[Thyroid gland function in patients with phasic affective disorders (cyclothymia) during lithium treatment].
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Biomedical subjects
Publications and source records attributed to P Bottermann.
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Recently, the radioimmunological determination of C-peptide came into interest because of the jugdement of the remaining function of the islet apparatus in insulin-dependent diabetics. As the degradation of C-peptide preferably takes place in the kidney we performed an intravenous glucose load in 32 patients with kidney diseases. The following results were obtained: 1. In patients with a healthy carbohydrate metabolism a clear correlation exists between the concentration of creatinine on the one hand, the creatinine-clearance and the fasting C-peptide concentration respectively the measured amount of C-peptide on the other hand. 2. The more advanced the renal insufficiency the better is the correlation between the parameter of the kidney function and the C-peptide concentration. 3. In diabetic patients there shows to be no clear correlation between the C-peptide levels and the kidney function. --In insulin-dependent diabetics the amount of C-peptide is only of diagnostic use if the renal function is well known.
In eight normal weight healthy volunteers it was proved by C-peptide assay whether high concentrations of insulin in serum would suppress the secretion of insulin in an autoregulative manner. Insulin combined with glucose, therefore was given intravenously as a single bolus injection as well as an infusion over a period of two hours. Moreover it was proved whether high levels of insulin would suppress the reactivity of the B-cell to sulphonylurea administration. It was demonstrated that the secretion of the B-cell is regulated only by the concentration of the blood sugar, but not by the level of serum insulin. Likewise the stimulation of the B-cell by sulphonyl-urea administration is not suppressed by high concentrations of insulin.
Determinations in 11 patients with anti-thyroid drug therapy of hyperthyreoidism showed, that a pronounced lag period exist between normalisation of thyroid hormone level and TRH responsiveness. The lag period range between 5 and 27 weeks. During this time it is not necessary to give simultaneously thyroid hormones in antithyroid drug therapy to compensate hyperresponsiveness of TSH. - Investigations in 12 volunteers with experimental hyperthyreoidism induced by administration of thyroxine suggest a longterm suppression of the hypophysis to be the cause of the lag period of TSH-secretion. There are some similarities to the ACTH-suppression in therapy with corticosteroids and to the so-called "syndrome of oversuppression" in long lasting treatment with contraceptive drugs.
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After ending a continous treatment with thyroxine the average dropping of the 2,3 DPG level was 0.4 mumol/ml. T4 decreased on the average by 7.6 microgram/ml. One time application of 1 mg thyroxine p.o. led within 24 hours to an increase of the 2,3 DPG level of -chi = 0.2 mumol/ml, the pH in the erythrocytes increased by 0.02 on the average. Blood incubation with thyroxine added in a concentration of -chi = 24 microgram/100 ml showed no increase of 2,3 DPG, pH and phosphate, while there was a significant acidosis and increase of phosphate in the control blood. The lactate production was significantly lower and glucose consumption was significantly higher in the blood with thyroxine.
In a total of 13 volunteers the changes in carbohydrate metabolism was investigated after administration of prednisolone, of buformin, and of a combination of prednisolone and buformin using 3H-labelled glucose. Under steady-state-conditions the glucose-turnover was estimated. Although, the changes of glucose assimilation of labelled and unlabelled glucose was observed to see the magnitude of glucose utilisation and of gluconeogenesis. It was concluded that biguanides enhance the glucose utilisation. Depending on the glucose level at the same time the gluconeogenesis is stimulated or inhibited.
Intravenous glucose tolerance test followed by combined intravenous glucose-glibenclamid tolerance test were performed to differentiate between sulfonylurea-dependent and insulin-dependent diabetics. As a criterion of sufficient sulfonylurea-induced insulin secretion the extent of the difference of the insulin secretion between both tests was taken. If the difference is more than 600/muE/h insulin treatment seems not to be necessary and oral treatment with sulfonylurea derivates seems to be successful. In comparison with the clinical course of 55 patients the criterion was right in 50 cases. 5 patients could not be classified by the clinical course. Their more-secretion of insulin was in between 200 and 550 muE/mlhour.
Calcium, phosphate and alcaline phosphatase levels were determined in the serum of 29 patients with suspected primary hyperparathyroidism. Phosphate clearance according to Kyle, 24 hours urine hydroxyproline excretion during collagen free diet, the excretion of cAMP in the 24 h urine during calcium restricted diet were examined with regard to the diagnostic value and relevance as compared to the consumption of laboratory and staff time. The elevation of the serum calcium levels are not specific and only of minor diagnostic value. It has been found that the highest diagnostic value is given by the Kyle-test using 15 mg Ca ions/kg body weight. No false positive results were recorded. The excretion of hydroxyproline and calcium are only of limited value. Serum alcaline phosphatase and cAMP excretion have no diagnostic significance whereas concentration of serum phosphate may have some value.
Intravenous glucose tolerance tests were performed and changes of blood glucose and insulin concentration were measured to examine whether the diabetogenic effect of glucocorticoides can be compensated by biguanides. Seven standard weight volunteers with a healthy metabolism were given prednisolone and buformin as well as a combination of both. In spite of the reactively higher insulin secretion after treatment with prednisolone the glucose tolerance was reduced. In contrast, treatment with biguanide improved the glucose tolerance while decreasing the insulin secretion. It was nearly possible to compensate the negative effect of prednisolone on the carbohydrate metabolism by biguanides. We, therefore, consider a preventive administration of biguanides to be effective in long term or high dosage administration of glucocorticoides.
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Gliquidone shows a good blood sugar lowering effect over the wide dose range of 30-60 mg in fasting subjects with a healthy metabolism, in spite of the wide range. This behavior suggests that a good therapeutic application is to be expected in diabetics being treated with sulfonylureas.
A study of 13 metabolically normal persons, 12 patients with asymptomatic or latent diabetes and 11 with manifest diabetes showed that 30 mg gliquidone orally prevents or delays the blood sugar rise during repeated small carbohydrate meals with simultaneous stimulation of insulin secretion. This effect was less marked in the normal and asymptomatic or latent diabetic subjects than after glibenclamide 5 mg, while there was no difference between the two drugs in those with manifest diabetes.
A non-recirculating, haemoglobin-free perfusion system was used to evaluate glycolysis in livers from fasted rats. Glycolysis was calculated from lactate and pyruvate production before and after infusion of glucose. In the absence of extracellular glucose glycolysis was small. Stimulation of glycolytic flux occured at extracellular glucose concentrations above 5 mM. Rates were proportional to glucose concentrations. Glycolysis was also investigated in the presence of extracellular lactate, which is a precursor of gluconeogenesis. High glucose concentrations (15-35 mM) were followed by lactate and pyruvate output suggesting that glycolysis was prevailing. Estimated flux rates, however, were significantly lower in the presence of the gluconeogenic precursor. Our results provide arguments that gluconeogenesis and glycolysis interact in order to regulate the peripheral glucose concentration.
The determination of the serum level of TSH, the essential factor in goitrogenesis, was the best indicator in order to recognize imminent recurrence of goitre in strumectomized patients. The functional reserve of the hypothalamic-pituitary system proved to be important: Elevation of basic TSH level and increase of TSH after stimulation with TRH was significantly higher in patients with recurrent goitre. We, therefore, recommend this test for the postoperative surveillance of patients after strumectomy.