***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    ***EXAMPLES*** 
    Input: Background Over the last few years , awareness and detection rates of hypopituitarism following traumatic brain injury ( TBI ) and subarachnoid hemorrhage ( SAH ) has steadily increased . Moreover , recent studies have found that a clinical ly relevant number of patients develop pituitary insufficiency after intracranial operations and radiation treatment for non-pituitary tumors . But , in a substantial portion of more than 40 % , the hypopituitarism already exists before surgery . We sought to determine the frequency , pattern , and severity of endocrine disturbances using basal and advanced dynamic pituitary testing following non-pituitary intracranial procedures . Methods 51 patients ( 29 women , 22 men ) with a mean age of 55 years ( range of 20 to 75 years ) underwent prospect i ve evaluation of basal parameters and pituitary function testing ( combined growth hormone releasing hormone (GHRH)/arginine test , insulin tolerance test ( ITT ) , low dose adrenocorticotropic hormone ( ACTH ) test ) , performed 5 to 168 months ( median 47.2 months ) after intracranial operation ( 4 patients had additional radiation and 2 patients received additional radiation combined with chemotherapy ) . Results We discovered an overall rate of hypopituitarism with distinct magnitude in 64.7 % ( solitary in 45.1 % , multiple in 19.6 % , complete in 0 % ) . Adrenocorticotropic hormone insufficiency was found in 51.0 % ( partial in 41.2 % , complete in 9.8 % ) and growth hormone deficiency ( GHD ) occurred in 31.4 % ( partial in 25.5 % , severe in 5.9 % ) . Thyrotropic hormone deficiency was not identified . The frequency of hypogonadism was 9.1 % in men . Pituitary deficits were associated with operations both in close proximity to the sella turcica and more distant regions ( p = 0.91 ) . Age ( p = 0.76 ) and gender ( p = 0.24 ) did not significantly differ across patients with versus those without hormonal deficiencies . Groups did not significantly differ across pathology and operation type ( p = 0.07 ) . Conclusion Hypopituitarism occurs more frequently than expected in patients who have undergone neurosurgical intracranial procedures for conditions other then pituitary tumors or may already exists in a neurosurgical population before surgery . Pituitary function testing and adequate substitution may be warranted for neurosurgical patients with intracranial pathologies at least if unexplained symptoms like fatigue , weakness , altered mental activity , and decreased exercise tolerance are present Neuro-endocrine deficiencies have been argued to be common sequelae after  aneurysmal subarachnoid hemorrhage ( aSAH ) . As this , however , does not resemble our clinical experience , we studied the incidence of neuro-endocrine and neuropsychological deficits after aSAH .  Twenty-six patients ( 20 females ) were prospect ively screened for neuro-endocrine and neuropsychological deficits 3 , 6 and 12 months after aSAH .  GH , IGF-1 , prolactin , LH , FSH , estradiol , testosterone , ACTH as well as cortisol during ACTH-stimulation were assessed . Neuropsychological analysis covered verbal comprehension , short term and working memory , visuospatial construction , figural memory , psychomotor speed , attention , and concentration . During the study period 5 individuals demonstrated neuro-endocrine dysfunction . Hypogonadotrophic hypogonadism resolved spontaneously in 2 patients and central hypothyroidism in one of these patients during the study . After 12 months three patients presented low IGF-1 levels . 73.9 % of our cohort was affected by neuropsychological deficits during follow-up . At 3 , 6 and 12 months the prevalences were 56.5 , 52.6 and 42.1 % , respectively . Interestingly , all patients with neuro-endocrine dysfunction presented impaired clinical outcome with a GOS 4 at some time point of the study ( GOS 4 vs. 5 , 45.5 % vs. 0 , P = 0.007 ) . We found a low prevalence of neuro-endocrine and a high prevalence of neuropsychological deficits in patients 3 , 6 and 12 months after aSAH without significant interrelation . Spontaneous recovery of neuro-endocrine alterations most likely presents an adaption to or dysfunction after severe illness . This hypothesis is strengthened by the fact that only patients with inferior clinical outcome after