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Biomedical subjects

L Tegler

Publications and source records attributed to L Tegler.

12 recordsLinked to original sources
PubMed1992

Hypoglycaemia and cardiac arrhythmias in patients with type 2 diabetes mellitus.

Improved blood glucose control by insulin treatment in patients with Type 2 (non-insulin dependent) diabetes mellitus increases the risk for hypoglycaemic episodes. Our objective was to investigate if hypoglycaemia causes electrocardiographic changes and cardiac arrhythmias in patients with Type 2 diabetes. Six insulin-treated patients with Type 2 diabetes and no known cardiac disease took part in the study. Hypoglycaemia was induced by insulin infusion aiming at a plasma glucose less than or equal to 2.0 mmol l-1 or hypoglycaemic symptoms. All patients experienced hypoglycaemic symptoms. The median lowest arterial plasma glucose was 2.0 mmol l-1. Arterial plasma adrenaline concentration increased from 0.4 +/- 0.1 (mean +/- SE) to 6.9 +/- 0.3 nmol l-1 (p less than 0.001) while serum potassium was lowered from 4.1 +/- 0.3 mmol l-1 to 3.5 +/- 0.2 mmol l-1 (p less than 0.001). The heart rate increased significantly during hypoglycaemia except in one patient who developed hypoglycaemic symptoms and a severe bradyarrhythmia at a plasma glucose of 4.4 mmol l-1. One patient developed frequent ventricular ectopic beats during hypoglycaemia while four patients showed no arrhythmia. ST-depression in ECG leads V2 and V6 was observed during hypoglycaemia in five patients (p less than 0.05) and four patients developed flattening of the T-wave. In conclusion, the study supports the hypothesis that hypoglycaemia in patients with Type 2 diabetes may be hazardous by causing cardiac arrhythmias.

Arrhythmias, Cardiac↗
PubMed1991

Thyroid epithelial cell proliferation in xenotransplanted human toxic nodular goitre is increased by Graves' IgG.

Human toxic nodular goitre tissue was xenotransplanted to athymic mice. Transplant function was analysed as 18-h thyroid transplant uptake of iodide-125 at day 21 and again at 10 weeks after transplantation. Graves' IgG or IgG from healthy donors was given intraperitoneally daily day 22-35. Epithelial cell proliferation in thyroid tissue transplants from human toxic nodular goitre and from normal thyroid glands was analysed by continuous [3H]thymidine administration for 4 days between day 21 and 24 and for 12 days between day 21 and 33 in separate series given daily injections of Graves' IgG or normal IgG during the same period. After administration of Graves' IgG, the 18-h iodide-125 uptake by the toxic nodular tissue transplants was 7 times higher at 10 weeks than at 3 weeks. Control IgG gave a corresponding 1.6-fold increase. The fraction of labelled cells after [3H]thymidine incorporation was 18 and 56% in toxic nodular goitre transplants and 4 and 48% in normal thyroid tissue transplants after daily Graves' IgG administration for 4 and 12 days, respectively, but only 1.3% in both types of tissue transplants after administration of normal IgG. Graves' IgG therefore seems to be able to stimulate cell proliferation in toxic nodular goitre tissue.

Animals↗
PubMed1990

Plasma exchange in endocrine ophthalmopathy.

We studied the effects of intensive plasma exchange on endocrine ophthalmopathy in 12 patients with Graves' disease and one with Hashimoto's thyroiditis. All patients were euthyroid at the time of plasma exchange. All but five had concomitant treatment with azathioprine. Each patient had a treatment period consisting of six plasma exchanges performed in 2-3 weeks; two patients were treated in two periods. Each time a mean of 2.4 liters plasma was exchanged. There was a prompt reduction in the concentration of circulating immune complexes and/or thyrotropin receptor antibodies following plasma exchange. Six of the 13 patients improved their proptosis; their median duration of eye symptoms before treatment was less than 8 months. In patients suffering from eye symptoms for more than 1 year improvement was rare. Overall the Hertel values were 24.1 +/- 4.4 (SD) before and 22.8 +/- 3.4 after plasma exchange for the left eyes (P = 0.07) and 23.8 +/- 4.0 before and 23.0 +/- 3.8 after for the right eyes (P = 0.09). Nine patients altogether improved their ophthalmopathy index and periorbital oedema. In patients with disabling endocrine ophthalmopathy plasma exchange may sometimes be of value to induce a relief of the ophthalmopathy; when it is used it should be instituted before fibrotic changes occur. We suggest that concomitant immunosuppressive drugs should be given to prevent rebound phenomenon induced by plasma exchange. To establish the role of plasma exchange in the treatment of endocrine ophthalmopathy controlled studies should be performed.

