Plasma Pituitary Hormone Levels in Severe Trauma with or without Head Injury

Chioléro, René; Lemarchand, T.; Schütz, Y.; Tribolet, N. de; Felber, J. P.; Freeman, Jessie S.; Jéquier, E

doi:10.1097/00005373-198809000-00011

Cited by 73 publications

(45 citation statements)

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“…In this regard, only a few authors have evaluated the relationship between outcome from TBI and the presence of pituitary dysfunction. As mentioned above, either positive or negative relationships between pituitary dysfunction and outcome from TBI have been observed in the early, acute phase post-TBI (41,46,47,61). We did not find any statistical correlation between outcome measures and presence of pituitary dysfunction, both in patients examined over a 5-year period after TBI (5) and in patients evaluated during the early rehabilitation period (48).…”

Section: Consequences and Treatment Of Pthpmentioning

confidence: 48%

Hypopituitarism after traumatic brain injury

Bondanelli

Ambrosio²,

Zatelli³

et al. 2005

eur j endocrinol

185

152

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Traumatic brain injury (TBI) is one of the main causes of death and disability in young adults, with consequences ranging from physical disabilities to long-term cognitive, behavioural, psychological and social defects. Post-traumatic hypopituitarism (PTHP) was recognized more than 80 years ago, but it was thought to be a rare occurrence. Recently, clinical evidence has demonstrated that TBI may frequently cause hypothalamic -pituitary dysfunction, probably contributing to a delayed or hampered recovery from TBI. Changes in pituitary hormone secretion may be observed during the acute phase post-TBI, representing part of the acute adaptive response to the injury. Moreover, diminished pituitary hormone secretion, caused by damage to the pituitary and/or hypothalamus, may occur at any time after TBI. PTHP is observed in about 40% of patients with a history of TBI, presenting as an isolated deficiency in most cases, and more rarely as complete pituitary failure. The most common alterations appear to be gonadotropin and somatotropin deficiency, followed by corticotropin and thyrotropin deficiency. Hyper-or hypoprolactinemia may also be present. Diabetes insipidus may be frequent in the early, acute phase post-TBI, but it is rarely permanent. Severity of TBI seems to be an important risk factor for developing PTHP; however, PTHP can also manifest after mild TBI. Accurate evaluation and long-term follow-up of all TBI patients are necessary in order to detect the occurrence of PTHP, regardless of clinical evidence for pituitary dysfunction. In order to improve outcome and quality of life of TBI patients, an adequate replacement therapy is of paramount importance.European Journal of Endocrinology 152 679-691

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Section: Consequences and Treatment Of Pthpmentioning

confidence: 48%

Hypopituitarism after traumatic brain injury

Bondanelli

Ambrosio²,

Zatelli³

et al. 2005

eur j endocrinol

185

152

View full text Add to dashboard Cite

show abstract

“…As mentioned above, either positive or negative relationships between pituitary dysfunction and outcome from TBI have been observed in the early, acute phase post-TBI. (39,40,41,42) We did not find any statistical correlation between outcome measures and presence of pituitary dysfunction, both in patients examined over a 5-years period after TBI (5) and in patients evaluated during the early rehabilitation period. (43) Autopsy studies demonstrated a high incidence (14-74%) of anatomical lesions in the hypothalamic-pituitary region; this suggests, therefore, that hypopituitarism might contribute to the poor prognosis of the TBI patients.…”

Section: Consequencesmentioning

confidence: 62%

Neuroendocrine Disturbances Following Head Injuries

Raje¹,

Biradar²,

Reddy³

et al. 2015

jemds

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“…Em humanos, os estímulos proporcionados pelo traumatismo resultam em mudanças celulares profundas e a reação geral ao trauma prossegue até níveis sistêmicos (AMARAL et al, 1988), ocasionando, entre outras alterações, respostas metabólicas e cardiovasculares coordenadas pelo hipotálamo (CHIOLERO et al, 1988). Sabe-se que diferentes causas de trauma podem expandir o espaço vascular, o que diminui a pressão venosa, o retorno venoso e o débito cardíaco.…”

Section: Resultsunclassified