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Biomedical subjects

S Aanderud

Publications and source records attributed to S Aanderud.

At least 19 recordsLinked to original sources
PubMed1991

[Rapid calcium infusion in the diagnosis of hypoglycemia].

The diagnosis of beta cell tumours of the pancreas is a clinical problem. It is also difficult to exclude this diagnosis in patients who are suspected of suffering from recurrent hypoglycemia, but do not have beta cell tumours. The most widely used diagnostic procedure has been suppression of endogenous insulin production with prolonged fasting up to 72 hours. This procedure is troublesome to the patient, time-consuming and expensive, and demands the complete cooperation of the patient. Therefore several diagnostic tests have been developed, but none has been generally accepted. A newly described test involving calcium infusion, 2 mg/kg in one minute, seems to give a diagnostic response in most patients with insulinomas, few false positive results and few side effects. We have used this test for four years and found it safe and easy to perform. It has given diagnostic response in three patients with insulinomas and no false positive results in 27 other patients.

Calcium Gluconate↗
PubMed1989

Chemotherapy and endocrine function in lung cancer.

To investigate whether cyclic chemotherapy for lung cancer influenced endocrine function, we monitored thyroxine, cortisol, testosterone, sex hormone binding globulin (SHBG), estradiol, FSH, LH, and transcortin every three weeks in 12 male patients. Treatment regimens consisted of cisplatin and etoposide in 9 patients, or vincristine, doxorubicin, and cyclophosphamide in 3 patients. SHBG and FSH level were significantly elevated after 6 to 9 weeks of therapy, whereas the other variables were unchanged. The results suggest that the therapy induces endocrine gonadal dysfunction. The increments in SHBG levels reflect a considerable fall in free testosterone, and may effect alterations in total androgen/estrogen ratios. The mechanism underlying the increased SHBG levels is unknown.

Aged↗
PubMed1988

ACTH deficiency, hyperprolactinemia and benign intracranial hypertension. A case report.

A 26-year-old female with ACTH deficiency, hyperprolactinemia and benign intracranial hypertension is reported. Her symptoms of adrenocortical insufficiency and persistent amenorrhea appeared after her last child birth one year previously. During an infectious disease she became critically ill with hypotension and was treated with iv penicillin. A bacterial infection was, however, not diagnosed. After 4 days she developed symptoms and signs of intracranial hypertension. She improved gradually within 10 days without specific therapy against the intracranial pressure. Endocrine investigation disclosed a secondary adrenocortical failure. The lesion appeared to be located in the pituitary gland since plasma ACTH and cortisol did not respond to CRH. A moderately elevated serum PRL was found, whereas the pituitary reserves of TSH, GH, LH and FSH were normal, as was a computed tomographic scan of the pituitary gland. The patient was given cortisone substitution therapy and recovered immediately. Within the following year she regained normal menstruations and became pregnant. A possible autoimmune etiology of her isolated ACTH deficiency precipitated in the puerperium is discussed.

Adrenal Cortex↗
PubMed1986

Effect of different beta-blocking drugs and adrenaline on the conversion of thyroxine to triiodothyronine in isolated rat hepatocytes.

The in vitro effect of various selective and non-selective beta-blocking drugs and adrenaline on the conversion of thyroxine (T4) to triiodothyronine (T3) was studied in suspensions of isolated rat hepatocytes after 90 min of incubation. Compared with the untreated controls propranolol caused a dose-related inhibition of the T4 to T3 conversion in conc of 100, 200 and 400 microM. The other beta-blocking drugs studied, timolol, oxprenolol, atenolol and metoprolol, were without any effect on this in vitro conversion. Propranolol did not interfere with the cellular association of T4 or the degradation of T4 and T3. Adrenaline 200 microM caused a small decrease of T3 in the medium and a corresponding increase in the intracellular content of T3. The inhibitory effect of propranolol 200 microM was not antagonized by equimolar concentrations of adrenaline. Our study suggests that the inhibitory effect of propranolol on the conversion of T4 to T3 in hepatocytes is caused by a direct chemical effect of the drug unrelated to its beta-blocking and membrane stabilizing properties.

Adrenergic beta-Antagonists↗
PubMed1985

Influence of glucose, insulin and sera from diabetic patients on the prostacyclin synthesis in vitro in cultured human endothelial cells.

