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Biomedical subjects

K Brismar

Publications and source records attributed to K Brismar.

At least 91 records · Page 5Linked to original sources
PubMed1990

The growth hormone, prolactin and TSH response to TRH and L-dopa in patients with hyperprolactinaemia and a normal-sized sella turcica may denote a pituitary adenoma.

Forty-one patients with hyperprolactinaemia and suspected prolactinomas were studied. Growth hormone (GH) and thyrotropin (TSH) secretory patterns after thyrotropin releasing hormone (TRH) were affected in the majority of patients. The disturbances were observed regardless of tumour size as indicated by the radiological sella size. In patients with hyperprolactinaemia and normal-sized sella turcica, an abnormal GH and TSH response to TRH can be helpful in the diagnosis of a microadenoma. The hyperprolactinaemia per se and its effect on dopaminergic hypothalamic neurones may be the cause of the GH and TSH response. By contrast, many patients with macroprolactinomas showed insufficient GH secretory capacity.

Adult↗
PubMed1989

Calcium and magnesium concentrations in affective disorder: difference between plasma and serum in relation to symptoms.

Morning (0800) plasma and serum and mean diurnal (24-h) serum calcium (Ca) and magnesium (Mg) concentrations were investigated in 56 depressed patients, 32 with acute major depression, 26 of these restudied in remission, 24 patients with longstanding depression, mainly treated with lithium, and in 27 healthy controls. All subjects were rated with the Comprehensive Psychopathological Rating Scale (CPRS). Significant differences between the groups were found for 0800 and 24-h serum Ca and Mg, 0800 plasma Mg, but not for 0800 plasma Ca. Elevations of serum Ca and Mg, plasma Mg but not plasma Ca were noted in the lithium-treated patients. Sex differences for plasma but not serum levels were seen in remission and in the controls. Depressive symptoms were negatively correlated to 0800 plasma Ca in the acute state and positively to 0800 and 24-h serum Ca and Mg in remission and longstanding depression. This difference between plasma and serum in relation to symptoms could reflect a change in a calcium binding factor present in plasma but not in serum, connected with biological factors of affective disease.

Adult↗
PubMed1988

Insulin regulates the 35 kDa IGF binding protein in patients with diabetes mellitus.

The serum levels of the low molecular form of insulin-like growth factor binding protein (IGFBP) was determined in 56 outpatients with diabetes mellitus by a radioimmunoassay developed for amniotic 35 kDa IGFBP. The mean level of 35 kDa IGFBP was found to be threefold higher in insulin dependent diabetes mellitus (IDDM), 112 +/- 13 ng/ml, than in age matched controls, 37 +/- 2 ng/ml, while the mean level in non-insulin dependent diabetes mellitus (NIDDM), 16 +/- 2 ng/ml, was decreased. In hospitalized IDDM patients there was a significant correlation (r = 0.91, p less than 0.01) between fasting blood-glucose and 35 kDa IGFBP levels, not found in NIDDM patients. During insulin infusion the 35 kDa IGFBP levels declined with a half-life of 60-120 min. The decline in IGFBP continued even after the establishment of steady state B-glucose at 4.7 mmol/l. In conclusion, the elevated 35 kDa IGFBP levels in IDDM can be attributed to insulin deficiency and may reflect a reduced bioavailability of the IGFs at the target cells.

Adult↗
PubMed1988

Melatonin secretion related to side-effects of beta-blockers from the central nervous system.

In two studies of hypertensive patients the relationship between beta-blocker-induced CNS side-effects and the nightly urinary secretion of melatonin was analysed. In one group (n = 10) placebo, atenolol (mean dose 86 mg/day) or propranolol (mean dose 305 mg/day) were given in a double-blind, randomised design. In the other (n = 13) 100-400 mg metoprolol was given daily (mean dose 197 mg). After 4 weeks of treatment all beta-blockers reduced melatonin excretion, but the effect was significant only for metoprolol. Sleep disturbance records revealed more disturbed nights in the metoprolol group compared with the propranolol and the atenolol groups, even when the difference in age between the groups was controlled for. In the metoprolol group a significant relationship (p less than 0.05) was found between the fall in melatonin and the percentage of disturbed nights. Severe CNS side-effects, such as nightmares, occurred only in patients treated with metoprolol (21%), which in all cases were accompanied by low levels of melatonin. Our data suggest that the CNS side-effects during beta-blockade are related to a reduction of melatonin levels.

Adult↗
PubMed1987

Depressed melatonin secretion in patients with nightmares due to beta-adrenoceptor blocking drugs.

Nocturnal urinary melatonin excretion was evaluated in six patients with nightmares and hallucinations during treatment with beta-adrenoceptor blocking agents, and compared to six control patients with similar diagnoses and treatment but without such symptoms from the central nervous system (CNS). Nightly melatonin excretion was lower in all cases with nightly CNS-symptoms than in the control patients. The results also suggest drug differences and dose dependency. It is concluded that in predisposed patients CNS side-effects induced by beta-adrenoceptor antagonists are related to depressed nightly melatonin secretion.

