Acute and chronic effects of octreotide on thyroid axis in growth hormone-secreting and clinically non-functioning pituitary adenomas

A. Colao, B. Merola, D. Ferone, P. Marzullo, G. Cerbone, S. Longobardi, C. Di Somma, G. Lombardi

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish
Pages (from-to)189-194
Number of pages6
JournalEuropean Journal of Endocrinology
Volume133
Issue number2
Publication statusPublished - 1995

Fingerprint

Octreotide
Pituitary Neoplasms
Growth Hormone
Thyroid Gland
Adenoma
Hormones
Insulin-Like Growth Factor I
Somatostatin
Thyrotropin-Releasing Hormone
Thyroglobulin
Triiodothyronine
Thyroxine
Therapeutics
Serum

ASJC Scopus subject areas

  • Endocrinology

Cite this

Acute and chronic effects of octreotide on thyroid axis in growth hormone-secreting and clinically non-functioning pituitary adenomas. / Colao, A.; Merola, B.; Ferone, D.; Marzullo, P.; Cerbone, G.; Longobardi, S.; Di Somma, C.; Lombardi, G.

In: European Journal of Endocrinology, Vol. 133, No. 2, 1995, p. 189-194.

Research output: Contribution to journalArticle

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abstract = "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.",
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AU - Colao, A.

AU - Merola, B.

AU - Ferone, D.

AU - Marzullo, P.

AU - Cerbone, G.

AU - Longobardi, S.

AU - Di Somma, C.

AU - Lombardi, G.

PY - 1995

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N2 - 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.

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