The effects of glucose, insulin and sera from Type 1 (insulin-dependent) diabetic patients on the synthesis of prostacyclin in vitro were studied in confluent primary cultures of human endothelial cells. The stable metabolite, 6-keto-prostaglandin F1 alpha, was measured in growth medium after 24 h of incubation with endothelial cells in a buffer incubated with the cells for 10 min on a rocker platform, and in a buffer solution of ruptured cells. Glucose (11, 15, 20 or 25 mmol/l) and glucose (11 mmol/l) plus insulin (10(3), 10(4) or 10(6) mU/l) in growth medium did not have any effects on the prostacyclin synthesis. The prostacyclin synthesis was significantly reduced in cell cultures incubated with medium supplemented with 10% serum from patients with Type 1 diabetes (p less than 0.01) compared with cultures incubated with pooled serum from healthy blood donors. These data suggest that diabetic sera inhibit the prostacyclin synthesis in cultured endothelial cells unrelated to the glucose and insulin levels.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Effects of intravenously infused porcine GIP on serum insulin, plasma C-peptide, and pancreatic polypeptide in non-insulin-dependent diabetes in the fasting state.

Eight fasting patients with non-insulin-dependent diabetes (NIDD) and six healthy controls were given an intravenous infusion of porcine gastric inhibitory polypeptide (GIP). During the GIP infusion mean plasma pancreatic polypeptide level increased significantly in both groups, whereas the mean serum insulin level increased in the NIDD group only, indicating a more important role for GIP in these patients than in healthy subjects.

Adult↗
PubMed1984

Amiodarone inhibits the conversion of thyroxine to triiodothyronine in isolated rat hepatocytes.

Previous studies have shown decreased T3 and increased T4 and rT3 serum levels in subjects treated with amiodarone. We studied the acute effect of amiodarone on the in vitro conversion of T4 to T3 in suspensions of isolated rat hepatocytes. Iodine and melperone, another class III antiarrhythmic drug, were included in the study as controls. Amiodarone (60 microM) totally blocked the formation of T3 from T4, whereas concentrations of 6 and 0.6 microM reduced T3 formation to 13.7 +/- 10.6% and 63.9 +/- 15.9% (+/- SD), respectively, compared with untreated controls. The drug solvent did not affect the conversion rate. Iodide (120 microM) had an inhibitory effect of approximately 10% compared with the controls, whereas melperone did not affect this in vitro conversion. Amiodarone (60 microM) caused a slight but significant reduction of the cellular uptake of [125I]T4 after 10 min of incubation, whereas the 60 min values were unaltered. Our study indicates that amiodarone inhibits the 5'-monodeiodination of T4 to T3 in a dose-related manner. It is suggested that the antiarrhythmic activity of the drug is related to its inhibitory effect on the conversion of T4 to T3.

Amiodarone↗
PubMed1983

Expression of FcIgG receptors on cultured fetal rat brain cells. Studies on normal, preneoplastic and malignant cells.

The expression of FcIgG receptor (FcR) was studied during various stages of growth and subculturing of: (1) fetal rat brain cells (FBC); (2) FBC during in vitro neoplastic transformation after a transplacental pulse of the alkylating carcinogen ethylnitrosurea in vivo, and (3) an established neoplastic brain tumor cell line. Hemadsorption of antibody-coated sheep erythrocytes was used for the detection of FcR-positive cells. Such cells were not detected in cryostat sections of fetal rat brains, but in primary cultures of FBC 1 day after the explantation. FcR-positive cells were present throughout the logarithmic-growth phase. When reaching confluency after 5-7 days in culture. FcR-positive cells could not be detected. In the secondary cultures the occurrence of FcR-positive cells showed a similar variation related to growth: The growth-related receptor was also present on cells growing into arteficial defects in confluent cultures, while the resting cells in the same cultures were FcR-negative. With further subculturing the cells became epithelioid and slowly growing without FcR. Morphologically induced differentiation of such epithelioid cells by 12-O-tetra-decanoyl phorbol-13-acetate did not change the FcR expression. We did not detect any change in the receptor expression related to the malignant transformation, and the malignant cell line was FcR-negative. Expression of FcR on FBC undergoing malignant transformation therefore seems to be mainly connected to the mode of growth (log-phase versus confluence).

