Traumatic Brain Injury as Frequent Cause of Hypopituitarism and Growth Hormone Deficiency: Epidemiology, Diagnosis, and Treatment

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.

Development and internal validation of a predictive score for the diagnosis of central adrenal insufficiency when morning cortisol is in the grey zone

“…The association between the number of other pituitary deficiencies and the probability of CAI is not surprising; in fact, the global function of the hypothalamus and pituitary gland is deeply interconnected, and the coexistence of different pituitary deficits is a feature frequently encountered in hypopituitarism [34][35][36][37][38]. Moreover, our finding that CAI was significantly associated with the presence of ≥ 3 other pituitary deficiencies, and not with a lower compromise of the pituitary function, is coherent with the notion that the ACTH secretion is one of the most resistant among pituitary ones [34][35][36][37][38]. The role of sex as a risk factor for CAI is in line with previous findings by other authors [39][40][41][42]; male sex, in fact, has been found to be associated with a higher chance of hypopituitarism in various clinical settings, even after adjustment for other concurrent predictors [39][40][41][42].…”

Long Non-coding RNAs and Circular RNAs: Insights Into Microglia and Astrocyte Mediated Neurological Diseases

“…The primary injury of TBI occurs directly in response to mechanical forces, like contusion, hemorrhage, hypoxia, etc. The primary injury can trigger the secondary injury that relates to several biochemical alterations, such as inflammation, nerve cell damage, and cerebral edema, contributing to exacerbating TBI progression (Alam et al, 2020;Gasco et al, 2021). Tumor necrosis factor receptor-related factor 6 (TRAF6) is a target of miR-873-5p.…”

COVID-19 and hypopituitarism

“…Hypopituitarism results from the failure of one or more pituitary hormones to be produced or released into the circulation by the pituitary gland, leading to specific systemic effects. Anterior pituitary failure is caused by several etiologic factors, including traumatic brain injury, sellar tumors, genetic mutations, infiltrative and infectious diseases [ 6 ].…”