Relationships among Plasma Cortisol, Adrenocorticotrophin, and Severity of Injury in Recently Injured Patients

Rn, Barton; Hb, Stoner; Sm, Watson

doi:10.1097/00005373-198704000-00007

Cited by 141 publications

(83 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In some cases, abnormalities in cortisol secretory dynamics (fasting hypercortisolemia, abolition of the normal diurnal rhythm and inadequate suppression after dexamethasone) may persist for many months after TBI (53). A positive correlation between cortisol concentrations and injury severity has been demonstrated in patients with mild or moderate TBI, but not in those with severe injury (51). On the contrary, adrenal insufficiency has been found in 16% of patients during the early phase post-TBI, suggesting post-traumatic damage at the hypothalamic -pituitary level (49).…”

Section: Consequences Of Tbimentioning

confidence: 96%

Hypopituitarism after traumatic brain injury

Bondanelli

Ambrosio²,

Zatelli³

et al. 2005

eur j endocrinol

185

152

View full text Add to dashboard Cite

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

show abstract

Section: Consequences Of Tbimentioning

confidence: 96%

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

“…1B). 30,[32][33][34] The values are highest in patients with the highest illness-severity scores 3,5,7,30,[32][33][34][35] and in those with the highest mortality, 5 and the values are very high (30 to 260 m g per deciliter [828 to 7173 nmol per liter]) shortly before death. 36 Adrenal function in severely ill patients is often evaluated by a corticotropin-stimulation test, in which serum cortisol is measured at base line and 30 to 60 minutes after the intravenous administration of 250 m g of cosyntropin.…”

Section: The Normal Response Of the Hypothalamic-pituitary-adrenal Axmentioning

confidence: 99%

Corticosteroid Therapy in Severe Illness

1997

View full text Add to dashboard Cite

“…Ağır TBH'lı hastalar hariç hafi f ya da orta TBH'lı hastalarda kortizol seviyeleri ile hasarın ciddiyeti arasında pozitif iliş-ki gösterilmiştir 26 . Tam tersine hastaların %16'sında hipotalamik-hipofi zer düzeyde post-travmatik hasarı akla getirecek şekilde TBH'nın erken döneminde adrenal yetersizlik bulunmuştur 27 .…”

Section: șEkil 3 Hastaların Gkssi Ile Yatıș Süreleri Arasındaki Ilișkiunclassified

“…TBH'nın erken döneminde ya da rehabilitasyon sı-rasında vakaların %25-67'sinde hipogonadizm göste-rilmiştir [26][27][28] . Orta ve ağır TBH'nın erken döneminde 50 hasta üzerinde yapılan bir çalışmada hiperprolaktinemili 18 hasta ile birlikte vakaların %80'inde santral hipogonadizm tespit edilmiştir 17 .…”

Section: șEkil 3 Hastaların Gkssi Ile Yatıș Süreleri Arasındaki Ilișkiunclassified

Evaluation of pituitary functions during acute phase of head trauma

Dogan¹,

Seyithanoğlu²,

Özkan³

et al. 2012

Kafkas J Med Sci

View full text Add to dashboard Cite

AIM: To evaluate the functional outcome of the pituitary gland after the traumatic brain injury and to present the pituitary functional changes during the acute phase of the trauma in order to identify the possible factors. METHODS: The study included records of 30 patients (22 male and GirișKafa travması, saçlı deri yaralanmasından, yaygın beyin hasarına kadar geniş bir spektrumda yer alan birçok patolojiyi içine alan klinik bir durumdur. Kafa travmalarının insidansı ve buna bağlı mortalite ve morbidite riski giderek artmaktadır 1,2 . Travma sonucunda merkezi sinir sisteminde primer doku hasarı meydana gelmektedir. Ancak, kafa travması sonucu oluşan hasardan sadece primer hasar sorumlu değil-dir. Primer doku hasarını takiben ortaya çıkan birçok karmaşık fi zyopatolojik olaya bağlı olarak sekonder hasar da oluşmaktadır [3][4][5] . Beyin hasarında rol oynayan

show abstract

Relationships among Plasma Cortisol, Adrenocorticotrophin, and Severity of Injury in Recently Injured Patients

Cited by 141 publications

References 0 publications

Hypopituitarism after traumatic brain injury

Hypopituitarism after traumatic brain injury

Corticosteroid Therapy in Severe Illness

Evaluation of pituitary functions during acute phase of head trauma

Contact Info

Product

Resources

About