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Biomedical subjects

A D Toft

Publications and source records attributed to A D Toft.

At least 91 records · Page 5Linked to original sources
PubMed1983

Hyperthyroidism due to a thyrotrophin-secreting microadenoma.

We report a 63-year-old female with a TSH-secreting pituitary adenoma causing hyperthyroidism. This case is apparently unique, and challenges the present concept of dividing patients with inappropriate TSH secretion into tumour and non-tumour groups on the basis of conventional pituitary fossa radiology.

Adenoma↗
PubMed1983

The effect of minor increments in plasma thyroxine on heart rate and urinary sodium excretion.

We studied day/night (D:N) patterns of urinary sodium excretion and the 24 hour ambulatory electrocardiogram in seven normal subjects before and during the administration of T4. Thyroxine increased thyroid hormone levels within the normal range and inhibited the plasma TSH response to TRH. This was associated with a significant decrease in D:N sodium excretion (P less than 0.01) and D:N urine flow (P less than 0.01), a significant increase in mean nocturnal heart rate (P less than 0.01), and a lesser increment in mean daytime heart rate (P less than 0.05). These responses to small changes in thyroid hormone levels suggest that the anterior pituitary is not alone in recognising minor thyroid hormone excess. The clinical implication is that some patients with a normal T3 and T4 but an impaired TSH response to TRH might benefit from antithyroid treatment.

Adult↗
PubMed1982

Abnormal left ventricular function in hyperthyroidism: evidence for a possible reversible cardiomyopathy.

We assessed the effects of exercise and beta-adrenoceptor blockade on left ventricular ejection fraction (LVEF) measured by radionuclide ventriculography in nine patients with uncomplicated hyperthyroidism. Patients were studied in both the hyperthyroid and euthyroid states. The hyperthyroid state was characterized by a high LVEF at rest but--paradoxically--by a significant fall (P less than 0.01) in LVEF during exercise. At the same workload and at the same heart rate, patients had a restoration of the normal rise in LVEF during exercise when they were euthyroid. The LVEF was greater during exercise (P less than 0.02) when the patients were euthyroid than when they were hyperthyroid. Pretreatment with propranolol caused similar reductions in resting LVEF in the hyperthyroid and euthyroid states; the drug attenuated the rise in LVEF during exercise when the patients were euthyroid, but did not influence the exercise-induced reduction in LVEF in hyperthyroidism. The abnormal left ventricular function observed during exercise in hyperthyroidism suggests a reversible functional cardiomyopathy, independent of beta-adrenoceptor activation, that is presumably a direct effect of an excess in circulating thyroid hormones.

Adult↗
PubMed1982

Does calcitonin cause hypocalcaemia after thyroidectomy?

Plasma calcitonin, parathyroid hormone, total thyroid hormones and calcium were measured in 6 patients before, during and after thyroidectomy for hyperthyroidism. In 4 patients, plasma calcium fell postoperatively by 0.23--0.46 mmol/l, but there was no change in calcitonin or parathyroid hormone levels. In one patient, in whom there was a postoperative fall in plasma calcium of 0.55 mmol/l, thyroid hormones rose to a peak at 1 h and calcitonin to a peak at 12 h after resection. However, the rise in calcitonin occurred 8 h after the initial decrease in plasma calcium. In this patient, parathyroid hormone levels showed a slight rise only. It is concluded that, while thyroid hormones and calcitonin may leak from the damaged thyroid remnant after surgery, it is unlikely that calcitonin is important in the production of postoperative hypocalcaemia. However, impaired parathyroid hormone secretion may be a contributing factor.

Adolescent↗
PubMed1982

Cardiovascular responses in hyperthyroidism before and during beta-adrenoceptor blockade: evidence against adrenergic hypersensitivity.

