Approach to and Treatment of Goiters

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What is a goiter?

Simple diffuse goiter (SDG) is an enlargement of the thyroid volume occurring in an iodine-sufficient area or, more frequently, in young individuals living in mild to moderate iodine-deficiency areas. The goiters should not have signs and symptoms related to autoimmune thyroid disorders or neoplasia. SDG volume has been clinically evaluated by palpation, which is considered inaccurate. More recently, ultrasonography of the thyroid gland conducted in schoolchildren4 has provided a more accurate

Epidemiology

Studies on the epidemiology of SDG and MNG in a given population have been hampered by selection criteria, influence of environmental factors, methodology for measuring size, and morphology, as well as methods for evaluating thyroid function.5, 6

Survey of a representative sample of the adult population from a geographic area of the United Kingdom7 indicated that 15.5% of the individuals had a palpable goiter, with a female/male ratio of 4.5:1. No relation to iodine excretion was found. In the

Evolution of SDG and MNG

The evolution of SDG (either endemic or sporadic) is limited to primary and secondary factors.6 Primary factors are functional heterogeneity of normal follicular cells, caused by genetics, and acquisition of new inheritable qualities by replicating epithelial cells. An important primary factor is gender (females are affected more than males). Later, with the evolution of SDG and MNG, several functional and structural anomalies in growing goiters emerge (Fig. 2).

Secondary factors are mostly

Genes associated with MNG

In contrast to sporadic goiters, caused by recessive genomic variation, most cases of familial goiter present an autosomal-dominant pattern of inheritance, indicating predominant genetic defects. Gene-gene interactions of various polygenic mechanisms (ie, synergistic effects of several variants or polymorphisms) could increase the complexity of the pathogenesis of nontoxic MNG and offer an explanation for its genetic heterogeneity.32, 33, 34, 35, 36, 37, 38, 39, 40 A strong genetic

Clinical evaluation

Most patients with SDG and MNG have few or no symptoms except for those with large MNG. Many patients are referred to hospital for cosmetic reasons or, more frequently, for compression of cervical structures causing tracheal deviation. Rarely dyspnea, cough, and dysphasia are present. Often patients have a family history of goiter and nodules removed by surgery in their relatives. SDG commonly develops slowly in school-age children during adolescence. Goiter asymmetry is common. In older

Laboratory investigation and imaging procedures

TSH assays are sensitive in detecting thyroid dysfunction and are therefore preferred as a first approach by more than half of clinicians.45, 46 Depending on the geographic localization of the attending physician (North and South America, Europe, and Asia/Oceania), thyroidologists frequently also ask for thyroid hormone determination (free T4, free T3, total T4, total T3) in the initial evaluation of the patient. Antithyroid peroxidase (anti-TPO) antibodies are measured by half of clinicians.

Treatment

There is no ideal therapeutic option for SDG.47 As discussed earlier, SDG results from a combination of genetic factors and environmental conditions. Frequently a mild iodine deficiency is present.4 Therefore, iodine supplementation seems to be an adequate approach (400 μg iodine for 8–12 months). A significant reduction was observed in SDG. However, in patients with MNG, iodine therapy may induce autoimmune thyroiditis and also the risk of iodine-induced hyperthyroidism (Jod-Basedow

Summary

SDG and MNG affect millions of people worldwide. The main causes are mild iodine deficiency, natural goitrogens, smoking, and other environmental agents. Clinical evaluation is based on TSH, free T4, and anti-TPO determinations followed by ultrasonographic imaging. Large goiters with substernal invasion may require CT or MRI. More recently, it has been accepted that there is a strong genetic influence in some familial goiters, and it is suggested that goiters are derived from a combination of

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    This article was partially supported by a grant from Instituto da Tiróide-São Paulo, Brazil- www.indatir.org.br.

    The authors declare that they have nothing to disclosure.

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