Prolactin (PRL)-Producing Pituitary Tumors
PRL-producing pituitary tumors, also known as prolactinomas and lactotroph adenomas, secrete PRL and are typically an intrasellar tumor. In women, these adenomas are often small (<10 mm). In either sex, however, they can become large enough to enlarge the sella turcica. These adenomas represent the most common hormone-producing pituitary tumors and account for 25% to 41% of tumor specimens.
Adrenocorticotrophic Hormone (ACTH)-Producing Pituitary Tumors
The major manifestation of ACTH-producing pituitary tumors, also know as corticotroph adenomas, is secretion of adrenocorticotropic hormone (ACTH), which results in Cushing syndrome. These tumors are initially confined to the sella turcica, but they may enlarge and become invasive after bilateral adrenalectomy (i.e., Nelson syndrome). These adenomas represent the second or third most common hormone-producing pituitary tumors, depending on the series; in one series, these tumors accounted for 10% of all tumor specimens.[1,3]
Growth Hormone (GH)-Producing Pituitary Tumors
GH-producing pituitary tumors, also known as somatotroph adenomas, produce GH, resulting in gigantism in younger patients and acromegaly in others. Suprasellar extension is not uncommon. These adenomas represent the second or third most common hormone-producing pituitary tumors, depending on the series; in one series these adenomas accounted for 13% of tumor specimens.[1,3]
Thyrotropin-Producing Pituitary Tumors
Thyrotroph-producing pituitary tumors, also known as thyrotroph adenomas, secrete thyroid-stimulating hormone (TSH), also known as thyrotropin, which results in hyperthyroidism without TSH suppression. Many are large and invasive, may be plurihormonal, and secrete both GH and/or PRL. These tumors are rare and account for no more than 2% of tumor specimens.[1,3,20]
Gonadotroph (FSH-Producing and/or LH-Producing) Adenomas
Gonadotroph adenomas may secrete FSH and/or LH, or the alpha or beta subunits that comprise these heterodimers, which, depending on gender, may result in ovarian overstimulation, increased testosterone levels, testicular enlargement, and pituitary insufficiency caused by compression of the pituitary stalk or destruction of normal pituitary tissue by tumor. Many gonadotroph tumors, however, are unassociated with clinical or biochemical evidence of hormone excess and may be considered to be nonfunctioning or endocrine-inactive tumors. Functional, clinically detectable gonadotroph adenomas are rare.
Plurihormonal tumors produce more than one hormone. Morphologically, they can be either monomorphous or plurimorphous. Monomorphous plurihormonal adenomas consist of one cell population that produces two or more hormones. The adenoma cells often differ from nontumorous adenohypophysial cells, and their cellular derivation may remain obscure despite extensive morphological studies. Plurimorphous plurihormonal adenomas consist of two or more distinct cell types, and each produces one hormone. Thyrotroph adenomas are often plurihormonal.
Nonfunctioning (Endocrine-Inactive) Adenomas
These tumors arise from the adenohypophysis and cause symptoms when they extend beyond the sella, which results in pressure on the surrounding structures rather than secretion of a hormonally active substance. Endocrine-inactive adenomas show positive immunostaining for one or more pituitary hormones; however, they are not associated with clinical and biochemical evidence of hormone excess. Gonadotrophic hormones, as detected by antisera to beta-FSH and beta-LH, are present in many clinically nonfunctioning adenomas. Some of these adenomas are recognized by electron microscopy to have gonadotrophic differentiation, but some have characteristics of less well-differentiated cells and resemble the null cells that were initially thought to be undifferentiated precursors of adenohypophysial cells. Endocrine-inactive pituitary adenomas comprise approximately 30% to 35% of the pituitary tumors in most series and are the most common type of macroadenoma.