Hypopituitarism Secondary to Head Trauma

Benvenga, Salvatore; Campennì, Alfredo; Ruggeri, Rosaria M.; Trimarchi, Francesco

doi:10.1210/jcem.85.4.6506

Cited by 340 publications

(276 citation statements)

References 23 publications

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“…In the Benvenga series, the occurrence of PTHP was about 60% in the patients aged 11 -29 years, with the third decade most at risk, and progressively declined with advancing age, suggesting young age as a possible risk factor for developing PTHP (79). However, more recent studies have not confirmed this hypothesis.…”

Section: Post-traumatic Hypopituitarism (Pthp)mentioning

confidence: 93%

“…The prevalence of PTHP appears to be similar in males and in females (5, 9, 30), although Benvenga et al (79) reported a greater prevalence of PTHP in males (84% vs 16% in females). In the Benvenga series, the occurrence of PTHP was about 60% in the patients aged 11 -29 years, with the third decade most at risk, and progressively declined with advancing age, suggesting young age as a possible risk factor for developing PTHP (79).…”

Section: Post-traumatic Hypopituitarism (Pthp)mentioning

confidence: 95%

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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: Post-traumatic Hypopituitarism (Pthp)mentioning

confidence: 93%

Section: Post-traumatic Hypopituitarism (Pthp)mentioning

confidence: 95%

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

“…Increased prolactin was the most commonly observed endocrine alteration. Hyperprolactinaemia is a wellknown phenomenon in the acute phase of a brain injury that may persist in 31% of patients during rehabilitation (30), and it was reported in up to 47% of the TBI patients who had other endocrine failures during long-term follow-up (31). Although hyperprolactinaemia may indicate pituitary stalk and/or hypothalamic injury, prolactin is one of the first hormones to increase in acute phases of severe illness, whereas prolactin is no longer as high in chronic phases (24).…”

Section: European Journal Of Endocrinologymentioning

confidence: 99%

Early endocrine alterations reflect prolonged stress and relate to 1-year functional outcome in patients with severe brain injury

Marina

Klose

Nordenbo

et al. 2015

European Journal of Endocrinology

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Objective: Severe brain injury may increase the risk of developing acute and chronic hypopituitarism. Pituitary hormone alterations developed in the early recovery phase after brain injury may have implications for long-term functional recovery. The objective of the present study was to assess the pattern and prevalence of pituitary hormone alterations 3 months after a severe brain injury with relation to functional outcome at a 1-year follow-up. Design: Prospective study at a tertiary university referral centre. Methods: A total of 163 patients admitted to neurorehabilitation after severe traumatic brain injury (TBI, nZ111) or non-TBI (nZ52) were included. The main outcome measures were endocrine alterations 3.3 months (median) after the brain injury and their relationship to the functioning and ability of the patients at a 1-year follow-up, as measured by the Functional Independence Measure and the Glasgow Outcome Scale-Extended. Results: Three months after the injury, elevated stress hormones (i.e. 30 min stimulated cortisol, prolactin and/or IGF1) and/or suppressed gonadal or thyroid hormones were recorded in 68 and 32% of the patients respectively. At 1 year after the injury, lower functioning level (Functional Independence Measure) and lower capability of performing normal life activities (Glasgow Outcome Scale-Extended) were related to both the elevated stress hormones (P%0.01) and the reduced gonadal and/or thyroid hormones (P%0.01) measured at 3 months. Conclusion: The present study suggests that brain injury-related endocrine alterations that mimic secondary hypogonadism and hypothyroidism and that occur with elevated stress hormones most probably reflect a prolonged stress response 2-5 months after severe brain injury, rather than pituitary insufficiency per se. These endocrine alterations thus seem to reflect a more severe disease state and relate to 1-year functional outcome.

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“…Central diabetes insipidus occurs in 1 in 5 to 1 in 3 patients with post‐traumatic hypopituitarism 7. Agha et al .…”

Section: Discussionmentioning

confidence: 99%

Post‐traumatic hypopituitarism: report of a child case

Aoki

Hagiwara

Murata

et al. 2016

Acute Medicine & Surgery

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CaseWe report a case of post‐traumatic hypopituitarism in a 9‐year‐old boy who was injured in a car accident.OutcomePost‐traumatic hypopituitarism might be caused by moderate to severe head trauma, and while this possibility has recently drawn attention in adults, few reports are available regarding children. Our patient experienced head and facial injury, resulting in post‐traumatic hypopituitarism. Six hours after injury he suffered from diabetes insipidus and hormone replacement therapy was started. On day 12 he underwent facial fracture reduction under general anesthesia. On day 24 he was discharged from the hospital. One year after the injury, secretory function and water dehydration tests suggested the possibility of post‐traumatic hypopituitarism.ConclusionWe experienced a child case of post‐traumatic hypopituitarism. Emergency physicians should pay attention to the possibility of post‐traumatic hypopituitarism in cases of traumatic brain injury.

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Hypopituitarism Secondary to Head Trauma

Cited by 340 publications

References 23 publications

Hypopituitarism after traumatic brain injury

Hypopituitarism after traumatic brain injury

Early endocrine alterations reflect prolonged stress and relate to 1-year functional outcome in patients with severe brain injury

Post‐traumatic hypopituitarism: report of a child case

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