Burgess J R, Dwyer T, McArdle K, Tucker P, Shugg D
Department of Diabetes and Endocrine Services, Royal Hobart Hospital, Australia.
J Clin Endocrinol Metab. 2000 Apr;85(4):1513-7. doi: 10.1210/jcem.85.4.6554.
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.
过去60年里,电离辐射暴露、碘营养水平变化以及临床上不重要的甲状腺肿瘤病理诊断增加,都被认为是全球甲状腺癌(TC)发病率上升的原因。塔斯马尼亚在地理上是碘缺乏流行地区。在本报告中,我们描述了在一个平均有45万人的人群中,21年间TC的发病情况,这一时期跨越了20世纪80年代中期全民碘预防措施停止后,社区从碘充足到碘缺乏的转变。利用塔斯马尼亚癌症登记处确定了1978年至1998年间在塔斯马尼亚诊断出的所有TC病例,并对组织病理学和人口统计学数据进行了回顾。共识别出289例TC病例。乳头状TC(PTC)、滤泡状TC、髓样TC和其他类型分别占病例的62%、23%、4%和11%。1978年至1984年以及1992年至1998年间,女性TC的年龄标准化发病率从每10万人2.45例增至5.33例,男性从每10万人0.75例增至1.76例。在此期间,主要变化是女性PTC发病率上升了4.5倍(P<),男性上升了2.1倍(无统计学意义)。同时,这些年里滤泡状TC相对于PTC的比例从0.35降至0.17(P<)。PTC发病率上升部分归因于直径1厘米及以下肿瘤发生率的增加。尽管如此,在研究期间,较大病变的发病率也上升了3倍。43例(24%)PTC病例有多灶性病变,其中17例(40%)有双侧肿瘤。在所有PTC病例中,9例(5%)被确定为家族性(常染色体显性)PTC。先前的研究将碘预防措施与分化型TC尤其是PTC比例的上升联系起来。我们的数据表明碘营养与甲状腺肿瘤发生之间存在复杂关系。碘营养变化与甲状腺肿瘤发生之间的长时间潜伏期、碘营养对甲状腺肿瘤发生影响的剂量阈值以及碘营养与甲状腺对电离辐射敏感性之间的相互作用等因素可能都起到了作用。