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Biomedical subjects

T E Isles

Publications and source records attributed to T E Isles.

At least 37 records · Page 2Linked to original sources
PubMed1981

The relationships between surgical histometry, outcome and pre-treatment in Graves' disease.

Quantitative histometric methods were used to established the relationships between the extent of thyroid lymphocytic infiltration at operation, and outcome exactly 18 months later in 50 surgically-treated Graves' disease patients prepared by carbimazole and triiodothyronine. Periods of pre-operative treatment, surgical technique, histometric analysis and diagnostic criteria were all standardised. Controls (107) were obtained from the forensic laboratory. Thirty-seven patients became euthyroid, but there was no relationship between outcome and epithelial or lymphoid content of the thyroid gland. Neither was there any correlation between the size of lymphoid infiltrate and epithelial mass of the resected thyroids, suggesting that simple lymphocyte infiltrations do not replace thyroid tissue as once thought. The variation in thyroid epithelial content was nearly 3-fold, so that a surgeon, even if able accurately to judge the anatomical mass of the remnant, would still have little or no idea of its functional mass. The scatter of epithelial content was even greater in glands from patients prepared for surgery by propranolol alone (38 glands, variation X 5.5) or propranolol and iodide (32 glands, variation X 5.9). Outcome after sub-total thyroidectomy for Graves' disease seems unrelated to the lymphocyte content of the gland and it is questionable to what extent the surgeon can either predict or control the outcome of thyroidectomy in individual Graves' disease patients.

Adult↗
PubMed1979

Short-term triiodothyronine in prevention of temporary hypothyroidism after subtotal thyroidectomy for Graves' disease.

To determine whether short-term thyroid hormone replacement prevents or merely delays temporary hypothyroidism after surgery for Graves' disease, serum T3, thyroid-stimulating hormone, and T4 were measured every 2 months for 18 months in two groups of Graves' disease patients who had had subtotal thyroidectomy. Group I (18 patients) were given T3 20 microgram four times daily from surgery through the twelfth postoperative month. Group II (18 patients) received no treatment. Hypothyroidism occurred at some time during the 18-month period in 10 group-II patients, but was temporary in 7. Temporary hypothyroidism did not occur in group-I patients, whose mean T4 level rose to that in group II within 2 months of T3 withdrawal. Short-term T3 replacement after surgery for Graves' disease thus prevents (and does not simply delay) temporary postoperative hypothyroidism without increasing the frequency of permanent hypothyroidism.

Adult↗
PubMed1979

Propranolol, triiodothyronine, reverse triiodothyronine and thyroid disease.

Propranolol alone was given to sixteen hyperthyroid, and concomitantly with thyroxine therapy to ten hypothyroid patients. Following treatment of the hyperthyroid group for 1-2 weeks there was a significant decrease in serum triiodothyronine (T3) which correlated with the plasma propranolol steady state concentration. The serum reverse T3 (rT3) rose significantly. Weight loss ceased in this group while weight gain occurred in patients who had a marked fall in serum T3. One patient with T3 toxicosis went into remission. The reduction in serum T3 was maintained in six patients receiving propranolol for more than 1 month. In the hypothyroid group the mean serum T3 level achieved with 0.15 mg thyroxine per day was significantly lower than in a control group who did not receive propranolol. In five patients following propranolol withdrawal there was a significant rise in T3, a fall in rT3 and TSH, and weight loss. Propranol may therefore have a clinically significant and direct action on the peripheral conversion of thyroxine to T3 and rT3.

Adolescent↗
PubMed1979

A boy with low-TSH hypothyroidism.

A case of long-standing mild hypothyroidism is described. This was caused by partial TSH deficiency probably of hypothalamic origin, with no other pituitary hormone deficiencies, although with a decreased response of FSH and LH to LHRH.

Child↗
PubMed1979

The behaviour of the thyroidal iodide trap after subtotal thyroidectomy for thyrotoxicosis and its implication for the T3-suppression test.

