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This condition is common, especially in iodine-deficient regions.
Most of these goitres do not cause significant symptoms and are best left untreated. When
treatment is warranted, the fact that L-T4 is of questionable effect, whether before30 or
after surgery (31), in addition to a number of patients declining surgery, has led a
number of centers (including ours) to offer 131I-therapy to an increasingly number of
patients (2,3,21). Starting with highly selected patients who were ineligible for or
refused surgery (20,32), the treatment is now the preferred one for the vast majority of
patients in Denmark (2). Only relatively few and small studies with less than 10 years of
follow-up are available (2,3), and the role of this therapy is still discussed (Table 4).
Generally, oral 131I doses of 100–150 µCi (3.7–5,5 MBq) per gram thyroid tissue corrected for 100% 24 h. 131I uptake have been given. There is at present no evidence of one regime being better than the other, and since most countries have a relatively low maximum upper limit of out-patient 131I dose, many patients receive less than the intended doses. This should logically lead to a suboptimal thyroid volume reduction. This is, however, at present unsolved since it is not known whether there is a linear dose response relationship between 131I dose and thyroid volume reduction. In monstrous long-standing goitre this does not seem to be the case (19). br> Thyroid volume can be reduced by approximately 40% after one year (2,3,32) and by approximately 50–60% after two years without further reduction (3,21). 60% of this decrease is seen within the first 3 months of therapy (21). There is no significant acute increase in thyroid volume or obstructive symptoms after therapy (12,19). In fact, a relief of compressive symptoms, decrease in upper airway obstruction – as estimated by pulmonary functioning testing and flow volume loops – and an increasing cross-sectional area of the tracheal lumen, can be expected in most patients. This is also valid for monstrous goitres with intrathoracic extension (3,19,20). The treatment can be repeated and additional volume reduction can be achieved (21). Normalization of thyroid volume is rare due to the generally large pretreatment size. Secondary increase in thyroid volume has been seen, although uncommon, and should raise the suspicion of malignancy. Radiation thyroiditis is seen in 3% within the first months of 131I-therapy (23) and easily treated with salicylates or corticosteroids. Graves’ like hyperthyroidism has been demonstrated in 9 of 191 patients (5%) (23). This is most likely triggered by 131I-related release of thyroid antigens and related to appearance of TSHRab. It can also be seen after surgery (33) or following subacute thyroiditis (34), and typically occurs 3 months after treatment. In principle, this could lead to development of thyroid associated ophthalmopathy, as evidenced by a recent case (35). The risk of hypothyroidism, including subclinical cases, is approximately 20% after 5 years or similar to that found in toxic multinodular goitre (18). This figure is much lower than that found in Graves’ disease and in diffuse non-toxic goitre, which is explained by the 131I being taken up only in the functioning (hot/warm) areas of the gland. Pretreatment presence of anti-TPOab seems to confer an increased risk of developing both Graves’ like hyperthyroidism (22%), hypothyroidism (29%) and radiation thyroiditis (11%) as compared to 2%, 13% and 2%, respectively, in anti-TPOab negative subjects (23). The risk of inducing thyroid carcinoma is as yet a theoretical consideration. More important, the risk of pretreatment presence of thyroid carcinoma in multinodular non-toxic goitre is probably as high as in solitary cold nodules (36). This should be taken into consideration and, in my opinion, lead to a more liberal use of diagnostic imaging as well as fine needle aspiration biopsy in patients offered non-surgical treatment. |
