The natural history of post-traumatic hypopituitarism: Implications for assessment and treatment

doi:10.1016/j.amjmed.2005.02.042

The American Journal of Medicine

Volume 118, Issue 12, December 2005, Pages 1416.e1-1416.e7

https://doi.org/10.1016/j.amjmed.2005.02.042 Get rights and content

Abstract

Purpose

Hypopituitarism has been reported in up to half of long-term survivors of traumatic brain injury. We attempted to define the natural history of post-traumatic hypopituitarism to devise guidelines for the optimal timing of patients’ assessment and hormone replacement.

Subjects and methods

Fifty consecutive patients with severe or moderate head trauma were enrolled in a prospective study of pituitary function during the acute phase, at 6 months, and at 12 months after injury. Growth hormone and adrenocorticotropin hormone reserves were assessed using the glucagon stimulation test. Baseline serum concentrations of other anterior pituitary hormones were measured. Results were compared with normative data obtained from matched healthy controls.

Results

Nine patients (18%) had growth hormone deficiency in the acute phase; at 6 months, 5 patients recovered function and 2 new deficiencies were detected; at 12 months, 1 patient recovered, leaving 5 patients (10%) with growth hormone deficiency. Eight patients (16%) showed subnormal cortisol response in the acute phase; at 6 months, 4 patients had recovered and 5 new deficiencies were detected; all 9 patients had persistent abnormalities at 2 months. Forty patients (80%) had gonadotropin deficiency in the acute phase, of whom 29 (73%) recovered by 6 months and 34 (85%) recovered by 12 months. Thyrotropin deficiency was present in 1 patient in the acute phase, who recovered by 6 months; 1 new case was diagnosed at 6 months, which persisted at 12 months.

Conclusion

After traumatic brain injury, early neuroendocrine abnormalities are sometimes transient, whereas late abnormalities present during the course of rehabilitation. A follow-up strategy with periodic evaluation is a necessary part of the optimal care for patients with traumatic brain injury.

Section snippets

Sample

Fifty white patients with head trauma, aged 15 to 65 years, who were admitted to the Beaumont Hospital neurosurgical unit between October 2002 and April 2003, were included in the study. The clinical characteristics of the patients were reported previously⁶ and are summarized in Table 1. All patients had severe or moderate injury, defined by the initial post-resuscitation and pre-sedation Glasgow Coma Scale scores,7, 8 and all had computed tomography evidence of brain injury.⁹ The cause of the

Method

The study was approved by the ethics section of the Beaumont Hospital Medical Research Committee. All patients (or next-of-kin) gave informed consent.

Patients were assessed on 3 occasions: acute phase (median 12 days, range 7-20 days), at 6 months (during intensive rehabilitation), and at 12 months (end of intensive rehabilitation) after injury. Functional recovery at 1 year was assessed using the Glasgow Outcome Scale.¹⁰

Results

All 50 patients completed the acute phase studies. Two patients died after hospital discharge; thus, follow-up data are available for 48 patients.

Discussion

Our data show that anterior pituitary hormone abnormalities, which occur soon after traumatic brain injury, are transient in some patients, and that recovery occurred by 6 months in the majority of patients. Hyperprolactinemia and gonadotropin deficiency are particularly likely to recover completely in the majority of patients. Although recovery of normal growth hormone production in two thirds of patients and cortisol production in one half of patients were demonstrated in the post-acute

References (27)

G. Teasdale et al.
Assessment of coma and impaired consciousnessa practical scale
Lancet.
(1974)
R.H. Rao et al.
Intramuscular glucagon as a provocative stimulus for the assessment of pituitary functiongrowth hormone and cortisol responses
Metabolism.
(1987)
H.R. Fish et al.
Endocrine and neurophysiological responses of the pituitary to insulin-induced hypoglycemiaa review
Metabolism.
(1986)
G. Van den Berghe
Endocrine evaluation of patients with critical illness
Endocrinol Metab Clin N Am.
(2003)
J.M. Mazaux et al.
Rehabilitation after traumatic brain injury in adults
Disabil Rehabil.
(1998)
D.F. Kelly et al.
Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhagea preliminary report
J Neurosurg.
(2000)
S.A. Lieberman et al.
Prevalence of neuroendocrine dysfunction in patients recovering from traumatic brain injury
J Clin Endocrinol Metab.
(2001)
A. Agha et al.
Anterior pituitary dysfunction in survivors of traumatic brain injury
J Clin Endocrinol Metab.
(2004)
G. Aimaretti et al.
Traumatic brain injury and subarachnoid haemorrhage are conditions at high risk for hypopituitarismscreening study at 3 months after the brain injury
Clin Endocrinol (Oxf).
(2004)
A. Agha et al.
Neuroendocrine dysfunction in the acute phase of traumatic brain injury
Clin Endocrinol (Oxf).
(2004)

International classification of impairments, disabilities, and handicaps

(1980)

G. Teasdale et al.

Computed tomographic and magnetic resonance imaging classification of head injury

J Neurotrauma.

(1992)

B. Jennett et al.

Assessment of outcome after severe brain damage

Lancet.