Animals↗
PubMed1983

Effects of hydrocortisone and protein synthesis inhibitors on FcIgG receptors on cultured fetal rat brain cells.

The in vitro effect of protein synthesis inhibitors on FcIgG receptor (FcR) expression was studied in secondary cultures of fetal rat brain cells (FBC). Hemadsorption of antibody-coated sheep erythrocytes was used for the detection of FcR-positive cells. The addition of actinomycin D 0.5 and 2.5 micrograms/ml or cycloheximide 1.0 and 5.0 micrograms/ml to the growth medium did not change the FcR activity after 4 and 12 h. When the cells were cultured in medium containing hydrocortisone 10(-6) and 10(-7) M for 1, 2 or 3 days, the number of FcR-positive cells increased markedly. Confluent cultures of FBC and FBC undergoing in vitro neoplastic transformation were FcR negative. Hydrocortisone did not induce FcR activity in these cultures. The results indicate that the persistence of FcR on cultured FBC is not dependent on de novo protein synthesis. Hydrocortisone seems to prolong the period of FcR expression in FcR-positive cells.

Animals↗
PubMed1983

Metabolism of thyroid hormones in isolated rat hepatocytes: studies on the influences of carbamazepine and phenytoin.

The in vitro handling of thyroid hormones was studied in isolated rat hepatocytes by measuring 1) the cellular uptake of T4, 2) the conversion of T4 to T3 and 3) the degradation of T4 and T3. The in vitro conversion of T4 to T3 increased significantly by adding ethanol 2% or carbamazepine (CBZ) 400 microM in ethanol 2% to the incubation medium. As there was no difference between ethanol and CBZ/ethanol on the T3 formation, this effect was probably caused by ethanol. The T3 formation was unaffected by phenytoin (PHT) in conc. up to 400 microM, while propylthiouracil (PTU) 100 and 400 microM inhibited the conversion completely. The T4 to T3 conversion in hepatocytes from rats pretreated with CBZ or PHT for 2 weeks was not significantly different from untreated controls. The cellular uptake of T4 was reduced by about 30% in the presence of PHT and unaltered by CBZ and ethanol. The degradation of T4 and T3 was not influenced by the in vitro addition of CBZ or PHT, nor was the degradation of T4 and T3 significantly different from untreated controls in hepatocyte suspensions from CBZ or PHT pretreated rats. Our findings suggest that the handling of thyroid hormones in isolated rat hepatocytes is not influenced by the in vitro or in vivo exposure to CBZ or PHT.

Animals↗
PubMed1982

Systolic time intervals in the evaluation of thyroid dysfunction.

Systolic time intervals, the pre-ejection period (PEP), left ventricular ejection time (LVET) and PEP/LVET ratio were studied in ten thyrotoxic and ten hypothyroid patients. LVET and PEP intervals were corrected for heart rate (LVETc and PEPc). The measurements were repeated after 1-28 months when the patients were euthyroid following appropriate therapy. Compared with the euthyroid values, the PEPc intervals and PEP/LVET ratios were significantly decreased (p less than 0.01) in the thyrotoxic and increased (p less than 0.001) in the hypothyroid patients. In both groups the LVETc intervals were significantly prolonged (p less than 0.001). In four of the hypothyroid patients the PEP/LVET ratios were markedly increased (above 0.60, mean 0.66), and above 0.41 in the euthyroid state (reference value 0.35 +/- 0.05). In the other hypothyroid patients and in thyrotoxic patients the euthyroid PEP/LVET ratios were within the reference values. The systolic time intervals were not influenced by propranolol therapy in the thyrotoxic patients. Our results suggest increased myocardial contractility unaffected by adrenergic blockade in thyrotoxicosis, and reduced contractility in hypothyroidism.

Adult↗
PubMed1982

Immunological characterization of mononuclear cells in thyroid gland and blood in Graves' disease, multinodular goiter and papillary carcinoma.

