Oxyphenbutazone-induced goitre.
A woman who had taken oxyphenbutazone for 4 years because of back pain presented with goitre and hypothyroidism. This was shown to be due to an organification defect, caused or aggravated by oxyphenbutazone.
Biomedical subjects
Publications and source records attributed to F Clark.
A woman who had taken oxyphenbutazone for 4 years because of back pain presented with goitre and hypothyroidism. This was shown to be due to an organification defect, caused or aggravated by oxyphenbutazone.
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The effect of graded doses of thyroxine (T4) and triiodothyronine (T3) separately on the pituitary-thyroid axis has been studied in normal subjects. It has been demonstrated that small doses (50 mug T4 or 20 mug T3) cause significant suppression of the pituitary-thyroid axis. There was a strong negative correlation between the TSH value 20 min after TRH and the dose of thyroid hormone. T4 supplements led to a progressive dose-related rise in serum T4 and no significant change in T3 until high daily doses (greater than 200 mug) were administered. T3 supplements led to a progressive reduction in serum T4 and there was no change in T3 until substantial supplements were given (greater than 50 mug/day). Concurrent administration of 6 PTU had no effect on the pattern of pituitary suppression or thyroid hormone concentrations in contrast to its reported effect in hypothyroid subjects.
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Triiodothyronine (T3) suppression and thyrotropin-releasing hormone (TRH) tests were used to study thyroid function in 50 patients with thyroid disease. The results of the thyroid function tests were compared with the levels of serum thyroid-stimulating immunoglobulins (TSI) measured by a radio-receptor assay. In euthyroid and hyperthyroid patients, the presence of TSI corresponded with the absence of TSH control of thyroid function. However, in two hypothyroid patients with serum TSI levels readily detectable in the receptor assay, T3 suppression and TRH tests indicated that thyroid function was under TSH control.
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Serial electrocardiographic (E.C.G.) recordings were taken in seven patients suffering from intracranial conditions, for which their intracranial pressure was directly and continuously monitored with a Konigsberg extradural transducer. The E.C.G. changes observed in patients with raised intracranial pressure were prominent U waves, ST-T segment changes, notched T waves, and shortening and prolongation of Q-T intervals. Two patients with normal intracranial pressure showed no E.C.G. abnormalities but also establish a relationship between E.C.G. abnormalities and changing intracranial pressure.
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Neonatal hyperthyroidism has been thought to result from transplacental passage of long-acting thyroid stimulator (L.A.T.S.) from a mother with Graves's disease. A case is presented here in which no L.A.T.S. was detected in the mother or neonate but another immunoglobulin, L.A.T.S. protector, a specific human thyroid stimulator, was shown to be present in the mother's serum. This stimulator may have been the cause of the neonatal hyperthyroidism.
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