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Hyperthyroidism caused by a solitary toxic nodule can be treated
with ATD, this however, does not result in lasting remission. Therefore, the treatment of
choice, in most centers, is often 131I (3,24) (Table 3).
Most often oral 131I doses of 100–150 µCi (3.7–5,55 MBq) per gram thyroid tissue corrected for 100% 24 h 131I uptake is recommended. There is at present no consensus on the best dose-algorithm and as previously stated many have given up dose calculation and give fixed low (5 mCi/185 MBq) or high (15 mCi/555 MBq) doses. Only 75% of patients become euthyroid within 3 months of 131I-therapy, given that ATD are not given25. 10–20% need additional 131I doses due to persistent or recurrent hyperthyroidism (24,25) and some need up to 5 treatment sessions25. As with the other types of hyperthyroidism the role of ATD on the effect of 131I is not clarified. Thyroid volume is reduced by 35% within 3 months and 45% after 2 years (25,26). The reduction is independent of pretreatment with antithyroid drugs (25) and no additional reduction beyond 2 years of therapy can be expected. There is no clinically significant acute increase in thyroid volume or obstructive symptoms after 131I administration (25). The treatment can be repeated with an expected additional volume reduction (25). This volume reduction is generally satisfactory and only extremely rarely is subsequent surgery required. The risk of hypothyroidism depends on the 131I dose. Using the above dose-algorithm it is generally believed to be less than 10% after 5 years, although higher figures have also been reported (24,25). These relatively low figures are due to most of the 131I being taken up by the hyperfunctioning nodule, while the suppressed extranodular tissue is in part protected. The fact that the prevalence of hypothyroidism after 131I is not nil, is supported by studies demonstrating extranodular uptake of 131I and a significant effect on extranodular volume (26). Radiation thyroiditis is rare (< 5% of patients)24,25. Graves’ like hyperthyroidism has been demonstrated in 1 of 49 patients (2%) with a solitary toxic nodule22. Pretreatment presence of anti-TPOab seems to confer an increased risk of developing both Graves’ like hyperthyroidism22 and hypothyroidism (22,27). The fact that 13 out of 149 (9%) consecutive patients with clinically and scintigraphically nodular (both solitary and multinodular) toxic goitre had pretreatment presence of TSHRab illustrates that it is not always easy to discriminate between nodular toxic goitre and Graves’ disease (22). Some of these patients could in fact have had simultaneous presence of Graves’ disease and nodular goitre (Marine-Lenhart syndrome). Since pretreatment presence of TSHRab and elevated anti-TPOab levels are associated with a significantly increased risk of developing post 131I hyper- and hypothyroidism, it could be speculated whether these antibodies need being measured before treatment, to give a better risk estimate. |
