14.09.2005

Hirnverletzung - Hormonelle Störungen


Neuere Untersuchungen zeigen, dass rund ein Drittel bis die Hälfte aller Hirnverletzten Störungen des Hormonsystems (v.a. aber nicht nur des Hypothalamus und der Hirnanhangdrüse) aufweisen. Derartige Störungen haben schwere Auswirkungen auf das Allgemeinbefinden, die Konzentrations- und Gedächtnisleistungen sowie die psychische Befindlichkeit etc. Bleiben sie unbehandelt, so beeinträchtigen sie die Gesundheit von Menschen mit einer Hirnverletzung in hohem Masse.


Störungen manchmal erst nach Jahren



Popovic et al. von der Universitätsklinik Belgrad haben in ihrer im Juni 2005 veröffentlichten Studie festgestellt, dass 35 - 40% der untersuchten Hirnverletzten unter hormonellen Störungen leiden. Die Störungen treten meist bald nach dem Unfall bzw. der Hirnblutung auf, können aber auch erst nach Jahren entstehen. Da sich nicht voraussagen lässt, welche Hirnverletzten unter hormonellen Störungen leiden werden (Samadani et al.), verlangen Aimaretti et al. dass bei Hirnverletzten nicht nur zu Beginn neuro-endokrinologische Untersuchungen durchgeführt, sondern auch Folgeuntersuchungen vorgenommen werden. Wie Urban et al. festgestellt haben, verursachen hormonelle Störungen nicht nur zahlreiche psychische und körperliche Beschwerden, sondern erhöhen auch das Risiko insbesondere von Herz-Kreislauferkrankungen und verkürzen generell die Lebensdauer.


Oft nicht erkannt



Da man bis vor kurzem glaubte, hormonelle Störungen nach Hirnverletzungen träten nur ganz selten auf, bleiben derartige Störungen auch heute noch oft unerkannt. In Zukunft wird eine endokrinologische Untersuchung bei PatientInnen mit Hirnverletzung deshalb sicher zum Standard gehören müssen.


Abstracts (Zusammenfassungen)



Im Anhang finden Sie Abstracts (Zusammenfassungen) der jüngsten Studien. Falls Sie die ganzen Studien bestellen möchten, können Sie dies beispielsweise über www.medline.ch tun.


:: 15.08.2006 / Jean Baptiste Huber, Rechtsanwalt, Zug




Growth Horm IGF Res. 2005 Jun;15(3):177-84. Epub 2005 Mar 21.


Hypopituitarism following traumatic brain injury.


Popovic V, Aimaretti G, Casanueva FF, Ghigo E.


Neuroendocrine Unit, Institute of Endocrinology, University Clinical Center, Dr
Subotic 13, 11000 Belgrade, Serbia.



Recent studies have demonstrated that hypopituitarism, and in particular growth
hormone (GH) deficiency, is common among survivors of traumatic brain injury
(TBI) tested several months or years following head trauma. In addition, it has
been shown that post-traumatic neuroendocrine abnormalities occur early and with
high frequency. These findings may have significant implications for the
recovery and rehabilitation of patients with TBI. Although data emerging after
2000 demonstrate the relevance of the problem, in general there is a lack of
awareness in the medical community about the incidence and clinical
repercussions of the pathology. Most, but not all, head trauma associated with
hypopituitarism is the result of motor accidents. The subjects at risk are those
who have suffered moderate-to severe head trauma although mild intensity trauma
may precede hypopituitarism also. Particular attention should be paid to this
problem in children and adolescents. Onset of pituitary deficits can evolve over
years following injury. For the assessment of the GH-IGF axis in TBI patients,
plasma IGF-I concentrations, plus dynamic GH testing is indicated. Some degree
of hypopituitarism is found in 35-40% of TBI patients. Among multiple pituitary
deficits, the most common ones were GHD and gonadotrophin deficiency. In most
series 10-15% presented with severe GHD and 15% with partial GHD after
stimulating GH secretion confirming that the most common isolated deficit is
GHD. Psychometric evaluation together with neurocognitive testing shows
variability of disability and the possibility that untreated TBI induced
hypopituitarism contributes to the chronic neurobehavioral problems seen in many
head-injured patients warrants consideration. Preliminary data, from small
pilot, open-label studies show that subjects treated with GH experience
significant improvements in concentration, memory, depression, anxiety and
fatigue. In conclusion, pituitary failure can occur even in minor head injuries
and is poorly recognized.

-------------------------------


Eur J Endocrinol. 2005 May;152(5):679-91.


Hypopituitarism after traumatic brain injury.


Bondanelli M, Ambrosio MR, Zatelli MC, De Marinis L, degli Uberti EC.


Section of Endocrinology, Department of Biomedical Sciences and Advanced
Therapies, University of Ferrara, Via Savonarola 9, 44100 Ferrara, Italy.



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.

-------------------------------


Brain Inj. 2005 May;19(5):349-58.


Anterior hypopituitarism following traumatic brain injury.


Urban RJ, Harris P, Masel B.


Department of Internal Medicine, Division of Endocrinology, University of Texas
Medical Branch, Galveston, TX, USA.



