ACUTE AND CHRONIC EFFECTS OF OCTREOTIDE ON THYROID AXIS IN GROWTH HORMONE-SECRETING AND CLINICALLY NONFUNCTIONING PITUITARY-ADENOMAS

The effect of somatostatin on thyroid function was studied in 12 patients with growth hormone (GH)secreting and eight patients with clinically non-functioning adenomas (NFA) and normal pituitary/thyroid axis; the patients were subjected to the administration of octreotide (OCT), which is a long-acting somatostatin analog. All the patients received an acute test with 100 mu g of OCT, both short term (1 month) and long term (6 months), with doses ranging from 300 to 600 mu g/day. Serum thyroxine (T-4), triiodothyronine (T-3), free T-4, free T-3, thyroglobulin and basal and thyrotropin (TSH)-releasing hormone (TRH)-stimulated TSH were evaluated before and after 1 and 6 months of therapy. Circulating GH and insulin-like growth-factor I (IGF-I) in acromegalics and GH, IGF-I and a-subunit in NFA were assessed at baseline and every month. The acute administration of 100 mu g of OCT significantly reduced the TSH response to TRH (p < 0.01) in both acromegalics and NFA. In all the patients OCT administration caused a significant decrease of GH, IGF-I and alpha-subunit levels (p ( 0.01). In addition, after 1 month of therapy both baseline and TRH-induced TSH secretion were decreased significantly in acromegalics and NFA. After 6 months of therapy, baseline and TRH-induced TSH was still reduced in NFA. Conversely, in acromegalics, baseline TSH levels were increased while TSH response to TRH was inhibited. No change of T-4, T-3, free T-4 and free Tg was observed in NFA, whereas a slight but significant increase of T-4 and decrease of T-3 was recorded in acromegalics. In conclusion, OCT does seem to possess long-term suppressive effects on TSH response to TRH, both in acromegalics and NFA. The lack of basal TSH level inhibition in acromegalics could depend on the restored peripheral conversion of T-4 into Tg due to the normalized GH levels during long-term OCT administration.