Raymond Oslapas

Long-term effect of radiation on thyroid function and tumor formation.

Abstract Cellular injury coupled with hypersecretion of thyroid stimulating hormone (TSH) is considered the mechanism for radiation-induced thyroid tumors. This hypothesis was tested by administering 40 μCi of 131 I to male and female rats. Serum thyroxine (T 4 ) decreased significantly overtime in male and female control and radiated animals. T 4 was essentially the same in 6- and 12-month-old radiated and control animals, but a significant decrease in T 4 was noted in radiated females at 21 months. TSH decreased overtime in control animals, but a significant increase in TSH was required in radiated animals to maintain T 4 levels. Thyrocalcitonin (TC) was significantly greater in 21-month-old control females than in males or radiated females. A significant increase in follicular cell thyroid neoplasms in radiated animals was associated with the elevated TSH levels. The importance of sex in thyroid tumor formation is illustrated by the fact that males had a significantly higher frequency of thyroid neoplasms than did females. C-cell hyperplasia and medullary thyroid carcinoma only occurred in control animals and accounted for their higher TC levels. This study confirms that administration of low doses of 131 I leads to an increased frequency of thyroid tumor formation in rats and that direct cellular injury plus hypersecretion of TSH seem responsible for these radiation-induced tumors.

Hyperparathyroidism induced by hypothyroidism

The coexistence of hyperparathyroidism and thyroid tumors and/or chronic thyroiditis has raised the possibility of an etiologic relationship. The present study was designed to test the hypothesis that the chronic elevation of thyroid‐stimulating hormone (TSH) is related to the development of hyperparathyroidism. Three groups of 24 rats each were treated for 12 weeks as follows: group 1 received propylthiouracil (PTU) in their deionized water; group 2 received PTU and thyroid hormone to suppress TSH and to serve as a control group for possible direct effects of PTU; and group 3 was not treated at all and served as another control group. At 12 weeks, 95% of group 1 rats (PTU only) showed hyperplasia of the parathyroids with a 30% mean increase in circulating parathormone.