PRIMARY OBJECTIVES: To review evidence that there exists a substantial
sub-population of patients with endocrine disorders as a result of traumatic
brain injury (TBI) and to underscore the importance of screening patients with
TBI considered most at risk for hypopituitarism with the goal of attaining
beneficial effects in terms of morbidity and quality of life. DESIGN AND
METHODS: Reviewed recent literature regarding the frequency of TBI-induced
hypopituitarism. MAIN OUTCOMES AND RESULTS: Studies by Kelly DF, Gaw Gonzalo IT,
Cohan P, et al. Hypopituitarism following traumatic brain injury and aneurysmal
subarachnoid hemorrhage: A preliminary report. Journal of Neurosurgery
2000;93:743-751, Lieberman SA, Oberoi AL, Gilkison CR, et al. Prevalence of
neuroendocrine dysfunction in patients recovering from traumatic brain injury.
Journal of Clinical Endocrinology and Metabolism 2001;86:2752-2756 and Aimaretti
G, Ambrosio MR, Di Somma C, et al. Traumatic brain injury and subarachnoid
haemorrhage are conditions at high risk for hypopituitarism. Screening study at
3 months after the brain injury, In press., found that about one-half to
one-third of patients with TBI had anterior pituitary hormone deficiencies,
including growth hormone (GH) deficiency in 15-21%, and subtle deficiencies in
thyroid, adrenal and gonadal axes. One or more hormonal deficiencies produce
diverse physical and psychological symptoms that may mimic symptoms attributed
to brain trauma and may impair rehabilitation. A more general concern is the
fact that hypopituitarism increases the risk of significant morbidity (e.g.
ischaemic heart disease) and mortality (shortened life span). CONCLUSIONS: To
attain maximal improvement in mental and physical functioning as well as in
quality of life for victims of TBI, it is crucial that anterior pituitary
hormonal function be assessed. Appropriate hormone replacement therapy for those
patients with both TBI and TBI-induced pituitary function impairment could, for
the first time, allow treatment and correction of underlying causes of TBI
sequelae rather than merely symptomatic treatment.

-------------------------------


Acta Neurochir Suppl. 2005;93:121-5.


Endocrine dysfunction following traumatic brain injury: mechanisms,
pathophysiology and clinical correlations.


Samadani U, Reyes-Moreno I, Buchfelder M.


Department of Neurosurgery, University of Gottingen, Gottingen, Germany.



Despite growing recognition among those who provide care for traumatic brain
injury patients, endocrine dysfunction following brain injury is an often
under-recognized phenomenon. From historical reports one would conclude that
endocrine dysfunctions hardly ever occurs following trauma to the head. However,
recent studies suggest that a significant proportion of patients suffer some
degree of hypopituitarism. To date, there are no clear predicting factors
identifying patients at risk for developing hormonal disturbances and thus no
parameters exist for screening. Several retrospective analyses and literature
reviews, and more recently, a few longitudinal studies of brain injured patients
have been performed.

-------------------------------


J Clin Endocrinol Metab. 2005 Sep 6; [Epub ahead of print]


Residual pituitary function after brain injury-induced hypopituitarism: a
prospective 12-month study.


Aimaretti G, Ambrosio MR, Di Somma C, Gasperi M, Cannavo S, Scaroni C, Fusco A,
Del Monte P, De Menis E, Faustini-Fustini M, Grimaldi F, Logoluso F, Razzore P,
Rovere S, Benvenga S, Uberti EC, De Marinis L, Lombardi G, Mantero F, Martino E,
Giordano G, Ghigo E.


Division of Endocrinology and Metabolism, Department of Internal Medicine,
University of Turin, Turin; Department of Biomedical Sciences and Advanced
Therapies, Section of Endocrinology, University of Ferrara, Ferrara; Departments
of Molecular and Clinical Endocrinology and Oncology, University of Naples
Federico II degrees , Naples; Department of Endocrinology and Metabolism,
University of Pisa, Pisa; Department of Medicine and Pharmacology - Section of
Endocrinology, University of Messina, Messina; Division of Endocrinology,
Department of Surgical and Medical Sciences, University of Padua, Padua;
Division of Endocrinology, Catholic University, Rome; Division of Endocrinology,
Galliera Hospital, Genova; Service of Endocrinology, Treviso Hospital, Treviso;
Division of Endocrinology, Bellaria Hospital, Bologna; Division of
Endocrinology, S. Maria della Misericordia Hospital, Udine; Division of
Endocrinology, University of Bari; Division of Endocrinology, S, Croce e Carle
Hospital, Cuneo; Italian Society of Endocrinology, Chairman of the Study group
on Physiopathology of GH secretion.



