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Query: UMLS:C1332347 (ADH)
2,230 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The frequency of growth hormone (GH) deficiency in patients operated for pituitary neoplasms of various size and type was investigated using the insulin tolerance test. 45 patients were included in the study. 20 of the patients had a non-hormone secreting pituitary neoplasm, 9 had GH-, 6 ACTH-, 7 prolactin secreting adenomas and 3 had a craniopharyngeoma. Complete endocrinological examination was obtained in all patients after pituitary surgery. Apart from patients operated for GH secreting adenomas, GH deficiency was very common after pituitary surgery (92%), even in patients operated for small lesions. Among the 45 patients LH/FSH deficiency was found in 33%, ACTH in 33%, TSH in 18% and ADH deficiency in 9% of the patients. In this study, impaired GH secretion was found to be independent of the size of the tumors and was present in nearly all patients after pituitary surgery (with exception of GH secreting adenomas). Deficiencies of other pituitary hormones were predominantly observed after surgery for large tumors.
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PMID:Impaired growth hormone secretion in patients operated for pituitary adenomas. 795 Sep 4

The restricted environmental stimulation technique or REST is a method of relaxation where the level of environmental sensory inputs is kept very low. A particular REST technique called tank flotation, or flotation REST, consists of 1 h sessions in a tank containing water with a high salt content and maintained at 35.5 degrees C. In this protocol, five normal subjects were studied before and during 2 h after a 60 min flotation REST session and a control session of 60 min in a supine position on a bed. Cortisol, thyreostimulating hormone (TSH), thyroxine (T4), prolactin, melatonin, luteinizing hormone (LH), growth hormone (GH), beta-endorphin, vasopressin (ADH), gamma-aminobutyric acid (GABA) and homovanillic acid (HVA) were measured in plasma. HVA, 5-hydroxy-indoleacetic acid (5-HIAA) and vanylmandelic acid (VMA) were measured in urine. There were no changes in hormones concentrations that could be attributed to flotation REST. The urinary excretion of VMA was lower after the flotation REST session. The psychological consequences of flotation REST were more easily demonstrated than the neuroendocrine changes that are assumed to reflect the state of relaxation. Flotation REST increased subjective levels of sedation and euphoria. The possible mechanisms by which flotation REST induces relaxation are discussed.
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PMID:Neuroendocrine and psychological effects of restricted environmental stimulation technique in a flotation tank. 800 91

The influence on pituitary function of 6 weeks of training on 6 days a week was examined in six recreational athletes. Endurance training on a bicycle ergometer for 31-33 min was performed on 4 days each week at 90-96% (weeks 1-3) and 89-92% (weeks 4-6) of the 4 mmol lactate thresholds determined on day 0 and day 21, respectively, with interval training of 3-5 x 3-5 min in addition on 2 days a week at 117-127% and 115-110%, respectively. Determination of the serum hormone levels and a combined pituitary function test (200 micrograms thyrotropin releasing hormone (TRH), 100 micrograms gonadotrophin-releasing hormone (GnRH), 100 micrograms corticotrophin releasing hormone (CRH), 50 micrograms growth hormone releasing hormone (GHRH)) were made before training, after 6 weeks of training and after another 3 weeks of recovery. Training increased performance at 2 mmol lactate by 25%, at 4 mmol by 12%, and maximum performance by approximately 12%. The releasing hormone-stimulable prolactin, thyroid stimulating hormone (TSH) and somatotrophic hormone (STH) synthesis-secretion capacity remained unchanged, the adrenocorticotrophic hormone (ACTH) was increased after training. Cortisol release was reduced, follicle-stimulating hormone (FSH)-synthesis-secretion capacity was increased after training, and the luteinizing hormone (LH)-synthesis-secretion capacity reduced. This had no influence on base or exercise-induced serum hormone levels (cortisol, aldosterone, insulin, prolactin, FSH, LH, TSH, ACTH, ADH and STH), which showed no dependence on training, except for free testosterone which showed a decreasing trend (P < 0.10) of 19-25% and post-exercise ACTH which showed an increasing trend of 33% (P < 0.10). Conditioning (cortisol sensitivity and ACTH response) or adaptation (FSH and LH responses) to changed testosterone serum levels and altered spermatogenesis is discussed.
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PMID:Influence of 6-week, 6 days per week, training on pituitary function in recreational athletes. 824 77