Mononuclear cell infiltrates in thyroid gland tissue sections from patients with drug-treated Graves' disease (n = 5), non-toxic nodular goiter (n = 12) and papillary carcinoma (n = 5) were characterized by immunological membrane receptors. T lymphocytes were identified using 2-aminoethylisothiouronium bromide hydrobromide (AET)-treated sheep erythrocytes (E) (E-AET). E sensitized with rabbit IgM antibodies (A) and human complement (C) (EAC) were used to detect receptors for C3b (B lymphocytes and monocytes) or C3d (B lymphocytes). E sensitized with rabbit IgG antibodies were used to detect receptors for the Fc portion of IgG (FcR; lymphocytes and monocytes). The results indicate that T and B lymphocytes infiltrate the thyroid gland in Graves' disease as well as in nodular goiter. T lymphocytes seemed to predominate in both disorders. In thyroid papillary carcinoma the number of B and T lymphocytes was negligible. However, EA absorbed strongly to sections from 3 of the 5 tumors studied, indicating the presence of FcR on tumor cells or infiltrating host cells. The percentage of active and total T lymphocytes in peripheral blood from the patients with drug-treated Graves' disease was markedly reduced (9 +/- 5 and 28 +/- 11%, controls 22 +/- 9 and 68 +/- 11%; p less than 0.01 and less than 0.001). In patients with nodular goiter the percentage of total T lymphocytes was slightly, but significantly decreased (p less than 0.05). We suggest that the marked decrease in blood T lymphocytes observed in Graves' disease might be caused by the drug therapy. In nodular goiter the predominance of T lymphocyte infiltration together with a slight decrease in blood T lymphocytes suggest that autoimmune mechanisms are involved in the pathogenesis.

Adult↗
PubMed1982

ACTH suppression after oral administration of cortisone in Addisonian and adrenalectomized patients.

Plasma cortisol and the corresponding ACTH concentrations were determined before, and for 6 h following a single oral dose of 25 mg cortisone acetate in 7 patients with Addison's disease, 6 patients adrenalectomized for Cushing's disease and 1 patient adrenalectomized for congenital adrenal hyperplasia. The basal plasma cortisol concentrations 12 h after an evening dose of cortisone acetate 12.5 mg were below 100 nmol/l, and the corresponding ACTH concentrations were markedly elevated in all patients. Great interindividual variations were found in cortisol peak concentrations (Cmax) and the time to peak values, but without significant differences between the two patient groups. The maximal ACTH suppression occurred within 60-330 min after the cortisol Cmax, and was not significantly different in the two groups. The suppressed plasma ACTH concentrations were considerably above normal in 3 of the patients with Addison's disease and in 4 of the 6 patients adrenalectomized for Cushing's disease, including 2 patients with Nelson's syndrome. A similar degree of impaired ACTH suppression in patients with Addison's disease as in adrenalectomized patients suggests the occurrence of a secondary hypothalamic-pituitary dysfunction with ACTH hypersecretion in Addison's disease. The adequacy of the commonly used adrenocortical replacement therapy and its possible relation to the impaired ACTH suppression is discussed.

Addison Disease↗
PubMed1981

Plasma cortisol concentrations after oral substitution of cortisone in the fasting and non-fasting state.

Nine corticosteroid-substituted patients received oral cortisone acetate in the fasting state and together with a breakfast meal. Plasma cortisol concentrations were determined before, after 30 min, and at 1-hour intervals until 6 hours after drug ingestion. There were great interindividual variations in the time to peak values (tmax), the peak concentrations (Cmax), and the areas under the time-concentration curves (AUC0--6h). The AUC and Cmax values were significantly increased when cortisone tablets were ingested with food compared to the values obtained in the fasting state (p less than 0.01 and p less than 0.05 respectively), whereas tmax values were not significantly different. The differences were minor and probably without clinical implications.

Addison Disease↗
PubMed1981

The influence of carbamazepine on thyroid hormones and thyroxine binding globulin in hypothyroid patients substituted with thyroxine.

Carbamazepine (CBZ) decreases the serum concentration of thyroid hormones. It is proposed that CBZ increases the extra-thyroidal metabolism of thyroid hormones. In order to test this hypothesis CBZ was given to nine hypothyroid patients substituted with thyroxine (T4). A significant decrease in serum concentrations of T4, calculated free T4 (FT4), triiodothyronine (T3), and calculated free T3(FT3) was found after 3 weeks of CBZ medication. The serum concentrations of TSH and the T4:T3 ratios were unaltered, while the serum concentrations of T4-binding globulin (TBG) increased markedly in eight of the nine patients. These findings support the hypothesis of a CBZ induced increase in the extra-thyroidal metabolism of thyroid hormones.

Adult↗