[Different etiology of thyrotoxicosis as a function of previous prevalence of goiter]

The high incidence of goiter is believed to modify the characteristics and etiology of thyrotoxicosis. The aim of the present was to study the etiologic types and clinical characteristics of thyrotoxicosis of patients from two areas of different endemic goiter.

Two hundred twelve patients (184 women and 28 males) were studied with clinical and analytical data of thyrotoxicosis. The patients were consecutively seen in the endocrinology units of two different hospitals over the last 4 years. One hundred eight patients pertained to the area of the Xeral Hospital in Lugo (inland zone) and 104 pertained to the area of the Juan Canalejo Hospital from La Coruña (coastal zone). The clinical data of thyrotoxicosis, thyroxin concentration and thyroid gammagraphies were evaluated.

The different etiological types were: Graves disease (GD): Lugo: 20 (19%), La Coruña 57 (55%; p less than 0.001). Toxic multinodular goiter (TMG): Lugo 53 (49%), La Coruña 29 (28%; p less than 0.001). Toxic adenoma (TA): Lugo 23 (21%), La Coruña 13 (13%). Hyperthyroidism by iodine: Lugo: 8 (7%), La Coruña 3 (3%). Other diagnosis: Lugo: 4 (3%), La Coruña 2 (2%). Although the frequency of thyrotoxicosis was much greater in women the percentage distribution of the etiologic types was similar in the two sexes. Symptoms were more frequent in patients with GD with respect to TMG. The presence of auricular fibrillation was more frequent in patients with TMG (38%) than in those presenting GD (4%; p less than 0.01).

Toxic multinodular goiter is the most common cause of thyrotoxicosis in the zones of high endemic goiter. On lowering endemic goiter the percentage of TMG is lowered and that of Graves disease is raised. The symptomatology of thyrotoxicosis is more evident in GD with relation to other etiologic types, but auricular fibrillation is more frequent in TMG. The high prevalence of toxic nodular goiter and hyperthyroidism by iodine suggests the important pathogenic role of the increase of the ingestion of iodine in the form of iodized salt or drugs with iodine.