Neuroendocrine dysfunction in patients recovering from subarachnoid hemorrhage

Institute of Neurosurgery, Belgrade, Serbia.
Hormones (Athens, Greece) (Impact Factor: 1.2). 07/2010; 9(3):235-44. DOI: 10.14310/horm.2002.1273
Source: PubMed


Subarachnoid hemorrhage (SAH) is a recently identified risk factor for hypopituitarism, particularly growth hormone (GH) and corticotrophins deficiencies. The aim of our study was to identify possible predictor(s) for neuroendocrine dysfunction in SAH survivors.
Pituitary function was evaluated in 93 patients (30 males, 63 females), aged 48.0+/-1.1 years (mean+/-SE), and with a Glasgow Outcome Scale score of 4.6+/-0.6 (mean+/-SE) more than one year following SAH. In the acute phase, SAH was complicated by vasospasm (VS) in 18 and by hydrocephalus (HDC) in 9 patients. Baseline serum values of insulin growth factor 1 (IGF-I), cortisol, thyroxine (T4), thyroid stimulating hormone (TSH), follicle stimulating hormone (FSH), luteinizing hormone (LH), testosterone (in males), estradiol (in females) and prolactin were determined.
According to the results of baseline hormonal evaluation, 47 patients (50.5%) had no hormonal abnormalities. Seven patients (7.5%) had multiple pituitary hormone deficiencies: Four patients (4.3%) had two (GH and cortisol), one patient had three (gonadal, adrenal and GH) and two patients had deficiency of all pituitary axes. Thirty-nine patients (42%) had one abnormal axis (13 adrenal, 2 thyroid, 4 gonadal and 20 GH). None of the subjects was treated with desmopressin or exhibited symptomatic polyuria. The VS and HDC during the acute phase of SAH were related to abnormal pituitary status (VS with low IGF-I levels and HDC with low cortisol levels).
Through a screening procedure, neuroendocrine dysfunction was identified in a substantial number of asymptomatic patients with previous SAH. Cerebral VS and HDC at the time of SAH emerged as risk factors possibly predicting development of pituitary dysfunction. Low basal levels of IGF 1 and cortisol may help in selecting patients requiring further evaluation of pituitary function.

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    ABSTRACT: Despite further improvement of diagnostic procedures and the management of patients with acute subarachnoid hemorrhage it is still a severe clinical condition often worsened by several secondary complications after the initial bleeding. The most important and most frequent are early rehemorraging, cerebral vasospasm and the development of hydrocephalus. In addition there are many other sequelae, such as disturbances of electrolytes, seizures and the general complications of intensive care medicine which can greatly influence clinical outcome. This report provides an overview of the possible mechanisms for the development of complications, the typical temporary course and the currently available therapeutic strategies, in particular focused on the role of diagnostic imaging in early detection of these pathological conditions.
    No preview · Article · Feb 2011 · Der Radiologe
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    ABSTRACT: Background Neuroendocrine changes have been reported after ischemic stroke, subarachnoid hemorrhage, and brain trauma. As there are no corresponding data in patients with intracerebral hemorrhage (ICH) we analyzed various neuroendocrine parameters to investigate possible alterations in hormone profiles of patients with ICH. Methods Twenty patients with ICH were prospectively enrolled in the study. Patients were a priori parted into two groups: Ten non-ventilated patients treated on the stroke-unit (hemorrhage volumes <20 ml, “small ICH”), and 10 ventilated patients treated on the neurocritical care unit (hematoma volumes >20 ml with possible additional ventricular involvement (“large ICH”). Neuroendocrine parameters were compared between both groups referring to reference values. The following parameters were obtained over a period of 9 days in 20 patients with spontaneous supratentorial ICH: thyrotropin, free thiiodothyronine and thyroxine, human growth hormone, insulin-like growth factor 1, luteinizing hormone, follicle-stimulating hormone, testosterone, prolactin, adrenocorticotropic hormone, and cortisol. Results Small ICH patients were in a median 71 (54–88) years old and had a mean ICH volume of 9.5 ± 6.5 ml, whereas large ICH patients were 65 (47–80) years old and showed a mean volume of 56 ± 30.2 ml. None of the patients revealed pathological alterations for thyrotropin, free thiiodothyronine, thyroxine, human growth hormone, insulin-like growth factor 1, and testosterone. There was only a mild decrease of adrenocorticotropic hormone and cortisol on day 3 in large ICH patients. Small ICH patients showed pathologically elevated levels of luteinizing and follicle-stimulating hormone throughout the observation period. Large ICH patients showed a marked increase of prolactin that developed during the course. Conclusions Overall, neuroendocrine changes in ICH patients are not as profound as reported for ischemic stroke or subarachnoid hemorrhage. The clinical significance of increased LH and FSH levels in small ICH is unclear, whereas elevation of prolactin in large ICH was anticipated. Future randomized controlled trials should also focus on neuroendocrine parameters to clarify the impact of possible hormonal alterations on functional outcome.
    Full-text · Article · Aug 2011 · Neurocritical Care
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    ABSTRACT: Traumatic brain injury and subarachnoid haemorrhage are important causes of morbidity and mortality in the developed world. There is a large body of evidence that demonstrates that both conditions may adversely affect pituitary function in both the acute and chronic phases of recovery. Diagnosis of hypopituitarism and accurate treatment of pituitary disorders offers the opportunity to improve mortality and outcome in both traumatic brain injury and subarachnoid haemorrhage. In this article, we will review the history and pathophysiology of pituitary function in the acute phase following traumatic brain injury and subarachnoid haemorrhage, and we will discuss in detail three key aspects of pituitary dysfunction which occur in the early course of TBI; acute cortisol deficiency, diabetes insipidus and SIAD.
    No preview · Article · Oct 2011 · Best Practice & Research: Clinical Endocrinology & Metabolism
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