LATE EFFECTS OF RADIOACTIVE IODINE IN FALLOUT
1237
tively small numberof genes regulating the
synthesis of proteins responsible for thyroid
net result could be the development of
mild hypothyroidism or the maintenance
roid gland occurs very rarely, and mitosis
of the normal gland. Consequently, the
tinued overstimulation by TSH. Under
such circumstances, those cells capable of
responding may grow and multiply. Fur-
very long time. After many years, the cell
thermore, if the radiation has produced a
nonlethal mutation, the progeny of the cell
lethal mutation may not be evident for a
begins to divide and perishes in the process.
The cumulative effect of cell death could
readily account for the observed accrual of
hypothyroid cases at the rather steady rate
of about 2%/year of those treated.
Thus, it is not unexpected to find thar
hypothyroidism developed insidiously in
certain of the exposed Marshallese children.
_ The radiation dose was not so large as to
cause extensive cell destruction in the acute
phase, but only later did the injured cells
succumb.
The twoclearly hypothyroid Marshallese
children, like patients developing hypothyroidism after radioiodine therapy for hyperthyroidism, did not have any goiter forma-
tion. Evidently, the cells are sufficiently injured in these instances so that they fail
to respond to the influence of the excess
TSH secretion that must accompany falling
thyroid function. This phenomenon was
demonstrated directly by Doniach (23) who
showed that rats treated with 30 ye 171, or
1,100 rads by X rays, fatled to develop
goiter when treated briefly with propylthiouracil. Maloof, Dobyns, and Vickery (24)
also observed this phenomenon and. postu-
lated that, since the stimulated glands
showed cellular hypertrophy but no increase in weight, there must have been an
impairment of the ability of such irradiated
cells to divide.
In the spectrum of radiation dosage tothyroid cells, one might expect to find the
situation in which the cell’s function is
partially impaired but its growth potential
is not. Alternatively, unequal damage to
This chain of events appears responsible
for the majority of the cases of thyroid abnormality among the Marshall Islanders
and is found in animals treated with appropriate doses of radioiodine especially
when further stimulated by low-iodine diet
or antithyroid drugs (19, 20). As pointedout in connection with the histological
findings, the thyroid glands of the exposed
Marshallese children showedresults characteristic of excessive and prolonged thyroid
stimulation. Such stimulation, with or
without preceding irradiation, leads to the
formation of thyroid nodules with a wide
variety of histological cell types. Nodular
goiter formation of this sort, however, is
not limited to children. The explanation
for the high prevalence of goiter in the
children and the much lower prevalence in
the exposed adults is most likely attributable to the fact that the small thyroid
glands of the children received a larger,
and hence more destructive, dose of radiation.
Sheline, Lindsay, McCormack, and Galante (25) also found in their follow-up of
patients treated with thyroid radiation for
thyroid disease that of the 8 patients de-
veloping thyroid nodules out of a total of
256, 6 had been irradiated before the age
of 20 years and 4 before the age of 10
years. Indeed, the latter 4 represented two
thirds of all those treated at an age younger
than 10 years. Most of them had multiple
nodules, much as were found in the Mar-
shall Islanders. It may be that these
younger subjects actually received larger
radiation doses than the older ones. On the
other hand, this seems unlikely to be the
ope me aetee
cells in the same gland may result in some
with impaired function and growth potential and others with less severe injury. The
may be abnormal.
oer
is almost never seen in histological sections
of euthyroidism only as a result of con-
maeeepel
cell function. Cell division in the adult thy-
8a Te Tee
Talend No6
so
Teme
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