Extract

Understanding the etiology of nodular thyroid disease is a fundamental prerequisite for its subsequent eradication (1–3). For this complex disorder, where the phenotypic presentation is based on an ill-defined interplay between genetic and environmental factors (3, 4), overwhelming evidence points at the amount of tobacco smoking (positively correlated) and decreasing iodine intake (negatively correlated) being the most important modifiable environmental triggers (3, 5, 6). Based on this, it is no surprise that the epidemiology and the phenotypic presentation vary with the population in focus. In a very simplified manner, at least at the level of the individual seeking medical care, the relative risk of harboring thyroid malignancy in a thyroid nodule, although still much lower than the likelihood of a benign disorder, is highest in an iodine-replete, nonsmoking individual. This is so because such individuals have a lower risk of having colloid goiter. It follows that the physician’s individualized risk assessment is probably a major determinant for the huge variation in the expert opinion regarding the diagnostic and therapeutic management of nodular thyroid disease, whether uni- or multinodular (1, 3).

You do not currently have access to this article.