Reports of the coexistence of hyperparathyroidism and thyroid disease
have raised the issue of a possible etiologic relationship. The presen
t study tests the hypothesis that chronic elevation of thyroid-stimula
ting hormone (TSH) is related to the development of hyperparathyroidis
m. Four groups of 60 female rats were treated as follows: group 1, con
trol; group 2, propylthiouracil (PTU) 0.0025%; group 3, PTU 0.0025% pl
us thyroxine, 5 mu g two times per week; and group 4, only thyroxine.
The animals' serum calcium, phosphorus, TSH, thyroxine, and parathyroi
d hormone (PTH) levels were evaluated at 0, 6, 12, and 18 months. Sign
ificant elevation of TSH was sustained throughout the 18 months in gro
ups 2 and 3. The PTH levels were also significantly elevated in both g
roup 2 and group 3 animals (P = 0.02), The histopathologic features of
the parathyroids were evaluated at 18 months. In the group 2 (PTU onl
y) animals, which had profound hypothyroid, 44% developed parathyroid
adenomas. In the group 3 (PTU plus thyroxine) animals, who had mildly
elevated TSH levels, 53% developed parathyroid adenomas. These finding
s are consistent with the hypothesis that prolonged TSH stimulation ma
y lead to hyperparathyroidism in the rat model.