Multinodular Goiter - In this disorder, many nodules develop inside the thyroid which causes an enlarged thyroid. Causes of a goiter include an imbalance in the thyroid gland and Goiter symptoms generally occur in a gland that is overactive, producing too much hormone (hyperthyroidism), or that is underactive, producing too little hormone (hypothyroidism). Today, in the United States, thyroid goiter is more commonly associated with too much production of thyroid hormone (hyperthyroidism), too little production of thyroid hormone (hypothyroidism), or multiple nodules within the thyroid gland itself (mulitnodular goiter).

However, because multinodular goiters are a risk factor for thyroid cancer, people with this type of goiter should be screened. It is not known what causes multinodular goiters in most cases, but iodine deficiency (i.e. too little iodine in the diet) and certain genetic factors have been shown to lead to multinodular goiters. The latter is termed multinodular goiter ( MNGMNG - Multinodular goiter; enlarged thyroid that contains multiple nodules ). There are two forms of multinodular goiter: 1) nontoxic MNGNontoxic MNG - multinodular goiter that produces normal levels of thyroid hormone and 2) toxic MNG.

For example, in hyperthyroid Graves disease, there is usually a diffuse or generalized goiter; and in toxic adenomas and toxic multinodular goiter, there are solitary and multiple nodules, respectively in the gland. Thyroid cancers and benign tumors (nodules) that may cause a so-called multinodular goiter. In the United States, where the use of iodized salt is common, a goiter is more often due to the over- or underproduction of thyroid hormones or to nodules that develop in the gland itself.

The feasibility of high dose iodine 131 treatment as an alternative to surgery in patients with a very large goiter: effect on thyroid function and size and pulmonary function. Because the aspects of surgery, 131I, and l-T4 therapy bear much resemblance to what has been detailed regarding the multinodular goiter, we will focus on the newest (experimental) modalities regarding treatment of the solitary nodule. A general reservation is not justified because, on average, 131I therapy is not followed by any significant acute thyroid enlargement ( 65 , 272 ), either in moderate or in very large multinodular goiters.

Only in very few European countries, like Denmark and to some extent The Netherlands, is 131I now the routine choice as treatment of the benign nontoxic multinodular goiter ( 8 , 9 ). In North America, for example, the thyroid iodine uptake is rather low due to the high dietary iodine intake. In addition, pretreatment with recombinant human TSH causes a more homogeneous distribution of 131I within the nodular gland by stimulating the 131I uptake relatively more in cold areas than in hot areas ( 271 ). These potential benefits of recombinant human TSH are very intriguing in the context of an amplification of the 131I therapy, but whether the goiter reduction can be improved and whether this leads to a change in attitude among clinicians remains to be proven. In most studies of nontoxic goiters ( 65 , 162 , 174 , 224 , 252 - 254 , 262 ), the administered 131I activity was 3.7-5.5 MBq/g thyroid tissue corrected for 131I thyroid uptake, aiming at an absorbed dose of approximately 100 Gy. However, it should be noticed that dose calculation based on 24-h 131I uptake and not half-life may strongly overestimate the intended dose to nodular goiters ( 263 ). In fact, an elaborated algorithm for dose calculation may not be worthwhile, as is also evident in the case of hyperthyroidism ( 264 , 265 ). Besides a poorly defined individual susceptibility to 131I, which remains to be identified, the thyroid 131I uptake displays a considerable variation with time ( 266 , 267 ). The iodine biokinetics is probably also affected by the 131I therapy itself ( 266 ). Finally, the absorbed dose may be influenced by shrinkage of the gland during therapy ( 268 ).