| Título : |
Pituitary pathology in traumatic brain injury: a review |
| Tipo de documento : |
documento electrónico |
| Autores : |
Luis Vicente Syro Moreno, |
| Fecha de publicación : |
2019 |
| Títulos uniformes : |
Pituitary
|
| Idioma : |
Inglés (eng) |
| Palabras clave : |
Hypothalamic-pituitary autoimmunity (HP-A) pathology pituitary post traumatic hypopituitarism (PTHP) Traumatic brain injury (TBI) |
| Resumen : |
Purpose: Traumatic brain injury most commonly affects young adults under the age of 35 and frequently results in reduced quality of life, disability, and death. In long-term survivors, hypopituitarism is a common complication. Results: Pituitary dysfunction occurs in approximately 20–40% of patients diagnosed with moderate and severe traumatic brain injury giving rise to growth hormone deficiency, hypogonadism, hypothyroidism, hypocortisolism, and central diabetes insipidus. Varying degrees of hypopituitarism have been identified in patients during both the acute and chronic phase. Anterior pituitary hormone deficiency has been shown to cause morbidity and increase mortality in TBI patients, already encumbered by other complications. Hypopituitarism after childhood traumatic brain injury may cause treatable morbidity in those survivors. Prospective studies indicate that the incidence rate of hypopituitarism may be ten-fold higher than assumed; factors altering reports include case definition, geographic location, variable hospital coding, and lost notes. While the precise pathophysiology of post traumatic hypopituitarism has not yet been elucidated, it has been hypothesized that, apart from the primary mechanical event, secondary insults such as hypotension, hypoxia, increased intracranial pressure, as well as changes in cerebral flow and metabolism may contribute to hypothalamic-pituitary damage. A number of mechanisms have been proposed to clarify the causes of primary mechanical events giving rise to ischemic adenohypophysial infarction and the ensuing development of hypopituitarism. Conclusion: Future research should focus more on experimental and clinical studies to elucidate the exact mechanisms behind post-traumatic pituitary damage. The use of preventive medical measures to limit possible damage in the pituitary gland and hypothalamic pituitary axis in order to maintain or re-establish near normal physiologic functions are crucial to minimize the effects of TBI. |
| Mención de responsabilidad : |
Aydin Sav, Fabio Rotondo, Luis V Syro, Carlos A Serna, Kalman Kovacs |
| Referencia : |
Pituitary. 2019 Jun;22(3):201-211 |
| DOI (Digital Object Identifier) : |
10.1007/s11102-019-00958-8 |
| PMID : |
30927184 |
| En línea : |
https://link.springer.com/article/10.1007%2Fs11102-019-00958-8 |
| Enlace permanente : |
https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_display&id=4256 |
Pituitary pathology in traumatic brain injury: a review [documento electrónico] / Luis Vicente Syro Moreno, . - 2019. Obra : PituitaryIdioma : Inglés ( eng) | Palabras clave : |
Hypothalamic-pituitary autoimmunity (HP-A) pathology pituitary post traumatic hypopituitarism (PTHP) Traumatic brain injury (TBI) |
| Resumen : |
Purpose: Traumatic brain injury most commonly affects young adults under the age of 35 and frequently results in reduced quality of life, disability, and death. In long-term survivors, hypopituitarism is a common complication. Results: Pituitary dysfunction occurs in approximately 20–40% of patients diagnosed with moderate and severe traumatic brain injury giving rise to growth hormone deficiency, hypogonadism, hypothyroidism, hypocortisolism, and central diabetes insipidus. Varying degrees of hypopituitarism have been identified in patients during both the acute and chronic phase. Anterior pituitary hormone deficiency has been shown to cause morbidity and increase mortality in TBI patients, already encumbered by other complications. Hypopituitarism after childhood traumatic brain injury may cause treatable morbidity in those survivors. Prospective studies indicate that the incidence rate of hypopituitarism may be ten-fold higher than assumed; factors altering reports include case definition, geographic location, variable hospital coding, and lost notes. While the precise pathophysiology of post traumatic hypopituitarism has not yet been elucidated, it has been hypothesized that, apart from the primary mechanical event, secondary insults such as hypotension, hypoxia, increased intracranial pressure, as well as changes in cerebral flow and metabolism may contribute to hypothalamic-pituitary damage. A number of mechanisms have been proposed to clarify the causes of primary mechanical events giving rise to ischemic adenohypophysial infarction and the ensuing development of hypopituitarism. Conclusion: Future research should focus more on experimental and clinical studies to elucidate the exact mechanisms behind post-traumatic pituitary damage. The use of preventive medical measures to limit possible damage in the pituitary gland and hypothalamic pituitary axis in order to maintain or re-establish near normal physiologic functions are crucial to minimize the effects of TBI. |
| Mención de responsabilidad : |
Aydin Sav, Fabio Rotondo, Luis V Syro, Carlos A Serna, Kalman Kovacs |
| Referencia : |
Pituitary. 2019 Jun;22(3):201-211 |
| DOI (Digital Object Identifier) : |
10.1007/s11102-019-00958-8 |
| PMID : |
30927184 |
| En línea : |
https://link.springer.com/article/10.1007%2Fs11102-019-00958-8 |
| Enlace permanente : |
https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_display&id=4256 |
|  |
Inicio
Pituitary pathology in traumatic brain injury: a review
