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

Departments of Diabetes and Endocrine Services (J.R.B.) and Anatomical Pathology (K.M.), Royal Hobart Hospital; Tasmanian Cancer Registry (D.S.), Menzies Centre for Population Health Research (T.D.), University of Tasmania; Hobart Pathology (P.T.), Tasmania, Hobart 7001, Australia

Address all correspondence and requests for reprints to: Dr. John R Burgess, M.D., FRACP, Department of Diabetes and Endocrine Services, Royal Hobart Hospital, GPO Box 1061L, Hobart 7001, Australia. E-mail: jburges{at}postoffice.utas.edu.au

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.

This article has been cited by other articles:

				K. Guttikonda, J. R. Burgess, K. Hynes, S. Boyages, K. Byth, and V. Parameswaran Recurrent Iodine Deficiency in Tasmania, Australia: A Salutary Lesson in Sustainable Iodine Prophylaxis and Its Monitoring J. Clin. Endocrinol. Metab., June 1, 2002; 87(6): 2809 - 2815. [Abstract] [Full Text] [PDF]