12 Diez et?al.20 performed a retrospective analysis of 75 individuals with SCT reporting a higher rate of progression in those with TSH?<?0��10?mU/l. T3 was not measured at baseline in all individuals, however, and 50% of subjects who developed ��overt thyroid hyperfunction�� were prescribed antithyroid medication for clinical reasons despite normal T4 and T3 concentrations. <a href="http://www.selleckchem.com/products/pifithrin-alpha.html
">PFT�� price We report here the largest published series examining the influence of aetiology on outcome in SCT. Underlying thyroid pathology determined on scintigraphy was an independent predictor of outcome with the cumulative percentage developing thyrotoxicosis at 5?years in the sGD, MNG and AN subgroups being 9%, 21% and 61%, respectively. Age, gender, family history of thyrotoxicosis, symptoms at presentation, thyroid nodule(s) on clinical examination, entry TSH level and antithyroid antibody status did not influence risk of progression. Two factors are likely to have contributed to the higher rates of progression reported here compared to previous studies. First, whereas radioiodine ablation of nontoxic AN��s and MNG��s is common in selected regions of the world,21 it has been the practice of our department to monitor patients without treatment, providing a unique opportunity to assess natural disease history. Second, despite the iodization of salt in New Zealand from 1924, with standardization of the salt iodine content (0��3?umol/g) in 1939, the click here
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continues to consider our region mildly iodine deficient,22,23 a factor that has been suggested to increase progression of autonomous thyroid hormone secretion in nodular thyroid disease.24,25 Consistent with a previous report,26 development of thyrotoxicosis in individuals with an AN occurred early during follow-up in our cohort with a predilection for T3 toxicosis. While nodule size has been reported to influence progression risk,26 this information was not collected. Progression of sGD was infrequent in our population with TSH fluctuation and normalization commonly seen. This finding is in contrast to that of Rosario, possibly reflecting the different study entry criteria and population dietary iodine intake. Of interest, two individuals with sGD in our study developed persistent hypothyroidism requiring long-term thyroxine replacement therapy. Spontaneous hypothyroidism is well described in patients with GD previously treated with antithyroid drugs, the pathogenesis of which is thought to involve TSH-blocking antibodies or development of chronic lymphocytic thyroiditis.27,28 While there is no information on this outcome in treatment na?ve individuals with sGD, a similar pathogenesis could be hypothesized.