(1975)

Cited by (134)

Anterior pituitary in acute phase of severe traumatic brain injury, a descriptive study
2023, Acta Colombiana de Cuidado Intensivo
El trauma craneoencefálico (TCE) es un problema de salud pública. El TCE es una de las principales causas de discapacidad y muerte en personas menores de 45 años; la disfunción endocrino hipofisiaria postraumática asociada al TCE severo produce múltiples consecuencias, reduce la calidad de vida y se asocia a trastornos neuropsicológicos y a una pobre rehabilitación.
Medir los niveles hormonales séricos en pacientes con TCE severo ingresados en la unidad de cuidado intensivo (UCI) en el periodo 2015-2017 en un hospital de referencia de alta complejidad del suroccidente colombiano.
Estudio de corte transversal que incluyó 64 pacientes; se midieron en suero los niveles de hormonas asociadas con la adenohipófisis dentro de las primeras 72 horas de la admisión.
Todos los pacientes tuvieron por lo menos los valores hormonales de un eje adenohipofisario alterado. La disfunción somatotropa fue la más frecuente, afectando a 42 pacientes (65,6%), seguida por la gonadotropa en el 57,8%. En el eje tirotropo se identificó en el 51,6%, perfil sugestivo de hipotiroidismo central, y finalmente el eje corticotropo estuvo alterado en el 6,3%.
Las alteraciones hormonales de la adenohipófisis en los pacientes con TCE severo que ingresan en la UCI es alto, con predominio del eje somatotropo, lo cual plantea la necesidad de estudios que correlación estos datos con desenlaces de morbimortalidad.
Traumatic brain injury (TBI) is a public health problem. TBI is one of the main causes of disability and mortality in people under 45 years of age. Post-traumatic pituitary endocrine dysfunction associated with severe TBI has multiple consequences, reduces quality of life, and is associated with neuropsychological disorders and poor rehabilitation.
To measure serum hormone levels in patients with severe TBI admitted to intensive care (ICU) in the period 2015-2017 in a high complexity referral hospital.
Cross-sectional study that included 64 patients were included, the levels of hormones associated with the adenohypophysis were measured in serum, within the first 72 hours of admission.
All patients had at least one altered adenohypophysis axis hormonal value. Somatotroph dysfunction was the most frequent, affecting in 42 patients (65.6%), followed by gonadotroph in 57.8%. In the thyrotrope axis, it was identified in 51.6%, a profile suggestive of central hypothyroidism, and finally corticotropic axis was altered in 6.3%.
Hormonal alterations of the adenohypophysis in patients with severe TBI admitted to the ICU is high with a predominance of the somatotropic axis, which calls for studies that coincide with these data with morbidity and mortality outcomes.
Adrenal insufficiency: Physiology, clinical presentation and diagnostic challenges
2020, Clinica Chimica Acta
Adrenal insufficiency (AI) is a serious condition, which can arise from pathology affecting the adrenal gland itself (primary adrenal insufficiency, PAI), hypothalamic or pituitary pathology (secondary adrenal insufficiency, SAI), or as a result of suppression of the hypothalamic–pituitaryadrenal (HPA) axis by exogenous glucocorticoid therapy (tertiary adrenal insufficiency, TAI). AI is associated with an increase in morbidity and mortality and a reduction in quality of life. In addition, the most common cause of PAI, autoimmune adrenalitis, may be associated with a variety of other autoimmune disorders. Untreated AI can present with chronic fatigue, weight loss and vulnerability to infection. The inability to cope with acute illness or infection can precipitate life-threatening adrenal crisis. It is therefore a critical diagnosis to make in a timely fashion, in order to institute appropriate management, aimed at reversing chronic ill health, preventing acute crises, and restoring quality of life.
In this review, we will describe the normal physiology of the HPA axis and explain how knowledge of the physiology of this axis helps us understand the clinical presentation of AI, and forms the basis for the biochemical investigations which lead to the diagnosis of AI.
Pituitary disorders following traumatic brain injury
2018, Encyclopedia of Endocrine Diseases
TBI is a leading cause of morbidity and mortality in the younger population. Although the literature varies depending on the methodology used, it is generally accepted that chronic hypopituitarism post TBI occurs in approximately 20%–30% of patients. This is therefore a significant clinical problem. This article discusses the published data on the prevalence of pituitary dysfunction in TBI patients along with the pathophysiology and natural history of this disorder. We will also examine the potential impact of posttraumatic hypopituitarism on recovery and rehabilitation after injury, as well as the need for the identification and management of this endocrine challenge.
Endocrine Dysfunction After Traumatic Brain Injury: An Ignored Clinical Syndrome?
2023, Neurocritical Care
High Urinary Sodium Concentrations in Severe SIADH: Case Reports of 2 Patients and Literature Review
2022, Frontiers in Medicine
The Role of Thyroid Hormone in Neuronal Protection
2021, Comprehensive Physiology

View all citing articles on Scopus

: This work was supported by an unrestricted education grant obtained in open competition from Pfizer International Research Grants.

View full text

Clinical research studyThe natural history of post-traumatic hypopituitarism: Implications for assessment and treatment

Abstract

Purpose

Subjects and methods

Results

Conclusion

Section snippets

Sample

Method

Results

Discussion

Lancet.

Metabolism.

Metabolism.

Endocrinol Metab Clin N Am.

Rehabilitation after traumatic brain injury in adults

Disabil Rehabil.

Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhagea preliminary report

J Neurosurg.

Prevalence of neuroendocrine dysfunction in patients recovering from traumatic brain injury

J Clin Endocrinol Metab.

Anterior pituitary dysfunction in survivors of traumatic brain injury

J Clin Endocrinol Metab.

Traumatic brain injury and subarachnoid haemorrhage are conditions at high risk for hypopituitarismscreening study at 3 months after the brain injury

Clin Endocrinol (Oxf).

Neuroendocrine dysfunction in the acute phase of traumatic brain injury

Clin Endocrinol (Oxf).

International classification of impairments, disabilities, and handicaps

Computed tomographic and magnetic resonance imaging classification of head injury

J Neurotrauma.

Assessment of outcome after severe brain damage

Lancet.

Clinical research study
The natural history of post-traumatic hypopituitarism: Implications for assessment and treatment