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Biomedical subjects

W Magnet

Publications and source records attributed to W Magnet.

16 recordsLinked to original sources
PubMed1984

[Sonographic detection of a wood splinter in the small intestine--a case report].

We report on a case of sonographic detection of a foreign body (wooden splinter) in the abdomen with covered perforation of the jejunum. The patient did not know about the existence of that foreign body. We found out later that this splinter must have been in the abdomen for more than two years without any symptoms. A few weeks ago he felt an increasingly sharp pain in that area--probably at the time the perforation of the jejunum took place.

Foreign Bodies↗
PubMed1983

The inhibiting effect of trilostane on testosterone synthesis. Hormonal and morphologic alterations induced by subchronic trilostane treatment in rats and healthy volunteers.

(2 alpha, 4 alpha, 5 alpha, 17 beta)-4, 5-[Epoxy-17-hydroxy-3-oxo-androstane-2-carbonitrile (Trilostane, Win 24450) is a new, orally active, competitive inhibitor of 3 beta-hydroxysteroid dehydrogenase currently being introduced into therapy of Cushing's disease and primary aldosteronism and being investigated in the treatment of low-renin essential hypertension. In adult male rats and in healthy, young, male volunteers the effect of trilostane on testosterone production was studied. Rats were treated with trilostane 150 mg or 300 mg/kg/d for 7 or 14 days. Testosterone in serum was measured by radioimmunoassay, testes were weighed and Leydig cell nuclear volume determined. In healthy volunteers, dehydroepiandrosterone sulphate (DHEAS) and responses of luteinizing hormone (LH), follicle stimulating hormone (FSH) and testosterone to luteinizing hormone releasing hormone (LHRH) stimulation were measured by radioimmunoassay before and during trilostane treatment (240 mg/d). In rats, trilostane treatment decreases testosterone and increases Leydig cell nuclear volumes without affecting testicular weight. In volunteers, basal testosterone is not changed during trilostane treatment but testosterone response to LHRH is impaired. DHEAS increases. LH or FSH levels are not altered. It is concluded that trilostane treatment may decrease testosterone synthesis.

Adult↗
PubMed1983

[Representative studies of the vitamin D status of 2-year-old children in Frankfurt am Main].

In a representative sample population of 421 two-year-old Frankfurt children studied for vitamin-D nutritional status, only one case of subclinical rickets was discovered. 93.3% of the children have been a regular vitamin-D supplements during the first 12 month of life, but only 32.7% of them continued to receive the supplement beyond the age of one year. Risk groups were not identified, neither with regard to ethnic groups, nor smaller vitamin-D doses, or any other aspect.

Child, Preschool↗
PubMed1982

[ACTH in the dexamethasone suppression test].

Despite the great clinical importance of the low-dose dexamethasone suppression test (determination of cortisol after dexamethasone 2 mg p.o. at 11.00 p.m. in the evening before) and of the determination of ACTH in plasma, so far only little is known about the ACTH response to dexamethasone in normal subjects. In the present study cortisol and ACTH were determined by radioimmunoassay in normal subjects at 8.00 a.m., 10.00 a.m. and noon before and after dexamethasone. Additionally the cortisol response to ACTH was tested under both conditions. The ACTH concentrations in the morning show a periodicity quite similar to the well-known circadian rhythm of cortisol secretion. Dexamethasone blocks this periodicity without decreasing ACTH significantly. The cortisol response to ACTH after dexamethasone is normal. In the morning only a basal and presumably biologically inactive ACTH is secreted which can not further be suppressed by dexamethasone. Therefore it is advisable for the diagnosis of hypercortisolism to measure ACTH only in stimulation tests, e.g. insulin-induced hypoglycemia.

Adrenocorticotropic Hormone↗
PubMed1982

[ACTH response in the dexamethasone suppression test].

Despite the great clinical importance of the low-dose dexamethasone suppression test (determination of cortisol after dexamethasone 2 mg p.o. at 11.00 p.m. in the evening before) and of the determination of ACTH in plasma, so far only little is known about the ACTH response to dexamethasone in normal subjects. In the present study cortisol and ACTH were determined by radioimmunoassay in normal subjects at 8.00 a.m., 10.00 a.m. and noon before and after dexamethasone. Additionally the cortisol response to ACTH was tested under both conditions. The ACTH concentrations in the morning show a periodicity quite similar to the well-known circadian rhythm of cortisol secretion. Dexamethasone blocks this periodicity without decreasing ACTH significantly. The cortisol response to ACTH after dexamethasone is normal. In the morning only a basal and presumably biologically inactive ACTH is secreted which can not further be suppressed by dexamethasone. Therefore it is advisable for the diagnosis of hypercortisolism to measure ACTH only in stimulation tests, e.g. insulin-induced hypoglycemia.

Adrenocorticotropic Hormone↗
PubMed1982

The inhibiting effect of trilostane on adrenal steroid synthesis: hormonal and morphological alterations induced by subchronic trilostane treatment in normal rats.

In adult male rats the effect of a subchronic treatment with trilostane, a new, orally active, competitive inhibitor of 3 beta-hydroxysteroid dehydrogenase, on adrenal steroid production and morphology was studied. Rats were treated with 150 mg or 300 mg trilostane/kg/day for 7 or 14 days and with 150 mg trilostane/kg/day for 10 days in combination with 75 mg propranolol/kg/day or 1 mg indomethacin/kg/day. Trilostane leads to a dose-dependent increase in adrenal weight and to a rather uniform increase in nuclear volumes of zona glomerulosa and zona fasciculata cells. The basal secretion of aldosterone and corticosterone is not significantly altered. Trilostane increases the excretion of sodium and potassium in urine. The stimulating effect of trilostane on plasma renin activity and the adrenal enlargement are not inhibited by propranolol or indomethacin. We conclude that trilostane induces latent adrenal insufficiency. Increased renin and ACTH maintain normal basal steroid levels, and might impair the therapeutic effectiveness of trilostane.

Adrenal Glands↗
PubMed1975

[Androgens in the plasma of women with hirsutism (author's transl)].

109 women with hirsutism were investigated (102 with idiopathic hirsutism, four with Stein-Leventhal syndrome, one each with adrenal adenoma, adrenal carcinoma and hilus-cell tumour). Levels of testosterone, dihydrotestosterone, androstenediol and dehydroepiandrosterone were measured, usually in the course of a combined adrenal-ovarian stimulation-suppression test. Measuring several plasma androgens made it possible to distinguish idiopathic hirsutism from other endocrine diseases with hirsutism. Mean plasma testosterone level in idiopathic hirsutism was not significantly different from that in healthy women. Elevated testosterone and(or) dihydrotestosterone levels were found in only 22 of 102 women. There was a marked increase in plasma testosterone after HCG injection in the patient with Stein-Leventhal syndrome. Androstenediol and dehydroepiandrosterone were both important in the diagnosis of autonomous adrenal steroid secretion.

Adenoma↗