Page 731 - Robbins Basic Pathology by Vinay Kumar, Abul K. Abbas, Jon C. Aster
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Hyperpituitarism and Pituitary Adenomas 717
TRH PIF CRH Hypothalamus GHRH GIH GnRH
(Dopamine)
(Somatostatin)
Stalk
Anterior Posterior
TSH PRL ACTH Pituitary GH FSH LH
Figure 19–2 The adenohypophysis (anterior pituitary) releases six hormones: adrenocorticotropic hormone (ACTH), or corticotropin; follicle-
stimulating hormone (FSH); growth hormone (GH), or somatotropin; luteinizing hormone (LH); prolactin (PRL); and thyroid-stimulating hormone
(TSH), or thyrotropin. These hormones are in turn under the control of various stimulatory and inhibitory hypothalamic releasing factors. The stimula-
tory releasing factors are corticotropin-releasing hormone (CRH), growth hormone–releasing hormone (GHRH), gonadotropin-releasing hormone
(GnRH), and thyrotropin-releasing hormone (TRH). The inhibitory hypothalamic factors are growth hormone inhibitory hormone (GIH), or somato
statin, and prolactin inhibitory factor (PIF), which is the same as dopamine.
HYPERPITUITARISM AND composed of a single cell type and produce a single
PITUITARY ADENOMAS predominant hormone, but there are some exceptions.
Some pituitary adenomas can secrete two different hor-
The most common cause of hyperpituitarism is an adenoma mones (growth hormone and prolactin being the most
arising in the anterior lobe. Other, less common, causes common combination); rarely, pituitary adenomas are
include hyperplasia and carcinomas of the anterior pitu- plurihormonal. At the other end of the spectrum, pitu-
itary, secretion of hormones by some extrapituitary tumors, itary adenomas also may be truly “hormone negative,” as
and certain hypothalamic disorders. Some salient features indicated by absence of immunohistochemical reactivity
of pituitary adenomas are as follows: or ultrastructural evidence of hormone production.
• Pituitary adenomas are classified on the basis of hormone(s) • Most pituitary adenomas occur as sporadic (i.e., non-
familial) lesions. In about 5% of cases, however, adeno-
produced by the neoplastic cells, which are detected by immu- mas occur as a result of an inherited predisposition (see
nohistochemical stains performed on tissue sections (Table later).
19–1). • Pituitary adenomas are designated, somewhat arbi-
• Pituitary adenomas can be functional (i.e., associated trarily, as microadenomas if they are less than 1 cm in
with hormone excess and clinical manifestations thereof) diameter and macroadenomas if they exceed 1 cm in
or nonfunctioning (i.e., demonstration of hormone diameter.
production at the tissue level only, without clinical • Nonfunctioning and hormone-negative adenomas are
manifestations of hormone excess). Both functional likely to come to clinical attention at a later stage and
and nonfunctioning pituitary adenomas usually are are, therefore, more likely to be macroadenomas than
Table 19–1 Classification of Pituitary Adenomas
Pituitary Cell Type Hormone Tumor Type Associated Syndrome*
Corticotroph ACTH and other POMC- Densely granulated Cushing syndrome
derived peptides Sparsely granulated Nelson syndrome
Somatotroph GH Densely granulated Gigantism (children)
Sparsely granulated Acromegaly (adults)
Lactotroph Prolactin Densely granulated Galactorrhea and amenorrhea (in females)
Sparsely granulated Sexual dysfunction, infertility
Mammosomatotroph Prolactin, GH Mammosomatotroph Combined features of GH and prolactin excess
Thyrotroph TSH Thyrotroph Hyperthyroidism
Gonadotroph FSH, LH Gonadotroph, “null cell,” Hypogonadism, mass effects and hypopituitarism
oncocytic adenomas
ACTH, adrenocorticotropic hormone; FSH, follicle-stimulating hormone; GH, growth hormone; LH, luteinizing hormone; POMC, pro-opiomelanocortin; TSH, thyroid-stimulating
hormone.
*Nonfunctioning adenomas in each category typically manifest with mass effects and often with hypopituitarism.
Data from Ezzat S, Asa SL: Mechanisms of disease: the pathogenesis of pituitary tumors. Nat Clin Pract Endocrinol Metab 2:220–230, 2006.
