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Treatment of Hyperthyroidism due to Inappropriate Secretion of Thyrotropin With the Somatostatin Analog SMS 201–995^*

Departments of Endocrinology, Universities of Milan (P.B.-P., G.M., G.P., M.R., G.F.), Pisa (S.M., A.P.), Roma "Tor Vergata" (A.Be.), and Roma "Cattolica del Sacro Cuore" (A.Ba) Italy
Höpital Lariboisiere (P.J.G., Ph.C) Paris, France

Address all correspondence and requests for reprints to: Paolo Beck-Peccoz, M.D., Istituto di Scienze Endocrine, Ospedale Maggiore IRCCS, Padiglione Sacco, Via Francesco Sforza 35, 1-20122 Milan, Italy.

The management of hyperthyroidism due to inappropriate secretion of TSH (IST) includes agents that selectively suppress TSH hypersecretion both in patients with TSHsecreting tumor [neoplastic IST (nIST)] in whom pituitary surgery was unsuccessful and in those with selective pituitary resistance to thyroid hormone action [nonneoplastic IST (nnIST)]. Among such agents, somatostatin administration has proven to be effective in blocking TSH hypersecretion, but its short plasma half-life prevented its use in long term therapeutic trials. The recent availability of a potent and long-acting analog of somatostatin (SMS 201–995, Sandostatin) prompted us to study its effects on serum TSH, -subunit, and free thyroid hormone (FT₄ and FT₃) concentrations in five patients with nIST and three patients with nnIST. During short term SMS 201–995 administration (100 µg, sc, three times daily for 5 days) both serum TSH and -subunit levels decreased in all patients with nIST (mean decrements, –86% and –85%, respectively), with concomitant normalization of serum FT₄ and FT₃ concentrations. In the three patients with nnIST, this treatment lowered serum TSH levels less well (mean decrement, –47%), although serum FT₄ and FT₃ levels normalized in one patient. Chronic SMS 201–995 (100 µg, sc, every 12 h for 1–7 months) treatment in four hyperthyroid patients (two with nIST and two with nnIST) resulted in a steady euthyroid state in both patients with nIST, with restoration of normal visual fields in one patient. In contrast, in both patients with nnIST, escape occurred after 2 weeks of therapy. We conclude that SMS 201–995 administration is effective treatment for patients with nIST, able to suppress TSH hypersecretion from the adenomatous thyrotrophs and, consequently, to restore clinical and biochemical euthyroidism in such patients. On the contrary, the inhibitory effects of SMS 201–995 on TSH secretion in patients with nnIST are weaker and transient.

^* This work was supported in part by grants from Ministero della Pubblica Istruzione and CNR Special Project "Oncology" (Rome, Italy). Presented in part at the 16th Annual Meeting of the European Thyroid Association, July 1987, Lausanne, Switzerland (Abstract 35).

Received April 26, 1988.

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