Acute and chronic effects of octreotide on thyroid axis in growth hormone-secreting and clinically non-functioning 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 longacting somatostatin analog. All the patients received an acute test with 100 μg of OCT, both short term (1 month) and long term (6 months), with doses ranging from 300 to 600 μg/day. Serum thyroxine (T₄), triiodothyronine (T₃), free T₄ free T₃, 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 μg 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 α-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 NEA. Conversely, in acromegalics, baseline TSH levels were increased while TSH response to TRH was inhibited. No change of T₄, T₃, free T₃ and free T₃ was observed ill NFA, whereas a slight but significant increase of T₄ and decrease of T₃ 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 T₄ into T₃ due to the normalized GH levels during long-term OCT administration.