Adrenocorticotropic Hormone (ACTH), Plasma

Adrenocorticotropic Hormone (ACTH), Plasma

Number
	004440
CPT
	82024 (per specimen)
Related Information
	Endocrine Appendix
Synonyms
	ACTH ; Adrenal Corticotropin ; Corticotropin
Special Instructions
	Instructions for suppression/stimulation tests involving ACTH measurement can be found in the Endocrine Appendix .
Specimen
	Plasma, frozen
Volume
	0.8 mL
Minimum Volume
	0.3 mL (Note: This volume does not allow for repeat testing.)
Container
	Plastic or siliconized glass lavender-top (EDTA) tube
Collection
	Collect into iced plastic or siliconized glass lavender-top (EDTA) tube, noting time of collection. After venipuncture, immediately immerse the tubes in an ice bath. Separate plasma from cells by centrifugation. Transfer the plasma into a LabCorp PP transpak frozen purple tube with screw cap (LabCorp N^o 49482). Freeze immediately and maintain frozen until tested. Contact LabCorp's supply department for special tubes. To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested.
Storage Instructions
	Freeze immediately.
Causes for Rejection
	Thawed specimen; serum or heparinized plasma specimen; specimen collected in nonsiliconized glass tube
Reference Interval
	6-48 pg/mL
Use
	Pituitary function test useful in the differential diagnosis of Cushing syndrome, ectopic ACTH syndrome (eg, carcinoma of lung, islet cell tumors, carcinoid tumors, medullary carcinoma of thyroid), Addison disease, hypopituitarism, and ACTH-producing pituitary tumors (eg, Nelson syndrome)
Limitations
	ACTH secretion is pulsatile so multiple specimen collections may be required. Collection in nonsiliconized tubes can result in falsely low results as ACTH adheres to glass.¹
Methodology
	Immunochemiluminometric assay (ICMA)
Additional Information
	Cortisol excess from any source is “Cushing syndrome.” Increased ACTH from the pituitary, causing the adrenal cortices to produce excessive cortisol, was described by Cushing and called “Cushing disease.” ACTH secretion is stimulated by insulin, metyrapone, and vasopressin and suppressed by dexamethasone. Cushing disease usually demonstrates suppression of ACTH and cortisol by high-dose dexamethasone, whereas in adrenal adenomas, adrenal carcinomas, and ectopic ACTH-producing tumors, ACTH and cortisol are not suppressed by high-dose dexamethasone. ACTH levels in Cushing disease may be elevated or in the high normal range (but inappropriately elevated for the patient's plasma cortisol level), with loss of the normal diurnal changes. ACTH levels in ectopic ACTH syndrome are usually very high, whereas in Cushing syndrome due to adrenal adenoma or carcinoma, ACTH levels are very low to undetectable. In primary adrenal insufficiency (Addison disease) due to destruction of the glands by tumor, infection, or immune mechanisms, ACTH plasma concentrations are elevated and cortisol levels are depressed. ACTH increases are found with congenital adrenal hyperplasia (adrenogenital syndrome). In secondary adrenal insufficiency (secondary to pituitary insufficiency), ACTH and cortisol both are low. For sequential follow-up, ACTH should always be drawn at the same time each day. The most common benign tumor producing the ectopic ACTH syndrome is bronchial carcinoid.² ACTH was increased in 30% of patients with oat cell carcinoma and 26% with large cell carcinoma of lung, in a series of 110 patients with lung cancer.³ The increased ACTH of pseudo-Cushing syndrome does not exhibit normal circadian rhythms and fails to suppress with dexamethasone. Pseudo-Cushing syndrome is a reversible entity related to alcohol abuse.⁴
Footnotes
	Demers LM, “Pituitary Function,” Tietz Textbook of Clinical Chemistry, 3rd ed, Burtis CA and Ashwood ER, eds, Philadelphia, PA: WB Saunders Co, 1999, 1470-99. Wickus GG, Pagliara AS, and Caplan RH, “Spurious Elevation of Plasma Immunoreactive Adrenocorticotropic Hormone in Cyclic Cushing's Syndrome,” Arch Pathol Lab Med, 1989, 113(7):797-9. Gropp C, Havemann K, and Scheuer A, “Ectopic Hormones in Lung Cancer Patients at Diagnosis and During Therapy,” Cancer, 1980, 46(2):347-54. Grizzle WE and Dunlap N, “Cushing's Syndrome - Diagnosis of the Atypical Patient,” Arch Pathol Lab Med, 1989, 113(7):727-8
References
	Abboud CF, “Laboratory Diagnosis of Hypopituitarism,” Mayo Clin Proc, 1986, 61(1):35-48 (review). Blunt SB, Sandler LM, Burrin JM, et al, “An Evaluation of the Distinction of Ectopic and Pituitary ACTH Dependent Cushing's Syndrome by Clinical Features, Biochemical Tests, and Radiological Findings,” Q J Med, 1990, 77(283):1113-33. Carpenter PC, “Cushing's Syndrome: Update of Diagnosis and Management,” Mayo Clin Proc, 1986, 61(1):49-58 (review). Findling JW, “Eutopic or Ectopic Adrenocorticotropic Hormone-Dependent Cushing's Syndrome? A Diagnostic Dilemma,” Mayo Clin Proc, 1990, 65(10):1377-80. Findling JW, Kehoe ME, Shaker JL, et al, “Routine Inferior Petrosal Sinus Sampling in the Differential Diagnosis of Adrenocorticotropin (ACTH)-Dependent Cushing's Syndrome: Early Recognition of the Occult Ectopic ACTH Syndrome,” J Clin Endocrinol Metab, 1991, 73(2):408-13. Jones KL, “The Cushing Syndromes,” Pediatr Clin North Am, 1990, 37(6):1313-32. Lisansky J, Peake GT, Strassman RJ, et al, “Augmented Pituitary Corticotropin Response to a Threshold Dosage of Human Corticotropin-Releasing Hormone in Depressives Pretreated With Metyrapone,” Arch Gen Psychiatry, 1989, 46(7):641-9. Siegel SF, Finegold DN, Lanes R, et al, “ACTH Stimulation Tests and Plasma Dehydroepiandrosterone Sulfate Levels in Women With Hirsutism,” N Engl J Med, 1990, 323(13):849-54. Stewart PM, Corrie J, Seckl JR, et al, “A Rational Approach for Assessing the Hypothalamo-Pituitary-Adrenal Axis,” Lancet, 1988, 1(8596):1208-10.