Adrenergic beta-Antagonists↗
PubMed1987

Melatonin, cortisol, prolactin, and calcitonin secretion in primary hyperparathyroidism before and after surgery.

The aim of the present study was to determine the diurnal secretion of melatonin, cortisol, prolactin, and calcitonin during chronic parathyroid hormone-dependent hypercalcemia. Eight women, aged 40-76 years, with primary hyperparathyroidism (PHPT) were studied before and after surgical removal of a parathyroid adenoma. The hormone concentrations in blood were determined at 08, 12, 16, 22, 02, 04, and 06 h. Concomitantly, the excretion of melatonin and cortisol in urine between 07-19 h and 19-07 h, and the clearance of calcium and creatinine were measured. Nyctohemeral serum prolactin and calcitonin were unaffected by moderate parathyroid hormone-dependent hypercalcemia. In contrast, serum cortisol and melatonin were significantly higher during active disease than after surgical cure. Mean 24-h variation of serum cortisol was 349 +/- 34 nmol/liter vs. 223 +/- 17 nmol/liter and mean serum melatonin was 0.13 +/- 0.04 nmol/liter vs. 0.06 +/- 0.02 nmol/liter. Endogenous creatinine clearance was similar before and after surgery, while the clearance of melatonin and cortisol significantly increased after surgery, indicating an increased tubular reabsorption of both hormones during active disease. Fasting morning glucose concentrations were also significantly decreased after successful surgery, 6.1 +/- 0.6 vs. 5.2 +/- 0.5 mmol/liter. It is suggested that the relative hypercortisolism may be the cause of the glucose intolerance in primary hyperparathyroidism. Three to 4 months after surgical cure the serum melatonin levels were significantly lower than those seen in age-matched controls, indicating a melatonin insufficiency in patients successfully treated for PHPT. The meaning of this finding is not yet understood but might be of importance in the development of primary hyperparathyroidism.

Adenoma↗
PubMed1985

Metyrapone: an agent for melatonin as well as ACTH and cortisol secretion.

The metyrapone-test was used to study the influence of pituitary-adrenal activity on the pineal function in man. We recorded in blood the circadian rhythmicity of melatonin, ACTH and cortisol and the excretion of melatonin, cortisol and Porter-Silber chromogens in urine before, during and after the administration of 750 mg metyrapone every 4 h during 24 h in two healthy volunteers and in two patients with asymptomatic, moderate hyperparathyroidism and a prolactin-secreting microadenoma, respectively. The present study confirmed our previous report on an increased excretion of melatonin per 24 h and per mmol creatinine during the administration of metyrapone. The excretory maximum preceded the maximal ACTH-adrenal response. Serum melatonin remained unchanged during the administration of metyrapone. A second finding was depressed serum melatonin the night after the test in the subjects with the most marked ACTH-cortisol response following the metyrapone-test indicating suppression of melatonin secretion when ACTH-cortisol secretions were increased. A third finding was a late increase in diuresis appearing the day after metyrapone-administration while glomerular filtration rates did not show significant alterations. Thus, it is shown that the metyrapone-induced cortisol inhibition stimulates both ACTH and melatonin secretion, while high ACTH and cortisol levels are accompanied by reduced S-melatonin levels.

17-Hydroxycorticosteroids↗
PubMed1982

Effects of long-term bromocriptine treatment on catecholamine excretion and on circulatory adaptation to orthostasis and to exercise in patients with hyperprolactinemia.

Sympatho-adrenally regulated mechanisms of the circulatory system have been studied in seven patients with hyperprolactinemia in order to evaluate the effects of long-term (1-3 months) treatment with bromocriptine. Before treatment catecholamine excretion was within the normal range. Blood volume was low and there was a marked heart rate reaction to orthostasis. ECG showed no abnormalities. Blood pressure and ECG reaction during exercise were normal. The blood pressure heart rate response to handgrip was less marked than in healthy young men. During bromocriptine treatment, serum prolactin levels normalized in all but one patient. Total catecholamine excretion was lowered. Body weight diminished. Resting heart rate and blood pressure fell significantly. Blood volume per kg body weight remained unchanged as did the orthostatic heart rate increase. The circulatory response to handgrip was less marked than before therapy. It seems that long-term bromocriptine therapy provokes a cardiovascular pattern reflecting an inhibition of sympatho-adrenal activity.

Adenoma↗
PubMed1982

Melatonin and corticosteroid response to metyrapone in patients with pituitary disease.

Melatonin secretion is dependent both on the environmental lighting and noradrenergic control and seems to be related to the ACTH-cortisol secretion. The aim of the present study was to further elucidate the relationship between ACTH-cortisol and melatonin. For this purpose we chose the Metyrapone test. The melatonin secretion was studied in 10 patients, and increased significantly in 8/10 during and in one after the Metyrapone administration. These results further support a relationship between melatonin and ACTH-cortisol secretion, possibly through a suprapituitary interaction.

