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Traumatic brain injury (TBI) is a crucially important public health problem around the world, which gives rise to increased mortality and is the leading cause of physical and psychological disability in young adults, in particular. Pituitary dysfunction due to TBI was first described 95 years ago. However, until recently, only a few papers have been published in the literature and for this reason, TBI-induced hypopituitarism has been neglected for a long time. Recent studies have revealed that TBI is one of the leading causes of hypopituitarism. TBI which causes hypopituitarism may be characterized by a single head injury such as from a traffic accident or by chronic repetitive head trauma as seen in combative sports including boxing, kickboxing, and football. Vascular damage, hypoxic insult, direct trauma, genetic predisposition, autoimmunity, and neuroinflammatory changes may have a role in the development of hypopituitarism after TBI. Because of the exceptional structure of the hypothalamo-pituitary vasculature and the special anatomic location of anterior pituitary cells, GH is the most commonly lost hormone after TBI, and the frequency of isolated GHD is considerably high. TBI-induced pituitary dysfunction remains undiagnosed and therefore untreated in most patients because of the nonspecific and subtle clinical manifestations of hypopituitarism. Treatment of TBI-induced hypopituitarism depends on the deficient anterior pituitary hormones. GH replacement therapy has some beneficial effects on metabolic parameters and neurocognitive dysfunction. Patients with TBI without neuroendocrine changes and those with TBI-induced hypopituitarism share the same clinical manifestations, such as attention deficits, impulsion impairment, depression, sleep abnormalities, and cognitive disorders. For this reason, TBI-induced hypopituitarism may be neglected in TBI victims and it would be expected that underlying hypopituitarism would aggravate the clinical picture of TBI itself. Therefore, the diagnosis and treatment of unrecognized hypopituitarism due to TBI are very important not only to decrease morbidity and mortality due to hypopituitarism but also to alleviate the chronic sequelae caused by TBI., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Context: Diagnosis of secondary adrenal insufficiency and GH deficiency requires evaluation by dynamic stimulation tests in most cases. Although insulin tolerance test (ITT) is accepted as the gold-standard test for the evaluation of both hypothalamo-pituitary-adrenal (HPA) and (GH)-IGF-1 axes, the test is cumbersome. In clinical practice, low-dose adrenocorticotrophic hormone (ACTH) stimulation test is a sensitive, safe and easily applicable alternative to ITT. Although it takes more time, glucagon stimulation test (GST) is also a good alternative to ITT and can evaluate both axes., Objective: The primary aim of this study was to compare the ITT, low-dose ACTH and GSTs in the evaluation of HPA and GH-IGF-1 axes in patients with pituitary disorders and to evaluate the repeatability of all three tests., Design: ITT, low-dose ACTH and GSTs were performed in all 129 patients, and the tests were repeated in 66 of these patients., Setting: Erciyes University Medical School, Department of Endocrinology., Patients or Other Participants: One hundred and twenty-nine adult patients (76 women, 53 men) with pituitary disorder were included in the study., Main Outcome Measure(s): The cortisol and GH responses of patients to dynamic tests., Results: Peak cortisol levels obtained during ITT were significantly lower than the values obtained during both low-dose ACTH and GSTs. Peak cortisol levels obtained during the GST were lower than those found during the low dose ACTH stimulation test. Peak GH responses were found to be higher in GST than in ITT. All three tests had good reproducibility., Conclusions: Any of 3 tests can be used in the evaluation of the HPA axis and either GST or the ITT can be used in the evaluation of the GH-IGF-1 axis but cut-off levels for the insufficiency of HPA or GH-IGF-1 axis should be individualized for each test., (© 2014 John Wiley & Sons Ltd.)

Abstract: Objective: The aim of the present study was to investigate the effects of growth hormone (GH) replacement on posterior pituitary functions of GH-deficient Sheehan''s syndrome (SS) patients. Design: Ten patients with SS and 14 healthy control women were included in this prospective study. All patients were given appropriate hormone replacement therapy other than GH, according to present hormone deficiencies. Patients were euthyroid and eucortisolemic at the time of baseline evaluation. Patients and the control group were evaluated with water-deprivation and saline-infusion tests at baseline and the tests were repeated in patients with SS after 3months of GH replacement therapy. Results: According to the water deprivation test, 3 patients had partial central DI at baseline. Urine osmolalities of the patients were slightly lower and plasma osmolalities were significantly higher than the control group at baseline, after water deprivation and following DDAVP injection and after hypertonic saline infusion. The osmotic threshold of serum for thirst perception was found to be significantly higher in SS patients than the control group, GH replacement therapy did not influence the results of water deprivation and saline infusion tests in SS patients. Conclusion: Patients with SS have subtle abnormalities in posterior pituitary functions and the threshold for thirst perception is increased. However GH replacement therapy does not seem to reverse or adversely affect the mildly deteriorated posterior pituitary functions of SS patients. [Copyright &y& Elsevier]

Abstract: Context: Impaired cognitive performance has been demonstrated in adults with GH deficiency and acromegaly by using different neuropsychological tests. P300 event related potential (ERP) application is a well established neurophysiological approach in the assessment of cognitive performance. Objectives: Evaluation of cognitive performance by using P300 ERPs has not been reported in acromegaly, and the comparisons of the P300 ERPs between the patients with GH deficiency and GH excess have not been done yet. Therefore present study was designed to investigate the effects of GH deficiency and GH excess on cognitive performance by using P300 ERPs. Design and Methods: The study comprised 19 patients with severe GH deficiency, 18 acromegalic patients and 16 age, education and sex matched healthy controls. Baseline auditory ERPs were obtained at Fz (frontal), Cz (central), Pz (parietal) and Oz (occipital) electrode sites in GH deficient group, GH excess group and control group. Results: There was a significant difference between mean serum IGF-I levels in the GH deficient and acromegalic patients (48±38ng/ml and 742±272ng/ml, respectively) (P =0.01). The mean P300 latency of the patients with GH deficiency was significantly (P =0.0001) prolonged when compared with that of normal controls and acromegalic patients at all electrode sites. The mean P300 amplitude of the patients with acromegaly was significantly (P =0.005) lower when compared with that of normal controls and GH deficient patients at all electrode sites. Conclusions: Using ERPs recordings, the present study indicates the prolongation of P300 latencies in patients with severe GH deficiency and reduction of P300 amplitudes in patients with acromegaly. This study provides the electrophysiological evidence for the presence of cognitive dysfunction in both GH deficiency and GH excess, and different components of the cognitive performance are impaired in these conditions. [Copyright &y& Elsevier]