Hypothalamic derangement in traumatized patients: growth hormone (GH) and prolactin response to thyrotrophin‐releasing hormone and GH‐releasing hormone

Marinis, De; Mancini,; Valle,; Bianchi, Antonio; Gentilella,; Liberale,; Mignani,; Pennisi, Maddalena; Corte, Francesco Della

doi:10.1046/j.1365-2265.1999.00721.x

Cited by 32 publications

(22 citation statements)

References 42 publications

(51 reference statements)

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“…Its anabolic role has been demonstrated in animal studies, increasing the production of neurones (Asberg et al, 2000) and enhancing cognitive functions of rats (Saatman et al, 1997). A recent prospective study of comatosed, head injured patients demonstrated an IGF-1 response (De Marinis et al, 1999) and improved cognitive functioning has been reported in response to treatment of growth hormone deficient adults (Deijen et al, 1998). Not surprisingly, raised levels of cytokines occur in common causes of delirium such as cancer, infection, heart failure and infection (Neibauer et al, 1999).…”

Section: Discussionmentioning

confidence: 96%

Plasma insulin growth factor—1 and incident delirium in older people

Wilson

Broadhurst

Diver

et al. 2005

Int J Geriat Psychiatry

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Section: Discussionmentioning

confidence: 96%

Plasma insulin growth factor—1 and incident delirium in older people

Wilson

Broadhurst

Diver

et al. 2005

Int J Geriat Psychiatry

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“…Kelly and colleagues emphasized that patients with subarachnoid haemorrhage (SAH) may also be at high risk for ensuing hypopituitarism [5]. This clinical picture was more recently confirmed by additional studies in both TBI and SAH [12][13][14][15][16][17][18][19][20]. The percentage of patients with hypopituitarism after TBI or SAH varied between 20% and 80%.…”

Section: Introductionmentioning

confidence: 93%

“…In the same years, Kelly and Lieberman found a high prevalence of anterior pituitary dysfunction in patients with a previous history of moderate and severe TBI [5,6]. The frequencies of GHD (15%) and low cortisol levels (46%) were striking and may have had important implications for the patients' health, sense of well-being, and rehabilitation potential [13]. Kelly and colleagues emphasized that patients with subarachnoid haemorrhage (SAH) may also be at high risk for ensuing hypopituitarism [5].…”

Section: Introductionmentioning

confidence: 94%

Variations of Pituitary Function Over Time after Brain Injuries: The Lesson from a Prospective Study

Giordano¹,

Aimaretti

Ghigo

2005

Pituitary

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Traumatic Brain Injury (TBI) and Subarachnoid Haemorrhage (SAH) are conditions at high risk to develop hypopituitarism as pointed out by many papers in scientific literature. But most of the papers were referred to retrospective evaluations, not considering the possible evolution of the pituitary function over time. Aim of our studies was to clarify whether pituitary deficiencies and normal pituitary function recorded at short term follow-up (3 months), would improve or worsen, respectively, at long term (12 months after the brain injury). In a multicenter study protocol, in patients who suffered TBI (n = 70; 50 Males, 20 Females; age 39.31 +/- 2.4 years; BMI 23.8 +/- 0.4 kg/m(2)) or SAH (n = 32; 12M, 20F; age: 51.9 +/- 2.2 year; BMI: 24.7 +/- 0.6 kg/m(2)) we tested 3 and 12 months after the pathological events the pituitary function. In TBI patients, the 3 month evaluation had shown some degree of hypopituitarism in 32.8% and the 12 months retesting demonstrated some degree of hypopituitarism in 22.7%. Total hypopituitarism was always confirmed at 12 months while Multiple and Isolated deficits recorded at 3 months was confirmed in nearly 25% only of the patients. On the other hand, in 5.5% of TBI with normal pituitary function at 3 months Isolated deficits were recorded at 12 months testing. Moreover, in 13.3% of TBI with Isolated deficit at 3 months Multiple hypopituitarism was demonstrated at 12 months retesting. In SAH patients, the 3 months evaluation had shown some degree of hypopituitarism in 46.8% and the 12 month retesting demonstrated some degree of hypopituitarism in 37.5%. No multiple hypopituitarism recorded at 3 months was confirmed at 12 months, but 2 patients with isolated deficits at 3 months showed multiple hypopituitarism at 12 month retesting. At 12 as well as at 3 months, both in TBI and SAH patients, the most common deficit was severe GHD (>20%) followed by secondary hypogonadism and then hypoadrenalism and hypothyroidism. In all, in patients who experienced TBI or SAH the risk to develop hypopituitarism is very high; early diagnosis of total hypopituitarism is always confirmed at the long term follow-up; however pituitary function in brain injured patients may improve over time, because, isolated and even multiple pituitary insufficiencies recorded at short term can be transient; on the other hand normal pituitary function recorder at short term may, become impaired 12 months after the injury. Thus, brain injured patients must undergo neuroendocrine follow-up over time in order to monitoring pituitary function and eventually providing appropriate placement.

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“…Lieberman et al (7) Aimaretti et al (6) Bondanelli et al (5) 2.1% (1) 48.6% (17) 26.9% (7) 41.4% (12) 28.8% (42) Severe GHD 50% (4) 14.6% (7) 60% (21) 15.4% (4) 27.6% (8) 30.1% (44) ACTH deficiency 12.5% (1) 10.4% (5) 22.8% (8) 0 44.8% (13) 18.5% (27) TSH deficiency 12.5% (1) 31% (15) 14.3% (5) 19.2% (5) 3.4% (1) 18.5% (27) Isolated deficiency 62.5% (5) 75% (36) 71.4% (25) 76.9% (20) 79.3% (23) 74.7% (109) Multiple deficiencies 37.5% (3) 25% (12) 17.1% (6) 23.1% (6) 17.2% (5) 21.9% ( of patients had panhypopituitarism. Diabetes insipidus was present in 2.7% of patients with PTHP (Table 6).…”

Section: Kelly Et Al (30)mentioning

confidence: 99%

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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Hypothalamic derangement in traumatized patients: growth hormone (GH) and prolactin response to thyrotrophin‐releasing hormone and GH‐releasing hormone

Cited by 32 publications

References 42 publications

Plasma insulin growth factor—1 and incident delirium in older people

Plasma insulin growth factor—1 and incident delirium in older people

Variations of Pituitary Function Over Time after Brain Injuries: The Lesson from a Prospective Study

Hypopituitarism after traumatic brain injury

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