It is important to distinguish between symptomatic response and immunological cure in thyrotoxicosis because it has been suggested that surgery, in addition to providing a rapid symptomatic response, may also cause the disappearance of thyroid-stimulating antibodies. The evidence, however, is based largely on suppression tests which we argue may not be valid in the post-operative period. Seventy thyrotoxicosis patients were treated for 6 months with a standard course of carbimazole and T3, at the end of which each patient was classified as suppressor (S) or non-suppressor (NS) according to the fall in radioiodine uptake. Group I (18 patients) and group II (18 patients) were then randomly selected for immediate surgery while group III (34 patients) continued on antithyroid drugs. All groups were reviewed every two months from the 6th month for 12 months, during which time group I was drug-free and groups II and III received T3. Twenty-min iodide uptakes were performed in all patients at each visit to compare the serial changes in mean iodide trapping capacity between treatment groups. Despite 10-fold differences in TSH levels between groups I and II, and irrespective of suppressibility before surgery, the mean uptakes in both these groups remained basal (less than 4%) throughout the period of study, while the serial mean uptakes in group III S (no TSH, by implication no TSAB, but intact iodide trap) were consistently higher than those of group I NS (high TSH, by implication TSAB as well, but reduced iodide trap size). The data points to an absence of dose-responsiveness between TSH and the surgical-remnant's iodide trap, implying that post-thyroidectomy suppression tests (at least during the first year) cannot measure changes in iodide trapping, and therefore do not measure the same phenomenon after subtotal thyroidectomy as they do before operation when the thyroid is intact. We therefore question the validity of comparing suppressibility before and after surgery and basing the frequency of surgical cure on the result.

Adult↗
PubMed1977

High TSH concentrations in "euthyroidism": explanation based on control-loop theory.

High concentrations of thyroid-stimulating hormone (TSH) in the serum have often been reported in apparently euthyroid patients with damaged thyroids. We have confirmed this finding in 14 patients 18 months after subtotal thyroidectomy for Graves's disease (group 1) and in 14 patients with manic-depressive psychosis (group 2) receiving lithium carbonate, which reduces thyroid reserve. One factor common to groups 1 and 2 but not to the controls was reduced thyroid reserve or functioning capacity, and, using established physical principles of servo-control, we have tried to define the mechanism. A series of curves were projected to indicate how TSH might be expected to vary with functioning thyroid capacity.

Adult↗
PubMed1977

Post-thyroidectomy hypocalcaemia: A feature of the operation or the thyroid disorder?

It has been suggested that post-thyroidectomy hypocalcaemia is related to the presence of a thyrotoxic osteodystrophy for which a high serum concentration of bone alkaline phosphatase is a marker. Changes in serum-calcium (corrected to a standard albumin concentration of 40 g/l), alkaline phosphatase (A.P.), inorganic phosphate, and albumin were studied prospectively in 54 euthyroid patients with drug-treated Graves' disease, and in 17 controls with simple non-toxic goitre, before and serially after partial thyroidectomy. All data were paired and results indicate that the pattern of biochemical change was the same in both types of patient and that the degree of change was not related to the serum-A.P. concentration in the Graves'-disease patients. Of the patients studied within the first 24 h of operation, 5 out of 12 with Graves' disease and raised serum-A.P. (group I), 9 of 20 with Graves' disease and normal serum-A.P. (group II), and 7 of 15 controls (group III) showed a fall in serum-calcium below the lower limit of the reference range. In all three groups there was a highly significant fall in serum-calcium 24 h after operation but there was no significant difference in serum-calcium between the groups either immediately before or 24 h after operation. Serum-calcium returned to pre-surgical concentrations within 7 days of thyroidectomy and serum-A.P. concentrations by 4 to 6 weeks in all groups. There was no evidence that post-thyroidectomy hypocalcaemia is related to thyrotoxic osteodystrophy and the pattern of the biochemical changes was thought to be consistent with release of thyrocalcitonin at operation.

Adult↗
PubMed1977

The actions of cyclic AMP, its butyryl derivatives and Na butyrate on the proliferation of malignant trophoblast cells in vitro.

Cyclic AMP, and its derivatives N6-monobutyryl cyclic AMP and dibutyryl cyclic AMP, have been found to inhibit the proliferation of trophoblast cells of the BeWo cell line in vitro. Sodium butyrate (1 mM), a possible degradation product of the butyrate derivatives, also inhibited cell proliferation, giving similar growth rates to equimolar dibutyryl cyclic AMP. The inhibition by butyrate was however, not sufficient to account for the action of 1 mM N6-monobutyryl cycli AMP, which, like cyclic AMP, completely inhibited cell proliferation. The potency, specificity and toxicity of the substances were compared. The results suggest different modes of action for cyclic AMP and dibutyryl cyclic AMP.

Bucladesine↗
PubMed1977

The behaviour of thyroid hormones in an infant with untreated neonatal thyrotoxicosis.

The clinical course from birth and serial measurements of serum T3, T4 and TSH in an infant with untreated neonatal thyrotoxicosis are reported. The thyroid hormone levels fell exponentially with time at rates very much slower than those previously reported for the maternally-transmitted thyroid stimulating antibody generally thought to cause the disorder. Steady physiological levels of thyroid hormones were achieved after 110 days (serum T3 = 3.4 NMOL/L, T4 = 118 nmol/l). TSH first rose to a measurable level after about 90 days.

Adult↗