The syndrome of water intoxication, resulting from dilutional hyponatremia and characterized by lethalgy, confusion, seizures, and coma was seen in two autistic boys living in the institution for mentally retarded children. Patient 1, a 19 year-old autistic boy showed loss of attention, inactiveness, sleepiness and delirium and then followed by overbreathing, severe vomiting and finally convulsive seizures several times, or coma, since October 1985. In August 1988, he was admitted with generalized tonic clonic convulsion associated with frequent vomiting EEG showed diffuse spike and wave complex with slow background activity. Laboratory data showed inappropriately high serum ADH level (8.5 pg/ml), low sodium concentration (121 mOsm/m/l), serum osmolality (237 mOsm/l) which was lower than urine osmolality (334 mOsm/l), and remarkable body weight gain (8.5 kg). He was diagnosed as water intoxication due to compulsive water drinking and SIADH. Diminished GH secretion to insulin-induced hypoglycemia and exaggerated prolactin response to LHRH stimulation suggested a hypothalamic lesion. Patient 2, a 17-year-old autistic boy, showed essentially the same symptoms and laboratory data as Patient 1, except that he had no epileptic discharge in EEG, and curious GH response to insulin-induced hypoglycemia. A remarkable daily body weight change suggested excessive water drinking and a possible episodic release of ADH. With mild water restriction, this became smaller. Since Patient 1 had epileptic attacks several times without hyponatremia and his EEG showed epileptic discharges, he was diagnosed as having epilepsy. Patient 2 has been seizure-free until now. Abnormality of hypothalamic or pituitary defects and polydipsia and possibility of water intoxication should always be considered when an autistic patients shows recurrent epileptic attacks or episodic strange behaviors with hyponatremia.
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PMID:[Two cases of infantile autism with intermittent water intoxication due to compulsive water drinking and episodic release of antidiuretic hormone (SIADH)]. 929 11

A retrospective study analyzing etiological, clinical and hormonal aspects in a population of 45 patients (14 males and 31 females) with permanent hypogonadism was performed, the most important findings were: 1) The most common cause of hypogonadism was gonadal failure (60% of all patients). This included-twenty-three females and four males. Eighteen patients had XO, two XY and two more XX gonadal dysgenesis. In the remaining cases, three patients had bilateral agonadism and two had testicular atrophy secondary to radiochemotherapy. 2) Eighteen patients had hypogonadotropic hypogonadism (40% of the cases). Ten were males and eight females. Eleven patients had gonadotropin deficiency associated with other pituitary dysfunctions. Deficiency of GH was found in all cases. TSH in ten, ACTH in nine and ADH in five. An increase in prolactin was observed in seven patients. The etiology of the hypopituitarism was intracranial tumors in five cases, idiopathic in three, perinatal hypoxemia in two and hypoplastic pituitary in one. In the remaining seven cases, isolated gonadotropin deficiency was found. Four cases were idiopathic, two cases had demyelinating diseases and one beta-thalassaemia. 3) Mean levels of testosterone were 4.20 +/- 6.5 (0, 20) pg/ml. Meal levels of estradiol of the total group, gonadal failure patients and those with hypogonadotropic hypogonadism were 8.51 +/- 14.7 (0, 50), 9 +/- 16 (0, 50) and 7.12 +/- 10.98 (0, 29) pg/ml, respectively. 4) Mean basal levels of LH and FSH in patients with gonadal failure were 35.57 +/- 60.66 (5, 320) and 53.19 +/- 53.92 (4, 230) mUi/ml, respectively. In hypogonadotropic hypogonadism patients, mean basal and peak levels of LH were 0.98 +/- 1.24 (0, 5) and 3.45 +/- 3.94 (0, 12) mUi/ml, respectively. Mean basal and peak levels of FSH after LHRH stimulation were 1.43 +/- 1.88 (0, 6) and 3.85 +/- 4.85 (0, 17) mUi/ml, respectively.
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PMID:[Etiological, clinical and hormonal characteristics of a group of patients with permanent hypogonadism]. 929 97