Adrenal Cortex Hormones↗
PubMed1981

CSF circulation in subjects with the empty sella syndrome.

The etiology to the empty sella syndrome (ESS) is not known. Increased intracranial pressure (ICP) has been suggested to be one of the possible causes. In the present study the CSF circulation was analyzed in 48 subjects with ESS with gamma cisternography, pneumoencephalography (PEG) and computed tomography (CT). In 80% of the subjects the CSF circulation was retarded with convexity block which was combined with widened CSF transport pathways and basal cisterns. These findings were correlated with the clinical signs and symptoms, most of which seemed to be related to the imparied CSF circulation (i.e. impared memory, balance disturbances, cerebellar ataxia, papilledema, hypertension and pituitary disorders). Headache, psychiatric symptoms, visual field defects and obesity, however, were not related to the impaired CSF circulation. It is concluded that impaired CSF dynamics leading to intermittent increase of ICP has a major impact on the development of the ESS and that most of the patients' complaints are related to this disturbance. Thus it is important to obtain information of the CSF dynamics concurrent with the diagnosis of ESS. For this purpose PEG or CT may be used as the first examination. Moreover, the patient should be examined at least every second year for symptoms and signs of progressive impairments of the CSF circulation.

Adolescent↗
PubMed1981

Prolactin secretion in the empty sella syndrome, in prolactinomas and in acromegaly.

Prolactin (PRL) secretion was studied in 47 patients with empty sella syndrome. Hyperprolactinemia (39-123 micrograms/l) was found in six of them. Intermittent increases in PRL were noted in another seven patients. In most subjects with empty sella syndrome and hyperprolactinemia, diurnal PRL variation was altered or impaired whereas the PRL response to TRH and L-dopa was normal. Low doses of bromocriptine (3.75-5 mg/day) normalized PRL. In patients with prolactinoma and acromegaly who had prolactin levels of 30-165 micrograms/l the diurnal PRL variation and PRL response to TRH were impaired. Patients with prolactinoma failed to suppress PRL during L-dopa test. The dose of bromocriptine required to normalize PRL ranged between 7.5 and 15 mg/day. It is concluded that in subjects with sellar changes and intrasellar cisternal herniation ("empty sella"), and with moderate increases in PRL, the responses to TRH and L-dopa and to bromocriptine may help to differentiate between the empty sella syndrome and a coexisting pituitary tumour.

Acromegaly↗
PubMedDate not supplied

Decreased IGF-I bioavailability after ethanol abuse in alcoholics: partial restitution after short-term abstinence.

IGF-I stimulates protein synthesis, lowers blood glucose, and affects cell differentiation. The main production site of IGF-I is the liver. One of its binding proteins, IGFBP-1, is also produced by the liver. It is well known that ethanol affects the function of the human liver. Long-term alcohol abuse may therefore not only cause considerable IGF-I and IGFBP-1 production changes, but also changes in IGF-I bioavailability, which at least in part is determined by the IGF-I/IGFBP-1 ratio. Not much is known about how the bioavailability of IGF-I is changed in alcohol abusers. Therefore, the objective of this investigation was to study that matter, and to elucidate how abstinence affects IGF-I bioavailability in man. Three study groups were formed: group N including normal non-addicted subjects, group E ethanol abusers without gross liver insufficiency, and group C alcohol abusers with liver cirrhosis and ascites. Serum concentrations of insulin, GH, IGF-1, and IGFBP-1 were determined in the morning in all participants, and the IGF-I/IGFBP-1 ratios were calculated. These values were compared in the three study groups. In group E comparison was also made between values recorded in the ethanol intoxicated and in the detoxicated states. Patients in group C had low IGF-I levels, high IGFBP-1 levels, and low IGF-I bioavailability as reflected by the IGF-I/IGFBP-1 ratios, which were several-fold reduced compared with subjects in group N (0.6+/-0.2 vs 10.2+/-2.3; p<0.001). Patients in group E had also a low IGF-I/IGFBP-1 ratio in the acute ethanol intoxicated state, which increased after detoxication (from 1.5+/-0.4 to 5.6+/-1.2; p<0.01). It is concluded that alcohol abuse lowers the hepatic production of IGF-I and increases the production of IGFBP-1. This results in a reduced IGF-I bioavailability. However, in patients with not yet clinically apparent liver damage the IGF-I bioavailability increases if the alcohol abuse is stopped. These findings could reflect an important, physiological adaptation, since hypoglycemia may be induced if the blood glucose-lowering power of IGF-I remains strong at a time of ethanol-induced inhibition of the hepatic gluconeogenesis. Chronic alcohol abuse, causing liver cirrhosis, also leads to markedly reduced IGF-I bioavailability, which appears to become permanent, since it prevails more than one week after stopping the alcohol abuse.

Adult↗