Adult↗
PubMed1987

Effect of therapy on the serum thyroglobulin concentration in patients with toxic diffuse goiter, toxic nodular goiter and toxic adenoma.

Serum thyroglobulin (S-Tg) was measured in 104 patients with thyrotoxicosis, 59 of whom had toxic diffuse goiter (Graves' disease), in 30 with toxic nodular goiter and in 15 with toxic adenoma. Before treatment, most patients had increased S-Tg concentrations, regardless of what type of thyrotoxicosis they had. After therapy the course of the S-Tg varied, two major patterns being observed: the S-Tg concentration increased in some patients but decreased in others, although no relationship could be found between these patterns and the outcome of therapy, the presence or absence of thyroglobulin antibodies (Tg-ab) or changes in the Tg-ab titer. However, the median pretreatment concentrations of S-Tg were significantly higher in patients with toxic nodular goiter and toxic adenoma than in those with toxic diffuse goiter (p less than 0.001 and p less than 0.05, respectively), but did not differ significantly between patients with toxic nodular goiter and toxic adenoma. The lowest posttreatment S-Tg concentrations were found after surgery, irrespective of type of thyrotoxicosis. The median pretreatment and posttreatment S-Tg concentrations in patients with toxic diffuse goiter who relapsed, did not differ from those patients in remission. This was also true of patients with toxic nodular goiter. In both groups, however, there was a tendency towards higher pretreatment S-Tg values in patients who subsequently relapsed. Serial determinations of S-Tg, on the other hand, are of limited value in predicting the risk of recurrence, independent of which type of thyrotoxicosis is involved.

Adolescent↗
PubMed1987

Effects of thyroid stimulating immunoglobulin on function and morphology of xenotransplanted toxic diffuse, toxic nodular and normal thyroid tissue.

In order to examine the properties of human thyroid tissue, toxic diffuse goiter (TDG), toxic nodular goiter (TNG) and normal thyroid tissue were transplanted to nude mice. Starting 3 and 10 weeks after the transplantation the mice were given 14 daily injections of control serum or serum containing thyroid stimulating immunoglobulin (TSI). The uptake and release of 125I were repeatedly measured externally. The uptake and unstimulated release of 125I was lowest in TDG transplants, highest in TNG transplants, and intermediate in transplants of normal thyroid tissue. The findings were similar at both 3 and 10 weeks. Injections of TSI reduced the biological half-time of the tracer in TDG and normal transplants, but had no significant effect on TNG transplants. Light and electron microscopic studies showed that hyperplastic TDG tissue underwent involution after transplantation, whereas TNG and normal thyroid tissue remained unchanged. Injection of TSI reactivated TDG tissue; morphometry showed that the absolute and relative volumes of the follicle cells were more than doubled, with a corresponding decrease in the volume of the follicle lumen, and mitotic figures were common. Similar findings were seen in normal transplants, whereas the effect of TSI on TNG tissue was less pronounced. In summary, our observations show that serum from a patient with Graves' disease stimulated iodine release and induced follicle cell hyperplasia and probably also follicle cell multiplication in transplanted normal and TDG tissue, but had a lesser effect on TNG tissue.

Animals↗
PubMed1979

Non-selective and selective beta-1-adrenoceptor blocking agents in the treatment of hyperthyroidism.

Treatment for one month with propranolol or atenolol, a selective beta-1-adrenoceptor blocking agent, was evaluated in 20 hyperthyroid patients. The patients improved to the same extent on either drug, as shown by a clinical diagnostic index. Basal metabolic rate decreased by 11% during both treatments, while it was unchanged in seven untreated hyperthyroid controls. Thyroxine concentration did not change during any treatment. During propranolol treatment T3 decreased from 4.6 to 3.9 nmol/l, while no changes were observed during atenolol treatment or in the control group. No significant changes were seen in free T4, free T3 or rT3 concentrations on any treatment, although free T3 was observed to decrease slightly during propranolol treatment. Thus, the improvement of the clinical symptoms of hyperthyroidism cannot be explained by diminished thyroid hormone concentrations in serum, since the reduction was small during propranolol and absent during atenolol treatment.

