Adrenocorticotropic Hormone (ACTH), Plasma

CPT CODE:

USEFUL FOR:

Determining the cause of hypercortisolism and hypocortisolism states

SPECIMEN REQUIRED:

Draw blood in an ice-cooled, lavender-top (EDTA) tube(s). Spin down in a refrigerated centrifuge, immediately separate plasma from cells, and send 1 mL of EDTA plasma frozen in plastic vial. Morning (6 a.m.-10 a.m.) specimens are desirable.

TRANSPORT TEMPERATURE:

Frozen\Refrig <12 hrs OK\Ambient NO

CLINICAL INFORMATION:

ACTH, the primary stimulator of adrenal cortisol production, issynthesized by the pituitary in response to corticotropin-releasing hormone (CRH), which is released by the hypothalamus. Plasma ACTH and cortisol levels exhibit peaks (6-8 a.m.) and nadirs (11 p.m.)
Cortisol, the main glucocorticoid, plays a central role in glucose metabolism and in the body's response to stress. Only a small percentage of circulating cortisol is biologically active (free form), with the majority of cortisol inactive (protein bound). Cortisol is inactivated in the liver and excreted in the urine as conjugated compounds (largely 17-hydroxysteroids). Urine free cortisol levels reflect circulating free plasma cortisol levels.
Disorders of cortisol production:   Hypercortisolism:      Cushing's syndrome:          Cushing's disease (pituitary ACTH-producing tumor)          Ectopic ACTH-producing tumor          Ectopic CRH          Adrenal cortisol-producing tumor          Adrenal hyperplasia (non-ACTH dependent, autonomous          cortisol-producing adrenal nodules)   Hypocortisolism:      Addison's disease - primary adrenal insufficiency      Secondary adrenal insufficiency:          Pituitary insufficiency          Hypothalamic insufficiency      Congenital adrenal hyperplasia - defects in enzymes involved      in cortisol synthesis

CLINICAL INTERPRETATION:

In a patient with hypocortisolism, an elevated ACTH indicatesprimary adrenal insufficiency, whereas a value that is not elevatedis consistent with secondary adrenal insufficiency from a pituitaryor hypothalamic cause.
In a patient with hypercortisolism (Cushing's syndrome), a suppressed value is consistent with a cortisol-producing adrenal adenoma or carcinoma, primary adrenal micronodular hyperplasia,or exogenous corticosteroid use.
Normal or elevated ACTH in a patient with Cushing's syndromeputs the patient in the ACTH-dependent Cushing's syndromecategory. This is due to either an ACTH-producing pituitary adenoma or ectopic production of ACTH (bronchial carcinoid, small cell lung cancer, others). Further diagnostic studies such as dexamethasone suppression testing, CRH stimulation testing, petrosal sinus sampling, and imaging studies are usually necessary to define the ACTH source.

REFERENCE VALUES:

10-60 pg/mL (a.m. draws)

No established reference values for p.m. draws

Pediatric reference values are the same as adults, as confirmed

by peer reviewed literature. (Petersen KE:  ACTH in normal children

and children with pituitary and adrenal diseases I. Measurement in

plasma by radioimmunoassay - basal values. Acta Paediatr Scand

1981;70:341-345)