomatic hypoglycaemia (
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