What is the role of lab studies in the diagnosis of pituitary macroadenomas?

Updated: Apr 20, 2020
  • Author: James R Mulinda, MD, FACP; Chief Editor: George T Griffing, MD  more...
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Laboratory tests include basal hormone levels and dynamic hormone measurements depending on the tumor studied.

All tumors should have screening basal hormone measurements, which may include prolactin, thyrotropin, thyroxine, adrenocorticotropin, cortisol, LH, FSH, estradiol, testosterone, growth hormone, insulinlike growth factor-1 (IGF-1), and alpha subunit glycoprotein.

Dynamic hormone tests are performed to assess the functionality of a tumor and assist in differential diagnosis. They also can be used to assess anterior pituitary reserve.

Thyrotropin-releasing hormone (TRH) causes elevation of serum prolactin and thyrotropin. Prolactinomas, hyperprolactinemic states, hyperthyroidism, and panhypopituitarism exhibit a blunted response. Gonadotropinomas respond paradoxically to TRH (LH, FSH, LH-beta, and alpha subunit should be measured).

GHRH produces an elevation in growth hormone. This response is blunted in growth hormone deficiency, Cushing disease, and hypothyroidism. Other agents that may be used for this test include insulin, L-dopa, arginine, and clonidine. Acromegaly may produce a paradoxical reduction in growth hormone.

Hyperglycemia suppresses serum growth hormone. This suppression does not occur in pituitary tumors secreting growth hormone, ectopic growth hormone–releasing tumors, Cushing syndrome, and anorexia nervosa. A paradoxical rise in growth hormone may be observed in acromegaly, acute illness, and chronic renal failure. Many people with acromegaly also show paradoxical growth hormone response to TRH and occasionally to GnRH.

CRH causes a rise in corticotropin. This response is exaggerated in Cushing disease but blunted in other causes of Cushing syndrome. When combined with inferior petrosal sinus sampling, this test may assist in differentiating Cushing disease from benign ectopic adrenocorticotropic hormone (ACTH) syndrome.

Insulin-induced hypoglycemia causes a rise in corticotropin, cortisol, and growth hormone. A blunted response is observed in Cushing syndrome, growth hormone deficiency, hypothyroidism, and hyperthyroidism.

Metyrapone causes a rise in morning serum 11-deoxycortisol and urinary 17-hydrocorticosteroids (17-OH steroids). An exaggerated response occurs in Cushing disease, but no response is observed in other causes of Cushing syndrome.

Dexamethasone suppression testing is used in Cushing syndrome evaluation. An overnight 1-mg dexamethasone dose fails to suppress morning serum cortisol in Cushing syndrome but is only a screening test. Low-dose and high-dose dexamethasone suppression tests assist, respectively, in establishing the diagnosis of Cushing syndrome and differentiating between Cushing disease and ectopic production of corticotropin.

Cosyntropin testing and corticotropin infusion testing assist in assessing the hypothalamic-pituitary-adrenal axis for adrenocortical insufficiency.

GnRH causes an increase in LH and FSH levels. This response is blunted in pituitary hypogonadism but exaggerated in primary hypogonadism. Test results, however, are not very dependable.

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