posely discontinued before testing. Therefore. except for those relatively few instances in which selected individuais were asked not to ‘ take thvroxin for four to six weeks prior to thy- ‘iency. Retrospective testing of six persons who nad thyroid hyvpofunction after thyroid surgerv revealed the hypofunction had been present earlier (Larsen et al.. 1982). The development of thyroid hypofunction in the exposed individuals continues to be a cause roglobulin testing or thyroid scanning, elevated toryor results of annual TSH testing, somewhat TSH levels were apparent only because of noncompliance. Some persons may have had normal TSH levels after surgery only because they are adhering satisfactorily to the prescribed thyroxin regimen. more than forty percent of exposed persons who are supposed to be taking thyroxin have evidence of irreguiar or noncomplicance with the prescribed medication regimen (Adamset al., 1983). It is desirable to minimize loss of thy- Itis unlikely that the differences in prevalence of postsurgical thyroid hypofunction among the groups result from different degrees of compliance in taking thyroxin after surgery. Furthermore, it is likely that. on the average, the for concern. While the routine use ofsuppressive doses of thyroxin should render this concern moot. it was noted that. based on medicaihis- roid tissue at surgery insofar as it is deemed ‘extent of resection of thyroid tissue was greater clinically safe to do so: in fact, this has been the practice of the thyroid surgerv consultant to the Marshall Islands Medical Program for almost in the unexposed persons undergoing thyroid surgery than in exposed individuals because of concern that the latter were more likely to have - twenty years. impaired thyroid reserve. As Table 6 shows,this concern was well-founded. Although present data are without doubt quantitatively inaccurate, thev are likely to be qualitatively adequate. The distinction between these data and those of Larsen et al. (1982) is that. whereas thyroid hvpofunction was found by the latter group to antedate thyroid surgery (as documented by retrospective analysis of stored sera collected before institution of thyroxin suppression in the exposed Rongelap group), the present data reveal an inordinantly high frequency of postsurgical thyroid hypofunction in exposed persons with previously normai TSH leveis. The importanceofthis finding Is that there appears Despite efforts to mitigate loss of thyroid tissue. however. there continues to be evidence of an inordinantly high frequency of postsurgical thyroid hypofunction among the exposed population.Table 6 showsdata obtained through 1987 illustrating this point. An increasein frequency of postsurgical thyroid hypofunction with increase in the 1954 thyroid radiation dose is apparent, even though all thyroid surgery patients were advised to take thyroxin. However, the data in Table 6 must represent a min- imum estimate of the prevalence of postsurgical thyroid hypofunction. In contrast to the study bv Larsen et al. (1982), thyroxin was not pur- TABLE 6: MARSHALLESE WITH PREVIOUSLY NORMAL TSH > LEVELS WHO HAVE DEVELOPED ELEVATED LEVELS FOLLOWING THYROID SURGERY. Exposure group Rongelap*** Utirik Comparison Adult thyroid dose (rad)* Number with surgery Number with hypothyroidism ** 1200 23 14 160 25 7 none tl l ~ Percent 61 . 28 8 * Average estimated dose for an aduit male. "* Biochemical evidence of thyroid hypofunction as indicatedby at least two determinations of thyroid stimulating hormone = 7.0 uU/1. Normaivaluesare less than 6.0 uU/1. *** Routune thyroxin suppression prescribed. JOON T 1b 16