Abstract
An attempt was made to classify 326 patients with hyperthyroidism due to Graves’ disease and due to autonomous goiter in an area of endemic iodine deficient goiter using the following two sets of criteria: 1) Primary criteria: the presence of endocrine ophthalmopathy (Graves’ disease) and the absence of endocrine ophthalmopathy and the absence of microsomal antibodies ≥: 1600 (autonomous goiter). Sixty-nine percent of the patients could be devided in the two groups with the aid of these criteria. 2) Secondary criteria: age > 50 years, presence of a goiter, presence of thyroid nodules, activity distribution in the scan, iodine intake determined by iodine excretion in the urine. These criteria had to be applied in the 31 % of the patients who could not be devided into one of the two groups using the primary criteria. The secondary criteria were accumulative. Using these criteria 55% of the 326 patients were classified as having Graves’ disease and 45% as having autonomous goiter. The probability of correct grouping when both primary and secondary criteria were applied was estimated to be 90% compared to 54% when we used only the classical terms, i.e. endocrine ophthalmopathy and diffuse goiter on the one hand and multinodular goiter without endocrine ophthalmopathy on the other hand. In a second group of 120 hyperthyroid patients classified in this way, thyrotropin displacing activity was determined independently. Its prevalence was 79% in patients classified as having Graves’ disease but only 3% in those classified as having autonomous goiter. The prevalence of TDA observed in patients who presumably had autonomous goiter was in the same range as in the following groups: 45 normal individuals; 126 patients with euthyroid goiter; and in 112 patients with euthyroid and hyperthyroid autonomous adenoma. Our results support the hypothesis that autonomous goiter in areas of endemic goiter due to iodine deficiency might not be of immunogenic origin.
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Schicha, H., Emrich, D. & Schireivogel, I. Hyperthyroidism due to Graves’ disease and due to autonomous goiter. J Endocrinol Invest 8, 399–407 (1985). https://doi.org/10.1007/BF03348523
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DOI: https://doi.org/10.1007/BF03348523