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Biomedical subjects

J Marek

Publications and source records attributed to J Marek.

At least 163 records · Page 9Linked to original sources
PubMed1988

The nature of cardiac hypertrophy in acromegaly: an echocardiographic study.

M-mode echocardiography was used to study cardiac involvement in 78 patients with acromegaly. Proportionate concentric or eccentric left ventricular hypertrophy (LVH) was a common finding. Calculated left ventricular mass (LVM) was increased significantly in a hormonally active disease group compared to an inactive disease group or a control group (153 +/- 7 vs. 96 +/- 8 and 89 +/- 3 g/m2 resp.; p less than 0.001 for both). The increase of LVM in hormonally active disease is due to predominantly LV dilatation, whereas associated hypertension, if present, aggravates the LVH exclusively due to thickening of the LV wall. Hypocorticalism, if present, does not influence the degree of LVH. Asymmetric septal hypertrophy was not found to be specific for acromegaly and was seen in only 7.7% of patients. There was no correlation between LVM and both the plasma levels of growth hormone and duration of disease. On the basis of a retrospective analysis of LVM in successfully treated patients the authors conclude that specific heart muscle disease in acromegaly, manifesting itself as LVH, is slowly reversible after cessation of the growth hormone hyperproduction.

Acromegaly↗
PubMed1988

Effect of human growth hormone and somatomedin on the recovery of sheep red blood cell receptor in peripheral T-lymphocytes.

The effect of growth hormone (GH) and somatomedin (SM) on the recovery of sheep red blood cell (SRBC) receptor in trypsinized human T-lymphocytes was studied either with the use of sera from patients with acromegaly or pituitary dwarfism or after the addition of exogenous GH, SM or thymosin to human sera. It was found that GH does not show any effect on the recovery of SRBC receptor, but it may act through the increase of SM level. It was concluded that the regulation of cellular immunity may be influenced by GH through its stimulatory action on the synthesis and release of somatomedins.

Acromegaly↗
PubMed1987

[Cysticercosis].

Explore the source record for details and available documents.

Adult↗
PubMed1986

Pharmacokinetics of oral terguride in patients with a prolactinoma.

The pharmacokinetics of oral terguride 1 mg was evaluated in a single-dose study in 8 patients with a prolactinoma and one with acromegaly. A radioreceptor assay was used to measure the plasma levels of terguride. The peak plasma concentration (2.3 +/- 0.7 ng/ml, mean +/- SEM) was attained within 1 h of drug administration. Moment analysis gave a mean residence time of 4.3 +/- 0.6 h. Plasma prolactin was also determined by radioimmunoassay. The plasma prolactin was reduced to 30 +/- 3% of its pretreatment value after 4 h.

Acromegaly↗
PubMed1986

The use of andriol in treatment of androgen deficiency in transsexual women.

In search of a non-invasive, long-term acting form of androgen to be used in female-to-male transsexuals, testosterone undecanoate (Andriol, Organon) was investigated from clinical and laboratory points of view. The therapy resulted in a significant elevation of androgens with a considerable increase of the free testosterone fraction, desired virilization and somatic changes to a masculine phenotype. Testosterone undecanoate provides sufficiently high androgen levels without significant influence on the hypothalamo-pituitary-gonadal axis. The treatment impaired neither liver function nor glucose tolerance. It is concluded that this drug is suitable for hormonal preparation before the reconstructive therapy to males.

Adult↗
PubMed1986

Decreased 133Xe clearance in the proximal femur in acromegaly.

Using the 133Xe tissue clearance method, the blood flow in the greater trochanter of the femur was studied in 30 patients with acromegaly. Both the washout rate constant (k2) and blood flow (P2) values are significantly decreased in acromegaly (p less than 0.01). There is a significant negative correlation (r = -0.42, p less than 0.05) between the flow values and mean daily concentrations of growth hormone in serum of acromegalic patients. The observations is presented as a preliminary evidence of a possible influence of growth hormone on the blood flow in bone.

Acromegaly↗
PubMed1986

Insulin binding to erythrocyte receptors in acromegalic patients in relation to the activity of acromegaly and to concomitant diabetes mellitus.

Insulin binding to receptors on erythrocytes was studied in patients with acromegaly (n = 27) and in control subjects without any endocrine pathology, diabetes or obesity (n = 13). According to fasting serum concentration of growth hormone (GH), acromegalics were divided into two groups: A) GH less than 10 ng/ml (n = 16) and B) GH above 20 ng/ml (n = 11), in which patients were further divided into subgroups with regard to the presence or absence of diabetes. Insulin binding was decreased both in active and inactive acromegalics when compared with controls. A greater decrease was seen in active acromegaly coupled with diabetes. This was not the case of inactive hyperglycaemic acromegalics, where a compensatory increase in the affinity of "empty" receptors might account for a lack of a greater decrease in insulin binding.

Acromegaly↗
PubMed1986

Correlation between mass of parathyroid adenoma and biochemical indicators of bone turnover in patients with primary hyperparathyroidism.

We related the weight of the parathyroid adenoma to biochemical variables of bone turnover in 53 patients submitted to parathyroidectomy for primary hyperparathyroidism. There was a positive correlation (r = 0.61, p less than 0.01) between iPTH (c-assay) and adenoma weight. No correlations were found between either concentration of circulating iPTH or weight of parathyroid adenoma and severity of skeletal change expressed by total activity of serum alkaline phosphatase and its bone isoenzyme and urinary excretion of hydroxyproline. We conclude that the severity of bone changes in individual patients with primary hyperparathyroidism does not result from the direct tissue effect of a single hormone (parathyroid hormone).

Adenoma↗