aSAH as assessed by GOS demonstrated neuro-endocrine dysfunction Objective To determine the diagnostic value of a ghrelin test in the diagnosis of GH deficiency ( GHD ) shortly after aneurysmal subarachnoid hemorrhage ( SAH ) . Design Prospect i ve single-center observational cohort study . Methods A ghrelin test was assessed after the acute phase of SAH and a GH-releasing hormone (GHRH)–arginine test 6 months post SAH . Primary outcome was the diagnostic value of a ghrelin test compared with the GHRH – arginine test  in the diagnosis of GHD . The secondary outcome was to assess the safety of the ghrelin test , including patients ' comfort , adverse events , and idiosyncratic reactions . Results Forty-three survivors of SAH were included ( 15 males , 35 % , mean age 56.6±11.7 ) . Six out of 43 ( 14 % ) SAH survivors were diagnosed with GHD by GHRH – arginine test . In GHD subjects , median GH peak during ghrelin test was significantly lower than that of non-GHD subjects ( 5.4 vs 16.6 , P=0.002 ) . Receiver operating characteristics analysis showed an area under the curve of 0.869 . A cutoff limit of a GH peak of 15 μg/l corresponded with a sensitivity of 100 % and a false-positive rate of 40 % . No adverse events or idiosyncratic reactions were observed in subjects undergoing a ghrelin test , except for one subject who reported flushing shortly after ghrelin infusion . Conclusion Owing to its convenience , validity , and safety , the ghrelin test might be a valuable GH provocative test , especially in the early phase of SAH Using logistic regression , we analyzed the predictive value of a number of entry variables with respect to the outcome variables delayed cerebral ischemia , rebleeding , and poor outcome ( death or severe disability ) in patients with aneurysmal subarachnoid hemorrhage . The entry variables were clinical condition on admission ( grade s on the Glasgow Coma Scale , Hunt and Hess system ) , the amount of subarachnoid and intraventricular blood and the presence of hydrocephalus on the admission computed tomogram , and antifibrinolytic treatment with tranexamic acid . We used data from a prospect ively studied population of 176 patients admitted within 72 hours after subarachnoid hemorrhage . The risk of delayed cerebral ischemia was best predicted by the amount of subarachnoid blood , intraventricular blood , and antifibrinolytic treatment  irrespective of clinical condition and hydrocephalus . The site of delayed cerebral ischemia was not related to the location of the subarachnoid hemorrhage . Antifibrinolytic treatment was the only entry variable ( negatively ) predicting the risk of rebleeding . Death or severe disability after 3 months was best predicted by the amount of subarachnoid blood and the initial clinical condition reflected by the grade on the Glasgow Coma Scale Background Somatotropic and thyroid hormones are probably important for the recovery after acute brain injury . Still , the dynamics of these hormones after spontaneous subarachnoid haemorrhage ( SAH ) is not well described . The purpose of this study was to investigate the relation between somatotropic and thyroid hormones and clinical factors after SAH . Methods Twenty patients with spontaneous SAH were included prospect ively .  Serum concentrations of TSH , fT4 , T3 , IGF-1 and GH were measured once a day for 7 days after SAH .  Hormone patterns and serum concentrations were compared to the severity of SAH , neurological condition at admission , clinical course and outcome of the patients . Results During the first week after SAH , all patients showed increased GH and IGF-1 concentrations . In the whole group , concentrations of TSH increased , whereas T3 and fT4 decreased . There were no relations of serum concentrations of IGF-1 or GH to clinical condition at admission , clinical course or outcome of the patients . Half of the patients showed low T3 serum concentrations . A complicated course was associated with a deeper fall in TSH and T3 concentrations . There were negative correlations for mean concentrations of TSH and T3 versus WFNS grade and a positive correlation for T3 versus GOS after 6 months , indicating that low concentrations of TSH and T3 were connected to worse SAH grade and poor outcome . Conclusions All patients showed increased GH and IGF-1 concentrations irrespective of the grade of SAH or clinical course . Patients with a complicated clinical course showed a more pronounced fall in TSH and T3 concentrations and low serum T3 concentrations were related to a more serious SAH and poor patient outcome . These results need to be studied further and they may contribute to the accumulated knowledge needed to underst and the complex mechanisms influencing the unpredictable clinical course after SAH Objective We describe the occurrence and course of  anterior pituitary dysfunction ( PD ) after aneurysmal subarachnoid haemorrhage ( SAH ) , and identify clinical determinants for PD in patients with recent SAH . Methods We prospect ively collected demographic and clinical parameters of consecutive survivors of SAH and measured fasting state endocrine function at baseline , 6 and 14 months . We included dynamic tests for growth-hormone function . We used logistic regression analysis to compare demographic and clinical characteristics of patients with SAH with and without PD . Results 84 patients with a mean age of 55.8 ( ±11.9 ) were included . Thirty-three patients ( 39 % ) had PD in one or more axes at baseline , 22 ( 26 % ) after 6 months and 6 ( 7 % ) after 14 months . Gonadotropin deficiency in 29 ( 34 % ) patients and growth hormone deficiency ( GHD ) in 26 ( 31 % ) patients were the most common deficiencies . PD persisted until 14 months in 6 ( 8 % ) patients : GHD in 5 ( 6 % ) patients and gonadotropin deficiency in 4 ( 5 % ) . Occurrence of a SAH-related complication was associated with PD at baseline ( OR 2.6 , CI 2.2 to 3.0 ) . Hydrocephalus was an independent predictor of PD 6 months after SAH ( OR 3.3 CI 2.7 to 3.8 ) . PD was associated with a lower score on health-related quality of life at baseline ( p=0.06 ) , but not at 6 and 14 months . Conclusions Almost 40 % of SAH survivors  have PD . In a small but substantial proportion of patients GHD or gonadotropin deficiency persists over time . Hydrocephalus is independently associated with PD 6 months after SAH . Trial registration number NTR 2085 Introduction Subarachnoid haemorrhage ( SAH ) may damage the hypothalamo-pituitary-adrenal gl and ( HPA ) axis and disturb cortisol metabolism . There are no available data that relates to the response of the HPA axis in the acute phase of SAH . We aim ed to characterise the behavior of serum adrenocorticotropic hormone ( ACTH ) , total cortisol , stimulated total cortisol and free cortisol concentrations in acute aneurysmal SAH . Methods A prospect i ve cohort study was conducted of patients with acute aneurysmal SAH ( n = 30 ) admitted to a tertiary university hospital . Patients admitted for elective aneurysmal surgery ( n = 16 ) served as the control group . An ACTH stimulation test was performed twice during the first week and at three months . The main outcome measure was description of the ACTH-cortisol response by calculating serum free cortisol and measuring total cortisol and ACTH concentrations . A mixed models method was used for testing between the groups , allowing heterogeneity between the groups . Results Patients with SAH had higher initial serum total cortisol ( mean + /- SD ; 793 + /- 312 nmol/L ) and free cortisol concentrations ( 83 + /- 55 nmol/L ) than control patients ( 535 + /- 193 nmol/L , p = 0.001 and 33 + /- 18 nmol/L , p < 0.001 , respectively ) . Thereafter , there were no differences in this respect . Serum free and total cortisol concentrations correlated but were unaffected by the severity of SAH . ACTH concentrations were comparable between SAH and control groups . Patients with Hunt-Hess grade s IV to V had higher ACTH concentrations at day one ( 10.7 + /- 7.1 pmol/l/L ) and day five ( 8.2 + /- 7.7 pmol/L ) than patients with grade I-III ( day one : 3.8 + /- 2.0 pmol/L , p = 0.002 ; day five : 4.7 + /- 1.8 pmol/L , p = 0.04 ) . Conclusions Calculation of serum free cortisol concentration was not helpful 
    Output:
    
Abnormalities in basal hormonal levels were more frequent when compared to induction tests , and the prevalence of a single pituitary hormone dysregulation was more frequent than multiple pituitary hormone dysregulation .
The prevalence of pituitary dysfunction did not correlate with the outcome of the patient .
Conclusions Neuroendocrine dysfunction is common after aSAH , but these abnormalities have not been shown to consistently impact outcome in the data available .