The relationship between the sympathetic nervous system and cardiovascular responses has been studied indirectly in ten hyperthyroid patients and age matched euthyroid controls. Nyctohemeral variations in heart rate, and heart rate and blood pressure responses to exercise were measured before and during beta-blockade with slow-release propranolol. Both groups showed a parallel variation in heart rate over 24 h, with an increase in heart rate inthe hyperthyroid group that was the same during the day (27.9 +/- 0.95 beats/min) and during the night (26.7 +/- 0.75 beats/min). Similarly, the increase in resting heart rate (32.7 +/- 4.4 beats/min) in the hyperthyroid group was close to the increase in peak exercise-induced heart rate (25.0 +/- 4.7 beats/min). Adequate beta-blockade was achieved in all subjects as evidenced by a percentage reduction in peak exercise heart rate of 25-45%. Propranolol caused a greater reduction in daytime than night-time heart rate in both groups and blunted the response to exercise. Following beta-blockade, the mean percentage reduction in heart rate and systolic blood pressure during exercise, and heart rate responses over 24 h were similar in hyperthyroid and euthyroid groups. The closest correlation between thyroid hormone levels and heart rate was that of serum total tri-iodothyronine (T3) and nocturnal heart rate during beta-blockade (r=0.92; P less than 0.0001). It is concluded that excess circulating thyroid hormones exert a direct effect on the cardiovascular system additive to the sympathetic nervous system and that there is no evidence of adrenergic hypersensitivity in hyperthyroidism.

Adult↗
PubMed1982

Nocturnal natriuresis in hyperthyroidism.

We measured urine flow and the renal excretion of total solute, sodium, potassium and calcium in eleven patients with hyperthyroidism before and after treatment. Mean nocturnal sodium excretion was significantly greater (P less than 0.05) during hyperthyroidism and was unaccompanied by any significant alterations in day time or 24-h values. As a result of this nocturnal natriuresis in hyperthyroidism significant changes were noted in the ratios of day/night sodium excretion (P less than 0.005) and urinary flow (P less than 0.05). The change in ratio of day/night sodium excretion resulting from treatment of hyperthyroidism was shown to correlate significantly with the change in plasma total triiodothyronine (r=0.73, P less than 0.01). Twenty-four hour urinary calcium output was significantly greater (P less than 0.02) in hyperthyroidism but there was no significant alteration in the day/night pattern of excretion.

Adult↗
PubMed1982

Left ventricular function in hypothyroidism. Responses to exercise and beta adrenoceptor blockade.

The effects of exercise and beta adrenoceptor blockade on left ventricular function were assessed in eight patients with hypothyroidism before and during thyroxine replacement treatment. Left ventricular ejection fraction, measured by radionuclide ventriculography, was reduced in hypothyroid patients at rest and on exercise. The rise in ejection fraction with exercise was, however, similar in both groups. Pretreatment with intravenous propranolol reduced the ejection fraction at rest 9% in both hypothyroid and euthyroid patients and reduced the rise on exercise. Directional changes in a second index of myocardial contractility based on the shape of the ventricular volume curve paralleled the changes in the ejection fraction. Left ventricular function is therefore reversibly depressed by thyroid hormone deficiency but responses to exercise and beta adrenoceptor blockade are normal. There is no evidence of altered adrenergic sensitivity in the control of myocardial contractility in hypothyroidism.

Adult↗
PubMed1982

What is the significance of raised plasma TSH levels after thyroid surgery?

Thyroid function was assessed prospectively for five years in 73 patients treated surgically for Graves's disease. No patient developed hypothyroidism after the sixth postoperative month, despite the presence of raised plasma TSH levels in 70 per cent of euthyroid patients at the end of the first year. Indeed, in those with evidence of temporary hypothyroidism (low T4, raised TSh at 3 months but normalisation of T4 at 6 months) plasma TSH continued to fall for up to three years. The majority (6) of patients developing recurrent hyperthyroidism did so within the first year, but in one of three patients who relapsed subsequently, plasma TSH had been elevated at one year. Plasma TSH cannot be used to predict thyroid status following surgery for Graves' disease. Although regular review remains necessary, it should not include measurement of TSH unless this is needed to confirm the validity of a low thyroxine level after the third postoperative month and before starting permanent replacement therapy.

