WATERCRESS (Nasturtium officinale, R.Br.) is a rich source of iodine, the amount it contains probably depending on the amount of iodine available to it during growth1. The availability of the iodine in cress to man was studied by von Fellenberg2, who concluded from balance studies on himself that only about 65 per cent of the iodine ingested was absorbed. We have examined this problem further by using watercress grown in water containing iodine-131. The plant was grown in a greenhouse in water culture, starting from shoots of commercial origin. After 4 weeks' growth, carrier-free iodine-131 was added to the nutrient solution. The watercress was harvested one week later, and amounts containing 25 µc. were fed to two hospital patients who were recovering from myocardial infarction. These patients also received carbim-azole in a dose of 15 mg four times daily in order to prevent the uptake of iodine-131 by the thyroid gland. Urine and fæces were collected for the next three days and their content of iodine-131 was measured. In both patients there was complete recovery of the ingested iodine-131 in the urine, and negligible amounts were detected in the fæces. This indicated complete absorption of the iodine from the gastro-intestinal tract.
Journal Article QUANTITATIVE STUDIES OF IODINE METABOLISM IN THYROID DISEASE Get access W. D. ALEXANDER, W. D. ALEXANDER University Department of Medicine, Gardiner Institute, Western InfirmaryGlasgow Search for other works by this author on: Oxford Academic PubMed Google Scholar D. A. KOUTRAS, D. A. KOUTRAS University Department of Medicine, Gardiner Institute, Western InfirmaryGlasgow Search for other works by this author on: Oxford Academic PubMed Google Scholar J. CROOKS, J. CROOKS University Department of Medicine, Gardiner Institute, Western InfirmaryGlasgow Search for other works by this author on: Oxford Academic PubMed Google Scholar W. W. BUCHANAN, W. W. BUCHANAN University Department of Medicine, Gardiner Institute, Western InfirmaryGlasgow Search for other works by this author on: Oxford Academic PubMed Google Scholar E. M. MACDONALD, E. M. MACDONALD University Department of Medicine, Gardiner Institute, Western InfirmaryGlasgow Search for other works by this author on: Oxford Academic PubMed Google Scholar M. H. RICHMOND, M. H. RICHMOND University Department of Medicine, Gardiner Institute, Western InfirmaryGlasgow Search for other works by this author on: Oxford Academic PubMed Google Scholar E. J. WAYNE E. J. WAYNE University Department of Medicine, Gardiner Institute, Western InfirmaryGlasgow Search for other works by this author on: Oxford Academic PubMed Google Scholar QJM: An International Journal of Medicine, Volume 31, Issue 3, July 1962, Pages 281–305, https://doi.org/10.1093/oxfordjournals.qjmed.a066970 Published: 01 July 1962 Article history Received: 25 November 1961 Published: 01 July 1962
A comprehensive study of iodine metabolism is reported in 40 cases of Hashimoto's thyroiditis. The results showed a dissociation between the mean absolute (or stable) iodine uptake by the thyroid (2.0 ;μg. per hour, which was normal) and the serum level of protein-bound iodine (2.5 μg. per 100 ml., which was significantly decreased). These findings indicate that the thyroid gland traps a normal quantity of iodine, but lacks the capacity to utilize it efficiently to form thyroid hormone. This faulty utilization of iodine is apparently a form of acquired dyshormonogenesis. Evidence of its nature is provided by the frequent discharge of iodine from the thyroid gland following administration of potassium perchlorate and by the presence of a butanol-insoluble iodinated protein in the plasma in many cases. The intrathyroidal exchangeable iodine was markedly reduced in almost all cases. This, and not the presence of the butanolinsoluble iodinated protein, explains the frequent discrepancy between the high level of PBI131 and the low level of PBI in serum. Standard radioiodine tests (thyroidal uptake and plasma activity) yield misleading results unless the foregoing abnormalities in stable iodine metabolism are taken into account.
ABSTRACT The results of radioiodine tests are dependent not only on thyroid function but also on the size of the iodine pools in which the radioiodine is diluted. The significance of the second factor is analysed in this paper and it is shown that there is a danger in interpreting radioiodine tests in isolation. The uptake of 131I is inversely related to the extrathyroidal inorganic iodine pool and the PB131I is inversely related to the intrathyroidal iodine pool. Both these pools may be diminished in euthyroid persons and thus a high uptake of 131I may be associated with a high PB131I and so lead to false diagnostic conclusions. In order to avoid diagnostic errors standard 131I tests should never be reported without some knowledge of relevant clinical features, for example, whether there is the possibility of prolonged iodine deficiency, of previous treatment, of Hashimoto's disease, or of dyshormonogenesis. In this way due weight can be given to factors which increase or decrease the iodine pools of the body and discrepancies between the clinical picture and radioiodine tests become obvious. More specific investigations can then be undertaken in appropriate cases.
Abbott, W. E., Krieger, H., and Levey, S. (1958). Ann. Surg., 148, 567. Adlersberg, D., and liammerschlag, E. (1947). Surgery, 21, 720. Anidrup, E., Hjorth, P., and Jorgensen, J. B. (1958). Brit. J. Radiol., 31, 542. Bruusgaard, C. (1946). Acta chir. scand., 94, Suppl. 117. Gilbert, J. A. L., and Dunlop, D. M. (1947). Brit. med. J., 2, 330. Glazebrook, A. J., and Welbourn, R. B. (1952). Brit. J. Surg., 40, 111. Haslewood, G. A. D., and Strookman, T. A. (1939). Biochem. J., 33, 920. Le Quesne, L. P., Hobsley, M., and Hand, B. H. (1960). Brit. med. J., 1, 141. Lundh, G. (1958). Acta chir. scand., Suppl. 231. Porter, H. W., and Claman, Z. B. (1949). Ann. Surg., 129, 417. Thomas, J. E. (1957). Phvsiol. Rev., 37, 453. Varley, H. (1958). Practical Clinical Biochemistry, 2nd ed. Heinemann, London. Vitkin, S. F. (1940). Ann. Surg., 111, 27.
I have chosen for these two lectures a title which will permit me to cover a very wide field, but which compels me, therefore, to be selective in my approach, and I should like first of all to explain what directed my choice of the topics on which I intend to speak.My interest in thyroid disease was first stimulated soon after I qualified, and since then I have seen and taken part in a steady advance in the diagnosis and treatment of thyroid dysfunction.The direction of my investigations has on several occasions been decided by events in my own particular career, and I hope I may be allowed the pleasure of a few reminiscences which will, I think, make clearer to you the shape of the lectures I am privileged to give to the College.An important influence on my career was a period spent as an experimental pharmacologist, since this taught me to look statistically at medical problems.Though it is nearly thirty years ago, Professor A. J. Clark, of Edinburgh, was even at that time emphasizing the great variability of biological material, and in particular the variation which the individual animal may show in its response to drugs.He was a pioneer in demonstrating that statistical methods were necessary to deal with this phenomenon, and he and his successor, Professor J. H. Gaddum, extended the scope of these techniques and applied them to human pharmacology.