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Biomedical subjects

H Vierhapper

Publications and source records attributed to H Vierhapper.

At least 199 records · Page 11Linked to original sources
PubMed1983

Initiation of gonadotropin responsiveness in hypothalamic hypogonadism: comparison of pulsatile and continuous nocturnal subcutaneous administration of LH-RH.

An enhanced secretion of LH and FSH was observed in two patients with hypothalamic hypogonadism following treatment with nocturnal s.c. administration of LH-RH. Using portable infusion pumps two forms of therapy were used for 9 nights with a two months interval in between: A) continuous nocturnal s.c. LH-RH; B) pulsatile nocturnal s.c. LH-RH with administration of a bolus dose at 90 min intervals. Both therapeutical regimens induced a rise in the 8:00 h concentrations of LH. The secretory response of LH during an infusion of LH-RH (200 micrograms i.v.; t = 4 hours) was increased after both forms of therapy, whereas FSH secretion was enhanced only after the pulsatile mode of LH-RH application.

Adolescent↗
PubMed1983

Effect of i.v. prostaglandin E2 on the secretion of pituitary hormones in healthy men.

The intravenous administration of prostaglandin E2 (PGE2) has been proposed as a diagnostic tool in the differentiation of hypothalamic and pituitary forms of growth hormone deficiency. We have therefore studied the effect of PGE2 (200 micrograms i.v.) on serum concentrations of GH, LH, FSH, PRL, TSH, and cortisol in six healthy, male subjects. Side-effects, reported as highly unpleasant, occurred within two minutes after i.v. PGE2 in each individual. The individual response in serum concentrations of GH and LH following PGE2 was variable. Thus, a stimulatory effect was seen in some, but not in all individuals. Concentrations of FSH, PRL, and TSH did not change after PGE2-challenge, but a transient rise in serum cortisol was observed (p less than 0.01). The release of GH and LH upon i.v. PGE2 may be part of a systemic reaction or be due to a direct action of PGE2 on the anterior pituitary. The inhomogeneity of the obtained results and the unpleasant side-effects of i.v. PGE2 disqualify its use for the evaluation of pituitary GH-releasing capacity.

Dinoprostone↗
PubMed1983

Impact of euglycaemia and hyperglycaemia on the release of growth hormone and prolactin in type II-diabetics.

The influence of different blood glucose concentrations on the arginine (30 g/30 min i.v.) and TRH (400 micrograms i.v.) induced release of growth hormone and prolactin was studied in six male type II-diabetic patients. Blood glucose concentrations were clamped at euglycaemic (4-5 mmol/l) or hyperglycaemic (12-18 mmol/l) levels by means of an automated glucose-controlled insulin infusion system. The response of growth hormone to arginine, and irregular spikes in growth hormone concentrations following TRH seen in the euglycaemic state were suppressed during hyperglycaemia. The suppression of the arginine-induced release of growth hormone by hyperglycaemia was observed both with and without concomitant administration of exogenous insulin. The rise in serum prolactin concentrations in response to arginine was unaffected by hyperglycaemia, whereas the TRH-induced release of prolactin was suppressed. Since arginine induces the release of growth hormone and prolactin via the hypothalamus, while TRH acts at the pituitary level, the glycaemic state appears to exert a modulatory effect on the secretion of growth hormone and prolactin in type II-diabetics at both locations.

Arginine↗
PubMed1983

Increased secretion of insulin but unchanged secretion of growth hormone in hyperglycaemic type II diabetics treated with acetyl-salicylic acid.

The effect of acetyl-salicylic acid (ASA, 3 g/d for three days) on basal and arginine-stimulated concentrations of insulin and growth hormone was studied in seven type II diabetics. From 120 min before until 120 min after the infusion of arginine-hydrochloride (30 g/30 min) blood glucose concentrations were clamped at hyperglycaemic levels both during treatment with ASA (blood glucose: 12.7 +/- 1.2 mmol/l) and during a control experiment without ASA (blood glucose: 12.9 +/- 1.3 mmol/l). Concentrations of serum insulin in the hyperglycaemic state prior to arginine infusion were increased during treatment with ASA, whereas increments of serum insulin induced by i.v. arginine were unaffected. No difference was seen in either basal or stimulated concentrations of growth hormone. Thus, ASA enhances glucose-induced secretion of insulin in type II diabetics but fails to potentiate the glucose-dependent suppression of arginine-stimulated growth hormone release. In contrast to the pancreatic beta-cell the glucose-sensitive regulatory mechanism of growth hormone release appears to be unaffected by the inhibition of endogenous prostaglandin synthesis.