Adult↗
PubMed1982

Prolactin response to metoclopramide in hyperthyroidism.

The response of PRL to the oral administration of the dopamine receptor-blocking agent metoclopramide and the effect of metoclopramide on the TRH-induced release of PRL and TSH were measured in eight patients with hyperthyroidism and in eight age- and sex-matched euthyroid controls. As expected from the known direct inhibitory influence of thyroid hormones on pituitary TSH secretion, there was no TSH rise in response to metoclopramide in either group. PRL levels, on the other hand, rose significantly after the administration of metoclopramide in both the hyperthyroid and euthyroid subjects (P less than 0.0005 at 60 and 120 min). However, the increase in PRL at 120 min was significantly less in the hyperthyroid subjects than in the euthyroid controls (P less than 0.0025). Furthermore, the administration of metoclopramide failed to reestablish normal responsiveness of either PRL or TSH to TRH in the hyperthyroid subjects. We have previously suggested that thyroid hormones inhibit PRL secretion by stimulating the hypothalamic secretion of dopamine. These results suggest, however, that elevated levels of thyroid hormones also inhibit PRL release directly at the anterior pituitary level.

Administration, Oral↗
PubMed1981

Atrial fibrillation and isolated suppression of the pituitary-thyroid axis: response to specific antithyroid therapy.

Four patients are described with persistent atrial fibrillation associated with normal plasma total thyroxine (T4) and triiodothyronine (T3) but an absent plasma thyrotrophin (TSH) response to intravenous thyrotrophin releasing hormone (TRH). Initial cardioversion failed to establish sinus rhythm in three of the four patients. Following specific antithyroid therapy to lower thyroid hormone levels sufficient to allow a normal TSH response to TRH sinus rhythm was established in all four patients, one spontaneously and three after cardioversion. Stable sinus rhythm has persisted in three patients over a 2-yr follow-up period. In the presence of atrial fibrillation, an absent plasma TSH response to TRH should be considered sufficient grounds for antithyroid therapy even if plasma total T4 and T3 are within the expected normal range.

Atrial Fibrillation↗
PubMed1981

Patterns of plasma cortisol and ACTH concentrations in patients with Addison's disease treated with conventional corticosteroid replacement.

Plasma cortisol and adrenocorticotrophin hormone (ACTH) profiles were estimated in twelve patients with Addison's disease following randomized oral administration of either cortisone acetate (25 mg) or hydrocortisone (20 mg) alternately, at 0900 h on consecutive days. Normal corticosteroid replacement therapy was discontinued from 1200 h on the day prior to the study period. In four patients elevated basal plasma ACTH concentrations were not suppressed to the limit of detection following the administration of either drug, and in three of these no suppression was found following the prolonged administration of pharmacological doses of dexamethasone. Diminished sensitivity of pituitary ACTH secretion to cortisol inhibition may result from chronic loss of negative feedback before and/or after diagnosis and treatment. In three patients elevated basal plasma ACTH concentrations were suppressed adequately during the administration of either drug, but in five, low basal ACTH concentrations following corticosteroid withdrawal suggested chronic inhibition of anterior pituitary corticotrophs by over-replacement with glucocorticoid. However, further study is necessary to determine whether the estimation of ACTH profiles is a more accurate reflection of the adequacy of corticosteroid replacement than the estimation of cortisol profiles alone, and whether this estimation leads to an improvement in patient management. Hydrocortisone (20 mg) achieved higher mean cortisol levels and lower mean ACTH levels than cortisone acetate (25 mg), but either drug may be suitable for glucocorticoid replacement provided the dose is tailored to the individual needs.

Addison Disease↗