Context. Traumatic Brain Injury (TBI) and Subarachnoid Hemorrhage (SAH) are
conditions at high risk to develop hypopituitarism. Objectives. To clarify
whether pituitary deficiencies and normal pituitary function recorded at 3
months would improve or worsen at 12 months after the brain injury. Design and
Patients. Pituitary function was tested at 3 and 12 months in patients who had
TBI, (n = 70) or SAH (n = 32). Results. In TBI, the 3 months evaluation had
shown hypopituitarism (H) in 32.8%. Pan (PH), multiple (MH) and isolated (IH) H
had been demonstrated in 5.7, 5.7 and 21.4%, respectively. The retesting
demonstrated some degree of H in 22.7%. PH, MH and IH were present in 5.7, 4.2
and 12.8%, respectively. PH was always confirmed at 12 months while MH and IH
was confirmed in 25% only. In 5.5% of TBI with no deficit at 3 months IH was
recorded at retesting. In 13.3% of TBI with IH at 3 months MH was demonstrated
at 12 months retesting. In SAH, the 3 months evaluation had shown H in 46.8%. MH
and IH had been demonstrated in 6.2 and 40.6%, respectively. The retesting
demonstrated H in 37.5%. MH and IH were present in 6.2 and 31.3%, respectively.
While no MH was confirmed at 12 months, 2 patients with IH at 3 months showed MH
at retesting; 30.7% of SAH with IH at 3 months displayed normal pituitary
function at retesting. In SAH, normal pituitary function was always confirmed.
In TBI and SAH, the most common deficit was always severe GHD. Conclusion. There
is high risk for H in TBI and SAH patients. Early diagnosis of PH is always
confirmed on the long term. Pituitary function in brain injured patients may
improve over time but, although rarely, may also worsen. Thus, brain injured
patients must undergo neuro-endocrine follow-up over time.


-------------------------------


Neuro Endocrinol Lett. 2005 Aug 30;26(4) [Epub ahead of print]


Delay in diagnosis of hypopituitarism after traumatic head injury: A case report
and review of the literature.


Dogru O, Koken R, Bukulmez A, Melek H, Ovali F, Albayrak R.


Department of Pediatrics, Afyon Kocatepe University Faculty of Medicine, Afyon,
Turkey. drdogru@hotmail.com.



The pituitary gland is only 0.5 ml in volume but plays a major role in the
endocrine system linking the endocrine system and the central nervous system
(CNS). The gland has 2 parts, anterior pituitary (adenohypophysis) and posterior
pituitary (neurohypophysis). Hormones secreted by the anterior pituitary are
thyrotropin, or thyroid-stimulating hormone (TSH), gonadotropins, or
follicle-stimulating hormone (FSH) and luteinizing hormone (LH), growth hormone
(GH), corticotrophin, or adrenocorticotropin hormone (ACTH), and prolactin
hormone (PRL). Hypopituitarism is defined as partial or complete insufficiency
of anterior pituitary secretion [1]. Although trauma is one of leading causes of
hypopituitarism, the diagnosis and treatment of hypopituitarism is generally not
considered as a high priority after traumatic brain injuries [2]. The diseases
caused by hormonal abnormalities related to the posterior pituitary gland such
as syndrome of inappropriate secretion of antidiuretic hormone and diabetes
insipidus are more commonly concerned but chronic neuroendocrine deficits among
patients with traumatic brain injury (TBI) are not considered important [2].
Underdiagnosis or delayed diagnosis of neuroendocrine problems in patients with
TBI diminishes the quality of life and may cause serious health problems [1,2].


-------------------------------


J Endocrinol Invest. 2005;28(5 Suppl):61-4.


Hypopituitarism following traumatic brain injury (TBI): call for attention.


Popovic V, Aimaretti G, Casanueva FF, Ghigo E.


Neuroendocrine Unit, Institute of Endocrinology, University Clinical Center,
Belgrade, Serbia. popver@Eunet.Yu



Recent studies have demonstrated that hypopituitarism, in particular GH
deficiency, is common among survivors of traumatic brain injury (TBI) years
tested several months or following head trauma. In addition, it has been shown
that post-traumatic neuroendocrine abnormalities occur early and with high
frequency. These findings may have significant implications for the recovery and
rehabilitation of patients with TBI. Although data emerging after year 2000
demonstrate the relevance of the problem, in general there is a lack of
awareness in the medical community about the incidence and clinical
repercussions of the pathology. Most, but not all, head trauma associated with
hypopituitarism is the result of motor vechicle accidents. The subjects at risk
are those who have suffered moderate-to-severe head trauma, although mild
intensity trauma may also precede hypopituitarism. Particular attention should
be paid to this problem in children and adolescents; onset of pituitary deficits
can evolve over years following injury. Plasma IGF-I concentrations, plus
dynamic GH testing, are indicated for the assessment of the GH-IGF axis in TBI
patients. Some degree of hypopituitarism is found in 35-40% of TBI patients.
Among mulitple pituitary deficits, the most common ones were GH deficiency (GHD)
and gonadotrophin deficiency. In most series, 12-15% presented with severe GHD
and 14% with partial GHD after stimulating GH secretion, confirming that the
most common isolated deficit is GHD. Psychometric evaluation and neurocognitive
testing show variability of disability, and these measures are needed and
important to support hormonal replacement. Preliminary data, from small pilot,
open-label studies show that subjects treated with GH experience significant
improvements in concentration, memory, depression, anxiety and fatigue. In
conclusion, pituitary failure can occur even in minor head injuries and is
poorly recognized.

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