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Thyrotropin-Secreting Pituitary Tumors^*

Institute of Endocrine Sciences, University of Milan, Ospedale Maggiore IRCCS Milan, Italy
Centro Auxologico Italiano IRCCS Milan, Italy
Molecular and Cellular Endocrinology Branch NIDDK, NIH, Bethesda, Maryland 20892
Endocrinology Division, Mayo Clinic Jacksonville Jacksonville, Florida 32224

Correspondence: Address reprint requests to: Paolo Beck-Peccoz, M.D., Istituto Clinico Humanitas, Via Manzoni 56, 20089-Rozzano (MI)-Italy.

Abstract

I. Introduction: The term "TSH-secreting pituitary tumors" includes two opposite clinical conditions: true thyrotroph neoplasia that results in secondary hyperthyroidism, also called "central hyperthyroidism," and pituitary hyperplasia resulting from longstanding primary hypothyroidism. The latter condition was first recognized 145 yr ago (1), while the former was not clearly identified until the RIA era (2–8). However, in the 1950s and 1960s, while it became clear that Graves' disease was not caused by hyperpituitarism (9, 10), scattered reports suggested a possible association between pituitary tumors and hyperthyroidism (11–15), although no measurement of TSH levels was available during this time. The first case of TSH-secreting pituitary adenoma (TSH-oma) was documented in 1960 by measuring serum TSH levels with a bioassay (16). In 1970, Hamilton et al. (17) reported the first case of TSH-oma proved by a RIA that was much more sensitive and specific than the previously used bioassays. Classically, TSH-omas were diagnosed at the stage of invasive macroadenoma and had the reputation of being difficult to cure. However, with the introduction of ultrasensitive immunometric assays, routinely performed as a first-line thyroid function test, patients with TSH-oma are more often recognized earlier, before the stage of macroadenoma.

Footnotes

^* Supported in part by grants from CNR-Rome and Ospedale Maggiore IRCCS-Milan (to P.B.-P.), and Centro Auxologico Italiano-Milan (to L.P.).

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