Aged↗
PubMed1983

Serum concentrations of gonadotrophins in hypergonadotrophic patients following stimulation by a long-acting analogue of luteinizing hormone-releasing hormone.

The effect of D-Ser(TBU)6-EA10-LRH, a long-acting analogue of luteinizing hormone-releasing hormone (LRH), was studied in patients with hypergonadotrophism due to orchidectomy (n = 8) or due to Klinefelter's syndrome (n = 6). Patients orchidectomized less than 7 days prior to the administration of the compound presented with maximum concentrations of LH (63.8 +/- 29.9 mIU/ml) within 60 min following iv injection of the LRH-analogue (10 micrograms). This behaviour of LH was qualitatively similar to that seen in healthy men. In patients orchidectomized more than 40 days prior to the administration of the LRH-analogue and in patients with Klinefelter's syndrome the occurrence of maximum serum LH-concentrations (115.0 +/- 39.4 and 149.4 +/- 134.5 mIU/ml, respectively) was delayed up to 240-360 min following iv LRH-analogue. This pattern of LH secretion is similar to that of healthy women. No qualitative differences in stimulated FSH-concentrations were observed between the described groups of hypergonadotrophic patients. These findings demonstrate a time-dependent increase in the 'second pool' of LH following orchidectomy. The similar behaviour of stimulated LH-release in healthy women and in male patients with long-term hypergonadotrophic hypogonadism could indicate an augmented production of endogenous LRH in these individuals as compared to healthy men, providing an explanation for the sexually related differences in the LH-response upon the administration of the LRH-analogue.

Aged↗
PubMed1983

Thyroid function in adrenocortical insufficiency during withdrawal and re-administration of glucocorticoid substitution.

The regulatory function of glucocorticoids on thyroid hormone concentrations was studied in patients with adrenocortical insufficiency (ACI, n = 8) and in healthy subjects (n = 6). In patients with ACI withdrawal of glucocorticoid substitution for 84 h led to an increase in serum concentrations of total triiodothyronine (TT3) from 110 +/- 20 to 133 +/- 22 ng/dl and a decrease of serum reverse-T3 (rT3) from 23 +/- 6 to 18 +/- 6 ng/dl, whereas subsequent administration of dexamethasone (0.5 mg po q.i.d. for 3 days) induced a fall in TT3 (129 +/- 22 to 88 +/- 16 ng/dl) and a rise in rT3 (17 +/- 5 to 37 +/- 11 ng/dl) concentrations. Serum levels of total thyroxine (TT4) were unchanged by either withdrawal or re-administration of glucocorticoids. Basal plasma thyrotrophin (TSH) concentrations were unchanged by glucocorticoid withdrawal and fell from 2.2 +/- 1.5 to 1.1 +/- 0.8 mU/l during subsequent dexamethasone therapy. In healthy subjects a decrease of TT3 (89 +/- 8 to 69 +/- 8 ng/dl) and an increase in rT3 (19 +/- 5 to 32 +/- 8 ng/dl) concentrations were seen after stimulation of endogenous cortisol production by prolonged infusion of ACTH1-24 (0.5 mg, t = 8 h on 2 consecutive days), whereas concentrations of TT4 remained unchanged. During subsequent administration of dexamethasone serum level of both. TT3 and rT3 returned to basal levels. Thus, changes in thyroid hormone concentrations are induced by alterations of substitution therapy in patients with ACI. In healthy subjects the application of 2 mg dexamethasone/day following prolonged maximal stimulation of endogenous cortisol by iv ACTH may represent a state of relative glucocorticoid deficiency, thus explaining the observed hormonal changes, which are inverse to those generally induced in healthy man by endogenous or exogenous glucocorticoids.

Adrenal Insufficiency↗
PubMed1982

[Androgen-producing adrenal adenoma in an 18 year-old woman: diagnosis by gas-chromatographic steroid analysis, histology and postoperative course].

Gas-chromatographic analysis of the urinary steroids in an 18 year-old girl with primary amenorrhoea and hirsutism revealed markedly elevated excretion of androsterone, etiocholanolone, dehydroepiandrosterone, and androstendiole, both under basal conditions and after oral dexamethasone (0.5 mg q.i.d. for three days). Adrenal scintigraphy revealed the presence of a tumour of the right adrenal gland, which was subsequently removed by unilateral adrenalectomy. Histologically, the tumour showed marked anisocytosis, but since there was no evidence of capsular or angioinvasion or of mitotic activity, it was classified as an adrenocortical adenoma. Postoperatively the patient showed regression of the virilizing syndrome and normal menstrual bleeding. Urinary steroid excretion has remained normal for four years after adrenalectomy. Androgen-producing tumours must be considered as a possible cause of hirsutism in young females and should, thus, be excluded in each case. Analysis of urinary steroids by gas chromatography is a valuable tool in accomplishing this task.

