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Current perspectives on the pathogenesis of clinically non-functioning pituitary tumours.

Pituitary tumours are classified by the characteristic clinical syndromes that accompany tumour hormone production. All of the constituent hormone-secreting cell types of the anterior pituitary are capable of undergoing neoplastic change, although it is evident from histochemical analysis that adenomas derived from pure, functional lactotrophs, corticotrophs, somatotrophs, gonadotrophs and thyrotrophs are the exception rather than the rule. Tumours frequently express more than one hormone (Scheithauer et al. 1986, Kovacs & Horvath 1988), most frequently growth hormone (GH) and prolactin (PRL), although immunohistochemical detection of hormones is not a marker of true secretory function. Pituitary tumours that secrete intact hormones result in clinical syndromes of hormone hypersecretion – PRL causing clinical features of hyperprolactinaemia, GH causing acromegaly or gigantism, adrenocorticotrophic hormone (ACTH) causing Cushing’s disease and thyroid-stimulating hormone (TSH) causing secondary hyperthyroidism. Approximately 25–30% of all anterior pituitary neoplasms, however, do not cause clinical syndromes of hormone hypersecretion and are termed non-functioning tumours (NFTs). The term non-functioning is strictly a clinical term, as it is now clear from the results of immunohistochemistry that the majority of these tumours do indeed synthesise, and sometimes secrete, hormones (Arafah 1986), predominantly subunits of the glycoprotein hormones (GPHs; luteinizing hormone (LH), follicle-stimulating hormone (FSH) and TSH) or, occasionally, intact GPHs (Snyder et al. 1979, 1984, Snyder 1985, Black et al. 1987, Jameson et al. 1987, Klibanski 1987, Warnet et al. 1994). Figure 1 shows typical immunostaining properties of an NFT.