Patients with multiple sclerosis sometimes show subthalamic lesions presenting syndrome of inappropriate secretion of ADH (SIADH), hypothermia, hyperprolactinemia, weight loss, and cachexia. Hyperprolactinemia also has been found in the patients with active systemic lupus erythematosus, because prolactin can be produced from human activated lymphocytes. We described a case of multiple sclerosis showing galactorrhea-amenorrhea syndrome with hyperprolactinemia. A 31-year-old woman showed a high level of prolactin in the serum (79.6 ng/ml) during remission stage 5 months after the onset of multiple sclerosis. She showed galactorrhea-amenorrhea syndrome 3 years later. She showed dysesthesia in her limbs, relapsing monoparesis, visual disturbance and Gd-enhanced plaques in Brain MRI for 6 years. She was admitted to our hospital on November 24, 1995. A neurological examination showed hyporeflexia of the upper extremities, hyperreflexia of the lower extremities, bilateral ankle clonus, truncal ataxia, and neurogenic bladder. Laboratory tests revealed increased level of serum prolactin, exaggerated secretion of serum prolactin after intravenous injection of 500 micrograms TRH, and marked suppression after oral administration of 2.5 mg bromocriptine. Brain MRI showed demyelinating lesions near the lateral ventricle, and cervical MRI (T2 image) showed high signal intensity lesions in the spinal cord from C2 to C5. In the previous case, galactorrhea-amenorrhea syndrome was found during the exacerbation stage of multiple sclerosis. Hyperprolactinemia may be caused from subthalamic lesions or by activated lymphocytes in multiple sclerosis. We considered that hyperprolactinemia and galactorrhea-amenorrhea syndrome in our patient might be caused from subthalamic lesions because lymphocytes were not activated during the remission stage of multiple sclerosis.
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PMID:[A case of multiple sclerosis with galactorrhea-amenorrhea syndrome]. 936 74

It is known that in severe acquired brain injuries there is process of neuroinflammation, with the activation of a local and general stress response. In our study we considered six patients with disorders of consciousness (five in vegetative state and one in minimal consciousness state) in subacute phase, which had both a clinical assessment and a functional imaging (fMRI): in all these patients we analised blood levels of osteopontin (OPN), a cytokin involved in neuroinflammation but also in neurorepair with a still discussed role. Besides we studied the lymphocyte subsets and blood levels of some hormones (ADH, ACTH, PRL, GH, TSH, fT3, fT4). We found a positive correlation between the levels of serum osteopontin (higher than normal in all subjects) and the severity of the brain injury, especially for prognosis: actually, the patient with the lowest level has emerged from minimal consciousness state, while the one with the highest level has died a few days after the evaluation. The lymphocyte subset was altered, with a general increase of CD4+/CD3+ ratio, but without a so strict correlation with clinical severity; the only hormone with a significant increase in the worse patients was prolactin. In fMRI we detected some responses to visual and acoustic stimuli also in vegetative states, which had no clinical response to this kind of stimulation but generally have had a better prognosis. So we conclude that osteopontin could be a good marker of neuroinflammation and relate to a worse prognosis of brain injuries; the lymphocyte alterations in these disorders are not clear, but we suspect an unbalance of CD4 towards Th2; PRL is the best endocrinological marker of brain injury severity; fMRI surely plays an important role in the detection of subclinical responses and in prognostic stratification, that is still to define with more studies and statistical analysis.
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PMID:Immune endocrinological evaluation in patients with severe vascular acquired brain injuries: therapeutical approaches. 2370 Dec 52


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