Adenoma↗
PubMed1982

[Endemic goiter in Austria. Is iodine deficiency the primary cause of goiter?].

In spite of government-regulated iodide admixture to table salt, the incidence of goiter is still high in Austria. Iodine excretion and thyroid function were therefore investigated in 80 patients suffering from ordinary goiter in whom thyroid size and resulting symptoms had increased lately. 25 euthyroid non-goitrous subjects served as controls. 48% of the goitrous patients investigated presented with iodine excretion of less than 70 micrograms/24 h, suggesting an insufficient iodine supply. Thyroid I131 uptake, basal and TRH-stimulated plasma TSH concentrations, and serum T3 levels were higher, whereas serum T4 levels were lower in these patients than in goitrous patients with higher iodine excretion and non-goitrous controls. Iodine deficiency thus appears to be of pathogenetic relevance in about half of the goitrous Austrian population. Other factors enhancing goiter development seem to assume particular importance in goitrous patients with a sufficient iodine supply.

Adolescent↗
PubMed1982

Adrenergic mechanisms and blood pressure regulation in diabetes mellitus.

Changes in blood pressure (BP) and plasma norepinephrine (NE) following various stimuli of the sympathetic, nervous system were studied in six healthy subjects and in 17 diabetic patients. The latter were subdivided in three groups: (1) six patients with neither peripheral neuropathy nor autonomic dysregulation, (2) six patients with severe peripheral neuropathy without autonomic dysregulation, and (3) five patients with autonomic dysregulation, three of whom suffered also from peripheral neuropathy. The following procedures were performed: (1) cold pressor test (2 min), (2) mechanical irritation of the skin by suction (0.75 kg/cm2, 10 min), (3) orthostasis (10 min), and (4) i.v. infusion of NE (50, 100, 200 ng kg-1 min-1 for 15 min each). Both the stimulated endogenous plasma NE levels and BP response to exogenous NE were the same in normal subjects, in diabetic controls and in diabetics with peripheral neuropathy without autonomic dysregulation. In contrast, diabetics with postural hypotension showed a less pronounced release of NE to standing (P less than 0.05), but not to cold pressor test and mechanical skin irritation. Furthermore, they showed increased vasoreactivity to the highest dose (P less than 0.05), but not to the lower doses of exogenous NE. Thus NE release and adrenergic BP regulation seem to be altered only in diabetics with clinical signs of autonomic dysregulation. These alterations can only be evaluated when patients are exposed to stimuli of higher intensity, such as orthostasis or infusion of a high NE dose.

Adult↗
PubMed1982

Reduced pressor effect of angiotensin II and of noradrenaline in normal man following the oral administration of the calcium-antagonist nifedipine.

The pressor response to both angiotensin II (5, 10 and 20 ng kg-1 min-1) and to noradrenaline (50, 100 and 200 ng kg-1 min-1) was reduced (P less than 0.05 to less than 0.005) in six healthy male subjects following the administration of the calcium-antagonist nifedipine (10 mg p.o.). Nifedipine induced a rise in basal plasma noradrenaline concentrations but did not alter the plasma concentrations of adrenaline, dopamine, renin and aldosterone. A slight reduction in the angiotensin II induced rise of plasma aldosterone by nifedipine was observed after the administration of the largest dose of angiotensin II only (P less than 0.05). The reduced responsiveness towards pressor agents following oral nifedipine is in keeping with the known antihypertensive effect of calcium-antagonistic drugs and could provide a concept for the effectiveness of these drugs in hypertensive crisis.

Administration, Oral↗
PubMed1982

Acute suppressive effect of ACTH-induced cortisol secretion on serum prolactin levels in healthy man.

