Euthyroid goiter with and without nodules--diagnosis and treatment

Abstract

Background: Thyroid enlargement and thyroid nodules are common in the general population. This review concerns their proper diagnostic assessment and treatment.

Methods: We selectively reviewed the literature from 1990 to 2012 and evaluated original articles and reviews retrieved from the PubMed database, as well as the recommendations of the following specialty societies: the German Societies of Endocrinology and Nuclear Medicine (Deutsche Gesellschaft für Endokrinologie, Deutsche Gesellschaft für Nuklearmedizin), the German Working Group for Endocrine Surgery (Chirurgische Arbeitsgemeinschaft Endokrinologie, CAEK), the European Thyroid Association, and the American Thyroid Association.

Results: There have been very few randomized trials concerning the diagnosis and treatment of goiter. Nodular goiter can be managed by watchful waiting, drug treatment (initially with levothyroxine and iodide), radioactive iodine therapy, or surgery.

Conclusion: Many patients with nodules need no treatment at all. Treatment is indicated, however, if the patient is symptomatic and/or has an autonomously functioning ("hot") nodule, or if cancer is suspected. Potentially cancerous nodules must be operated on. If euthyroid nodular goiter is to be treated with the main goal of size reduction, either surgery or radioactive iodine therapy can be used. Drug treatment is an option for small nodules or goiters, but iatrogenic hyperthyroidism must be avoided at all costs. The type of follow-up that is required depends on the chosen treatment.

Figure 1

The multifactorial origin of goiter: The most important known, preventable cause of thyroid enlargement is iodine deficiency. The prevalence of goiter is directly related to iodine deficiency and tends to decrease when the iodine intake of a population is increased. The risk factors for goiter include intrinsic biological factors (which account for the five- to tenfold higher prevalence of goiter among women) as well as cigarette smoking, naturally occurring goitrogens, selenium or zinc deficiency, and emotional stress.

Figure 2

Hypothetical model of the pathogenesis of nodular goiter: Nodular goiters are very heterogeneous in their functional, structural, and molecular genetic features (4). It is currently thought that, in persons with both a genetic predisposition and an iodine deficiency, a “mutagenic environment” arises (increased cellular proliferation and formation of free radicals) that promotes the appearance of somatic mutations in thyrocytes. A clonal thyroid tumor forms when the genetic defect is not repaired and the mutation is of a type that gives the proliferating cells a selective advantage