posely discontinued before testing. Therefore, except for those relatively few instances in which selected individuals were asked not to take thyroxin for four to six weeks prior to thyroglobulin testing or thyroid scanning, elevated 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. ciency. Retrospective testing of six persons who had thyroid hypofunction after thyroid surgery revealed the hypofunction had been present earlier (Larsen et al., 1982). The development of thyroid hypofunction in the exposed individuals continuesto be a cause for concern. While the routine use of suppressive doses of thyroxin should render this concern moot, it was noted that, based on medical history or results of annual TSH testing, somewhat more than forty percent of exposed persons who are supposed to be taking thyroxin have evidence of irregular or noncomplicance with the prescribed medication regimen (Adams et al., 1983). It is desirable to minimizeloss of thyroid tissue at surgery insofar as it is deemed clinically safe to do so: in fact, this has been the practice of the thyroid surgery consultant to the Marshall Islands Medical Program for almost It is 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 extent of resection of thyroid tissue was greater in the unexposed persons undergoing thyroid surgery than in exposed individuals because of concern that the latter were morelikely to have impaired thyroid reserve. As Table 6 shows,this concern was well-founded. Although present data are without doubt quantitatively inaccurate, they are likely to be qualitatively adequate. The distinction between these data and those of Larsen et al. (1982) is that, whereas thyroid hypofunction was found by the latter group to antedate thyroid surgery (as documented by retrospective analysis of stored sera collected before institution of thyroxin suppressionin the exposed Rongelap group), the present data reveal an inordinantly high frequency of postsurgical thyroid hypofunction in exposed persons with previously normal TSH levels. The importanceof this finding is that there appears twenty years. 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 shows data obtained through 1987 illustrating this point. An increase in 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 minimum estimate of the prevalence of postsurgical thyroid hypofunction. In contrast to the study by 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 )* Numberwith surgery Number with hypothyroidism ** 1200 23 14 61 160 25 7 28 none 11 1 8 * Average estimated dose for an adult male. Percent ** Biochemical evidence of thyroid hypofunction as indicatedbyat least two determinationsof thyroid stimulating hormone = 7.0 uU/1. Normal values are less than 6.0 uU/1. *** Routine thyroxin suppression prescribed. 16