[Reversible hypophyseal disfunction and hyperplasia in two cases of primary hypothyroidism]

Some patients with primary hypothyroidism (HP) develop massive thyrotrope cell hyperplasia determining pituitary hyperplasia with suprasellar enlargement and pituitary dysfunction. Although TRH secretion undoubtedly has some influence, the intervention of other possible factors determining this hyperplasia and dysfunction has been little assessed.

Two patients with primary hypothyroidism with a serum TSH > 1,000 mU/I were studied. By means of CT and MR a pituitary hyperplasia was ascertained in the two patients. The pituitary functional reserve was investigated by the serum response of TSH and prolactin to the administration of TRH (400 micrograms, i.v.), bromocriptine (BRC, 5 mg, oral route), somatostatine (ST, 50 micrograms/kg/min, i.v. perfusion), and gonadotropin releasing hormone (GnRH, 100 micrograms, i.v.).

The TRH induced increment of TSH was 145% and 193%, respectively, compared with basal values. After the administration of BRC, TSH decreased to 57% and 84% of basal values, and PRL to 46% and 43%, respectively. TSH and PRL concentrations did not change after the administration of ST or GnRH. In both cases, hyperplasia and pituitary dysfunction returned to normality after substitutive therapy with levothyroxine.

Basal hyperprolactinemia and TSH and PRL responses to BRC administration suggest that central dopaminergic activity is decreased or abolished in patients with HP and pituitary hyperplasia. The massive thryrotrope cell hyperplasia and hypothyroidism itself determine pituitary dysfunction, which reverts after therapy with levothyroxine, a fact which is scarcely documented in literature.