The Changing Incidence and Spectrum of Thyroid Carcinoma in Tasmania (1978–1998) during a Transition from Iodine Sufficiency to Iodine Deficiency¹

Abstract

Exposure to ionizing radiation, changing levels of iodine nutrition, and increased pathologic diagnosis of clinically unimportant thyroid neoplasia have all been proposed as explanations for a worldwide rise in the incidence of thyroid carcinoma (TC) over the past 6 decades. Tasmania is geographically an area of endemic iodine deficiency. In this report, we describe the spectrum of TC in a population averaging 450,000 persons during a 21-yr period that spans the communities transition from iodine sufficiency to iodine deficiency after discontinuation of universal iodine prophylaxis in the mid 1980s. The Tasmanian Cancer Register was used to ascertain all cases of TC diagnosed in Tasmania between 1978 and 1998. Histopathological and demographic data were reviewed. A total of 289 cases of TC were identified. Papillary TC (PTC), follicular TC, medullary TC, and other species accounted for 62%, 23%, 4%, and 11% of cases, respectively. The age standardized incidence rate for total TC increased from 2.45 to 5.33 per 100,000 for females and 0.75 to 1.76 per 100,000 for males between 1978 and 1984 and 1992 and 1998, respectively. A rise in the incidence of PTC by 4.5-fold (P < 0.05) in females and 2.1-fold in males (not significant) was the dominant change over this period. In parallel, the proportion of follicular TC relative to PTC fell from 0.35 to 0.17 during these years (P < 0.05). The rise in PTC incidence was, in part, due to an increase in the occurrence of tumors 1cm or less in diameter. Nonetheless, a 3-fold rise in incidence of larger lesions was also observed during the study period. Forty-three (24%) PTC cases had multifocal disease, 17 (40%) of whom had bilateral tumors. Familial (autosomal dominant) PTC was identified in nine (5%) total PTC cases. Prior studies have linked iodine prophylaxis to a rise in the proportion of differentiated TC, particularly PTC. Our data suggest a complex relationship between iodine nutrition and thyroid tumorigenesis. Factors such as a long latency between changes in iodine nutrition and thyroid tumorigenesis, a dose threshold for the effect of iodine nutrition on thyroid tumorigenesis, and an interaction between iodine nutrition and thyroidal sensitivity to ionizing radiation may all play a role.

Association between Hashimoto’s Thyroiditis and Thyroid Cancer in 64,628 Patients

“…Some countries have introduced iodized salt programs and have since observed increasing trends of TC (1, 57–62), while other countries have not introduced these programs or observed a decrease in iodine intake although the incidence of TC continues to increase here as well (3, 63). …”

Thyroid carcinoma in children, adolescents, and young adults in Brazil: A report from 11 population-based cancer registries

“…High iodine in diet has been associated with thyroiditis, hypothyroidism, hyperthyroidism, increased risk of papillary carcinoma, and decreased risk of follicular carcinoma [30,31]. In this study, there was a smaller number of follicular carcinomas and no trends were observed in children and AYAs.…”

“…The role of iodine in the pathogenesis of thyroid cancer is controversial, and the difference has been documented according to tumor histology. Iodine deficiency is associated with follicular carcinoma, whereas excess iodine increases the risk of papillary type of thyroid cancer [30].…”

Downregulation of miR-146b-5p via iodine involvement repressed papillary thyroid carcinoma cell proliferation

“…To verify that high iodine contributes to the cell cycle distribution in PTC cells, DNA content was measured (Burgess et al 2000) by flow cytometry. We observed that treatment of PTC cells with 10 −3 M NaI enhanced the proportion of cells in the G0/G1 phase compared to that in control cells (Fig.…”