Iodine and Anaplastic Thyroid Carcinoma

Abstract

s programs of iodine prophylaxis have been im-plemented in many European countries in the recentpast, the report of Besic and colleagues (1) about associatedalterationsinthefrequencyofanaplasticthyroidcancer(ATC)is particularly timely. Alterations in dietary iodine supplyhave been shown to result in changes in the presentation of avariety of thyroid disorders (2). These include hyperthyroid-ism,whichcanpresentastoxicnodulargoiterwhentheiodinesupply is increased in a previously iodine-deficient popula-tion (Jod Basedow), or hypothyroidism as a consequence ofdisruption of thyroid hormonogenesis when a significantlyincreased amount of iodine is ingested (Wolff–Chaikhoff ef-fect). Even small changes in iodine supply have been shownby Laurberg and his colleagues (2) to alter the prevalence ofdisorders of thyroid function. These reported changes in thepresentation ofthyroid disorders do not only apply to alteredthyroid function. Many studies have shown that the rate ofdifferentiated thyroid cancer (DTC) presenting in the follicu-lar (FTC) or anaplastic histologic form was relatively morefrequentinareasofiodinedeficiency,whilethepapillaryform(PTC) predominated in iodine-replete populations (3). Whatis less clear is whether the overall rate of thyroid cancer isinfluenced by the dietary iodine status of a population (3,4).Although conclusive evidence exists showing that thyroidcancer rates are higher in animals fed an iodine-deficient dietand that carcinogen-induced thyroid carcinomas can be po-tentiated by iodine deficiency, proof of a direct causative rolefor iodine deficiency remains elusive (5–7). It has also beensuggested that iodine administration can prevent the trans-formation of DTC to ATC (8).Manystudieshaveshownanincreaseinthepapillaryformof thyroid cancer following iodine prophylaxis (5). Althoughthe rate of ATC has been reported as being greater in areas ofiodine deficiency, there have been few reports on the effect ofiodine prophylaxis on ATC frequency. Besic et al. cite twoconflicting reports on ATC rate from different regions ofAustria (9,10). In Carinthia, the incidence was the same (9),and in Tyrol (10), the incidence was lower, when the iodiza-tion of salt was changed from 10mg I/kg to 20mg I/kg. Thereport of Besic and colleagues is in agreement with that fromtheTyrolinthattheynotedafallintheincidenceofATCfrom3.25 per million (lower salt iodization 10mg I/kg) to 1.9 permillion (higher salt iodization 25mg I/kg). There are alwayscaveats, particularly relating to diagnostic methodology (5),which must be factored in when comparing epidemiologicalfindings for thyroid cancer incidence. However, this is prob-ably less relevant when dealing with ATC, and Besic andcolleagues detail how diagnostic criteria did not change overthe two study periods in their study.While the debate continues as to the importance of iodineprophylaxis in altering the rate of all thyroid cancers, in-cluding ATC, the significance of the findings in terms oftherapeutic possibilities that increasing iodine intake maydiminish the frequency of ATC remains unclear. In practice,excess iodide, by inhibiting thyroid hormone production(Wolff–Chaikhoff effect), may stimulate thyroid growth viaincreased thyrotropin (TSH). However this effect is self-limiting because iodide is also known to suppress iodidetransportviaNa