Other pituitary adenomas are associated with hormonal disorders not considered part of hyperpituitarism, or are nonfunctional and do not produce hormonal disturbances.
Gonadotroph adenomas are so named because they produce hormones (luteinizing hormone [LH] and follicle-stimulating hormone [FSH]) that act on reproductive organs (gonads). These adenomas can be difficult to recognize because they secrete hormones inefficiently and variably and the secretory products usually do not cause a recognizable clinical syndrome. They are typically detected when the tumors become large enough to cause signs and symptoms related to local mass effects, such as impaired vision, headaches, diplopia, or pituitary apoplexy. The neoplastic cells usually demonstrate immunoreactivity for the common gonadotropin α-subunit and the specific β-FSH and β-LH subunits; FSH usually is the predominant secreted hormone.
Thyrotroph (thyroid-stimulating hormone [TSH]–producing) adenomas account for about 1% of all pituitary adenomas and constitute a rare cause of hyperthyroidism.
Nonfunctioning pituitary adenomas are a heterogeneous group that constitutes 25% to 30% of all pituitary tumors. Not surprisingly, the typical presentation is characterized by mass effects. These lesions also may impinge on the residual anterior pituitary and produce hypopituitarism, which may appear slowly due to gradual enlargement of the adenoma or abruptly because of acute intratumoral hemorrhage (pituitary apoplexy).
Pituitary carcinomas are exceedingly rare. In addition to local extension beyond the sella turcica, these tumors virtually always metastasize to distant sites.
Prolactinomas: amenorrhea,galactorrhea,lossoflibido,andinfertility
Growth hormone (somatotroph cell) adenomas: gigantism(children),acromegaly(adults),andimpairedglucosetoleranceanddiabetesmellitus
Corticotrophcelladenomas:Cushingsyndrome,hyperpigmentation
Allpituitaryadenomas,particularlynonfunctioningadenomas,maybeassociatedwithmasseffectsandhypopituitarism.
Clinically significant hypopituitarism may occur with loss or absence of 75% or more of the anterior pituitary parenchyma. It may be congenital (exceedingly rare) or result from a wide range of acquired intrinsic abnormalities of the pituitary. Less frequently, disorders that interfere with the delivery of pituitary hormone–releasing factors from the hypothalamus, such as hypothalamic tumors, cause hypofunction of the anterior pituitary. Hypopituitarism accompanied by evidence of posterior pituitary dysfunction in the form of diabetes insipidus (discussed later) is almost always of hypothalamic origin. Most cases of anterior pituitary hypofunction are caused by the following:
Ischemic necrosis of the anterior pituitary, called Sheehan syndrome, or postpartum necrosis of the anterior pituitary, is the most common form of clinically significant necrosis of the anterior pituitary. During pregnancy, the anterior pituitary enlarges, mainly because of an increase in the size and number of prolactin-secreting cells. This hyperplasia is not accompanied by an increase in blood supply from the low-pressure hypophyseal portal venous system. The enlarged gland is thus vulnerable to ischemic injury, especially in women who experience hypotension during the peripartal period. By contrast, the posterior pituitary receives its blood directly from arterial branches and is much less susceptible to ischemic injury. Pituitary necrosis also may occur in the setting of disseminated intravascular coagulation, sickle cell anemia, elevated intracranial pressure, traumatic injury, and shock of any origin.