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S. PAPADOPOULOS
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S. MacFARLANE
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R. McG. HARDEN
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D. K. MASON
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W. D. ALEXANDER
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SUMMARY

The excretion of iodine in urine, saliva, gastric juice and sweat has been studied by using 131I-labelled monoiodotyrosine in a patient with the dehalogenase type of dyshormonogenesis. Iodinated components 'x', iodide, monoiodotyrosine and 'y' were found in the urine. A previously undescribed component (compound 'u') accounted for a large fraction of the urinary radioactive iodine. Organic iodinated compounds were not excreted in the saliva. Only inorganic iodide was found in the gastric juice. No organic iodine was detected in the sweat. The plasma inorganic iodine (PII) derived from salivary iodine measurements gave low values indicative of iodine deficiency. The PII values obtained from the urinary iodine were falsely high due to the presence of organic iodinated compounds.

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J. M. C. Connell
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D. C. McCruden
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M. Small
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M. M. Ferguson
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W. D. Alexander
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[35S]Methimazole and [35S]propylthiouracil were shown to accumulate in mouse sub-mandibular gland in vivo, with maximal tissue: plasma ratios being achieved at the lowest dose of drug studied (0·1 μg/animal). Autoradiography of submandibular glands showed that the drugs were localized to the intralobular ductal epithelium and within the lumen of the convoluted granular tubule, which was identical to the localization of radiolabelled iodide. Histochemical studies indicated that this was the site of peroxidase activity within the gland. Drug accumulation persisted when iodide trapping was competitively inhibited using perchlorate. These data suggest that antithyroid drug accumulation by this tissue is not dependent on the anion trap; the localization of drug and iodide at the site of peroxidase activity suggest that this may be an important factor in the mechanism of drug accumulation, possibly related to subsequent drug metabolism.

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J. M. C. Connell
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M. M. Ferguson
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D. S. C. Chang
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W. D. Alexander
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Radiolabelled [35S]propylthiouracil and [35S]methimazole were shown to accumulate in mouse thyroid gland in vivo, with maximal tissue/plasma ratios and maximal intrathyroidal levels of 35S-labelled drug being seen at the lowest dose of drug studied (0·1 μg/animal). Pretreatment with sodium perchlorate (10 mg) abolished iodide trapping by the thyroid and caused a fall in accumulation of both [35S]methimazole and [35S]propylthiouracil, although this effect was not seen at higher doses of drug, when tissue/plasma ratios approached unity. These data suggest that thiourylene antithyroid drug accumulation by the thyroid gland does not depend directly on the anion trap, and it is suggested that this accumulation might depend on subsequent intrathyroidal drug metabolism.

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W. WATSON BUCHANAN
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D. A. KOUTRAS
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J. CROOKS
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W. D. ALEXANDER
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W. BRASS
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J. R. ANDERSON
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R. B. GOUDIE
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K. G. GRAY
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SUMMARY

The significance of a positive thyroid complement-fixation (c.f.) test in thyrotoxicosis has been investigated by studying the correlation between various features of the disease in 468 patients. A significant correlation was found between the positivity of the c.f. test and (1) the degree of lymphocytic infiltration in the gland; (2) incidence of postoperative hypothyroidism; (3) size of the goitre; (4) previous treatment with radioiodine, and (5) a family history of thyroid disease. No correlation was found between the results of the test and the incidence of reactions to antithyroid drugs. The results suggest that thyrotoxic patients with positive c.f. tests should be treated initially with antithyroid drugs unless there is a definite indication for surgery.

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R. McG. HARDEN
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M. T. HARRISON
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W. D. ALEXANDER
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B. E. C. NORDIN
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SUMMARY

Certain aspects of calcium and phosphorus metabolism have been studied in thirty-six patients with thyrotoxicosis.

The plasma calcium and inorganic phosphorus concentrations were not significantly different from normal.

The basal phosphate excretion index was low (− 0·08 ± 0·01) and there was an impaired response to high phosphate feeding.

These findings suggest that parathyroid function is reduced in thyrotoxicosis.

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