Adolescent↗
PubMed1976

Controlled treatment of primary hypertension with propranolol and spironolactone. A crossover study with special reference to initial plasma renin activity.

Twenty-seven patients with hypertension were randomly allocated to a 10 month crossover study. Treatment consisted of spironolactone (200 mg/day for 2 months), propranolol (320 mg/day for 2 months) and combined administration of both drugs at half the dosage. Between treatment periods placebo was given for 2 months. Fourteen patients were previously untreated. The average pretreatment blood pressure for the entire group was 188/114 +/- 16/7(mean +/- standard deviation) mm Hg supine and 188/118 +/- 20/9 mm Hg standing. Both spironolactone and propranolol reduced blood pressure significantly in both the supine and standing positions. Upright plasma renin activity was determined by radioimmunoassay of angiotensin I. The average initial level was 1.9 +/- 1.2 (range 0.4 to 5.0) ng/ml/hr. There was a close correlation between plasma renin activity and the effects of the drugs: With increasing renin level the response to propranolol was better whereas the opposite was true for spironolactone. The combination of spironolactone and propranolol decreased the blood pressure still further in the supine and standing positions, irrespective of initial plasma renin activity. All patients achieved a normal supine pressure. Blood pressure and plasma renin activity returned toward pretreatment values during placebo administration. It is concluded that pretreatment levels of plasma renin activity can predict the antihypertensive response to propranolol and spironolactone. The combination of the two drugs, which have different modes of action, will effectively reduce blood pressure in hypertension. The results support the concept that the renin-angiotensin-aldo-sterone system may be involved in primary hypertension.

Adult↗
PubMed1976

Renin concentrations and effects of propranolol and spironolactone in patients with hypertension.

In a crossover study 32 patients with hypertension were randomly allocated to treatment with spironolactone 200 mg/day for two months, propranolol 320 mg/day for two months, and a combination of both drugs at half the dose. Between the treatments placebo was given for two months. Both spironolactone and propranolol lowered the blood pressure significantly in both positions. The initial plasma renin activity (PRA) levels ranged from 0-4 to 5-0 mug angiotensin I l-1 h-1, and there was a close correlation between these levels and the effects of the drugs: with increasing PRA the response to propranolol was better while the opposite was true for spironolactone. Spironolactone reduced the blood pressure more at eight than at four weeks, while no such difference could be shown for propranolol. Spironolactone and propranolol together decreased the blood pressure still further irrespective of the initial PRA. All patients achieved a normal supine blood pressure.

Administration, Oral↗
PubMed1976

Thyroid function after subtotal thyroidectomy for hyperthyroidism. A follow-up study with special reference to thyroid stimulating hormone (TSH) and the thyrotropin releasing hormone (TRH) stimulation test.

193 patients operated on for hyperthyroidism were examined at follow up a mean 4.5 years after operation (range 1-6 years). The patients were examined clinically and biochemically. It was found that 4.6% had a permanent paralysis of the recurrent nerve and 2.6% a permanent hypoparathyroidism. Recurrent hyperthyroidism was found in 2.6%. The patients were grouped according to the results of basal S-TSH and the TRH-stimulation test. Within the groups it was found that all patients with a normal basal TSH were clinically euthyroid. 35 patients had a raised basal TSH or a hypothyroid pattern in the TRH-test, or both. Among these, 14 clinically hypothyroid patients were found. The remaining 21 patients were euthyroid clinically and were classified as subclinically hypothyroid. The levels of basal TSH were significantly higher in subclinically hypothyroid patients than in euthyroid patients and still higher in clinically hypothyroid patients. The response to TRH stimulation was also higher in the hypothyroid patients than in the subclinically hypothyroid patients. It was also found that the proportion of clinically hypothyroid patients was significantly higher, after 5 years than after one year. Since it cannot be decided if the patients with a subclinical hypothyroidism are at risk for manifest disease a close follow up of these patients is recommended.

Adolescent↗