The effect of ACTH on serum prolactin concentrations was studied in 6 healthy women in the follicular phase of the menstrual cycle, in 5 healthy men and in 6 patients (5 males, 1 female) with adrenocortical insufficiency. In healthy women prolactin levels decreased from basal, 14.4 +/- 2.1 (SEM) microgram/l to 9.4 +/- 0.9 microgram/l after 30 min and to 8.1 +/- 0.7 micrograms/l after 60 min of iv administration of synthetic ACTH1-24 (0.25 mg). Upon continuous infusion of ACTH1-24 (0.25 mg for 8 h) prolactin fell to 4.4 +/- 0.6 microgram/l in healthy women and to 4.6 +/- 1.5 micrograms/l (basal: 10.6 +/- 1.8 micrograms/l) in healthy men. In patients with adrenocortical insufficiency prolactin concentrations remained unchanged following an 8 h infusion of ACTH1-24 (before ACTH: 14.5 +/- 2.3 micrograms/l, after ACTH: 16.3 +/- 3.1 micrograms/l). After treatment with dexamethasone (2 mg/day for 3 days) however, prolactin concentrations were suppressed both in healthy women (-52 +/- 7%) and men (-25 +/- 11%) and in patients with adrenocortical insufficiency (-21 +/- 10%). Thus the effect of ACTH on prolactin appeared to be mediated via enhanced cortisol secretion. It is suggested that an acute increase in cortisol levels within the physiological range may modulate prolactin secretion.

Addison Disease↗
PubMed1982

Impaired secretion of TSH in critically ill patients with 'low T4-syndrome'.

Thyroid and pituitary function was studied in 10 male and 6 patients female during critical non-endocrine disease. Low concentrations of TT3 were observed in each case. Seven patients out of whom 3 survived, presented with low levels of TT4 due to deficiency in TBG in the presence of normal values of FTI and FT4, whereas a 'low T4-syndrome', characterized by low concentrations of both TT4 and FT4 was seen in 9 patients, 8 of whom died 1 to 16 days after evaluation of pituitary function. A diminished response of TSH to iv TRH (400 micrograms), as observed in 4 patients with normal FT4 and in all patients with 'low T4-syndrome', was not accompanied by a concomitant lack in stimulated release of LH, FSH and Pr1 in the majority of cases. However, the secretory maximum of LH and FSH following stimulation by LRH (100 micrograms iv) was delayed in 10 and in 9 patients, respectively, including patients both with normal and subnormal concentrations of FT4. From the above it appears that low stimulated concentrations of TSH in the presence of subnormal concentrations of FT4 indicate an extremely poor prognosis in critically ill patients. The abnormal behaviour of TSH in this group of patients cannot be explained by generalized pituitary insufficiency or by an increase in FT4.

Adult↗
PubMed1982

Gonadotrophin-secretion in adrenocortical insufficiency: impact of glucocorticoid substitution.

In patients with deficient endogenous glucocorticoid production due to primary adrenal insufficiency (n = 4) or bilateral adrenalectomy (n = 2) a rise in LRH-stimulated concentrations of LH was seen following withdrawal of substitution therapy for 84 h. Consecutive re-administration of glucocorticoids (dexamethasone 2.0 mg/day for 3 days) resulted in increased basal concentrations of LH and FSH and a diminished secretory response of LH upon iv LRH (100 micrograms). Five patients substituted with glucocorticoids because of adrenocortical insufficiency presented upon the administration of exogenous ACTH1-24 with unchanged basal and LRH-stimulated concentrations of LH and FSH as compared to a placebo experiment. These data suggest that the withdrawal and subsequent re-administration of gluco-corticoid substitution alters basal and stimulated concentrations of gonadotrophins in patients with adrenocortical insufficiency, thus providing evidence for the importance of adequate glucocorticoid supply in the regulation of gonadotrophin secretion.

Addison Disease↗
PubMed1982

Pituitary-thyroid dysfunction in severe non-thyroidal disease: "low-T4 syndrome".

Thyroid function tests were obtained from 335 consecutive patients admitted to an intensive care unit. Twenty patients suffering from severe non-endocrine diseases (septicaemia, fulminant hepatic and renal failure, acute pancreatitis, polytrauma, cerebral haemorrhage) were found to have serum thyroxine levels in the hypothyroid range (less than 4 micrograms/dl). Serum concentrations of total thyroxine (2.3 +/- 0.2 micrograms/dl), triiodothyronine (0.23 +/- 0.03 ng/ml), and thyroxine binding globulin (15.1 +/- 1.3 micrograms/ml) were reduced, but were above normal for reverse triiodothyronine (0.43 +/- 0.06 ng/ml). Response of TSH secretion to iv TRH was found to be either normal, lowered or absent. Primary hypothyroidism was excluded, as no enhanced TSH response was observed in any case. Although decreased thyroxine levels may be due to increased thyroid hormone degradation it appears that associated impaired TSH responsiveness to TRH may result from illness-related inhibition of pituitary TSH release. Although the finding of decreased thyroid hormone levels is not rare in care patients, it represents an index of poor prognosis. Differentiation between this "low-T4 syndrome" and true hypothyroidism depends essentially on clinical symptoms and course of disease.

Acute Disease↗