Test Code CINP Cortisol, Mass Spectrometry, Serum

Reporting Name

Cortisol, S, LC-MS/MS

Useful For

Second-order testing when cortisol measurement by immunoassay (eg, CORT / Cortisol, Serum) gives results that are not consistent with clinical symptoms, or if patients are known to, or suspected of, taking exogenous synthetic steroids (order SGSS / Synthetic Glucocorticoid Screen, Serum to confirm the presence of synthetic steroids)

An adjunct in the differential diagnosis of primary and secondary adrenal insufficiency

An adjunct in the differential diagnosis of Cushing syndrome

This test is not recommended for evaluating response to metyrapone; DOCS / 11- Deoxycorticosterone, Serum is more reliable.

Testing Algorithm

For more information see Steroid Pathways.

Method Name

Liquid Chromatography Tandem Mass Spectrometry (LC-MS/MS)

Performing Laboratory

Mayo Clinic Laboratories in Rochester

Specimen Type

Serum Red

Ordering Guidance

The preferred screening test for Cushing syndrome is the 24-hour urinary free cortisol excretion, order CORTU / Cortisol, Free, 24 Hour, Urine.

When patients are not taking, or are not suspected to be taking, exogenous glucocorticoids, order CORT / Cortisol, Serum.

Specimen Required

Collection Container/Tube: Red top (serum gel/SST are not acceptable)

Specimen Volume: 0.6 mL

Submission Container/Tube: Plastic vial

Collection Instructions:

1. Morning (8 a.m.) and afternoon (4 p.m.) specimens are preferred.

2. Include time of collection.

3. Centrifuge and aliquot serum into a plastic vial.

Additional Information: If multiple specimens are collected, send a separate order for each specimen.

Specimen Minimum Volume

0.25 mL

Specimen Stability Information

Specimen Type	Temperature	Time
Serum Red	Refrigerated (preferred)	28 days
	Ambient	28 days
	Frozen	28 days

Reject Due To

Gross hemolysis	OK
Gross lipemia	Reject
Gross icterus	OK

Special Instructions

Steroid Pathways

Reference Values

5-25 mcg/dL (a.m.)

2-14 mcg/dL (p.m.)

Pediatric reference ranges 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

Day(s) Performed

Monday through Friday

CPT Code Information

82533

LOINC Code Information

Test ID	Test Order Name	Order LOINC Value
CINP	Cortisol, S, LC-MS/MS	87429-7

Result ID	Test Result Name	Result LOINC Value
84279	Cortisol, S, LC-MS/MS	2143-6
23606	AM Cortisol	9813-7
23607	PM Cortisol	9812-9

Clinical Information

Cortisol, the main glucocorticoid (representing 75%-95% of the plasma corticoids), plays a critical role in glucose metabolism and in the body's response to stress. Both hypercortisolism and hypocortisolism can cause disease.

Cortisol levels are regulated by adrenocorticotropic hormone (ACTH), which is synthesized by the pituitary in response to corticotropin releasing hormone (CRH). CRH is released in a cyclic fashion by the hypothalamus, resulting in diurnal peaks (6-8 a.m.) and troughs (11 p.m.) in plasma ACTH and cortisol levels.

The majority of cortisol circulates bound to corticosteroid-binding globulin and albumin. Normally, less than 5% of circulating cortisol is free (unbound). Free cortisol is the physiologically active form and is filterable by the renal glomerulus.

Pathological hypercortisolism due to endogenous or exogenous glucocorticoids is termed Cushing syndrome. Signs and symptoms of pathological hypercortisolism may include central obesity, hypertension, hyperglycemia, hirsutism, muscle weakness, and osteoporosis. However, these symptoms and signs are not specific for pathological hypercortisolism. The majority of individuals with some or all of the symptoms and signs will not suffer from Cushing syndrome.

When Cushing syndrome is present, the most common cause is iatrogenic, due to repeated or prolonged administration of, mostly, synthetic corticosteroids. Spontaneous Cushing syndrome is less common and results from either primary adrenal disease (adenoma, carcinoma, or nodular hyperplasia) or an excess of ACTH (from a pituitary tumor or an ectopic source). ACTH-dependent Cushing syndrome due to a pituitary corticotroph adenoma is the most frequently diagnosed subtype; most commonly seen in women in the third through fifth decades of life. The onset is insidious and usually occurs 2 to 5 years before a clinical diagnosis is made.

Hypocortisolism most commonly presents with nonspecific lassitude, weakness, hypotension, and weight loss. Depending on the cause, hyperpigmentation may be present. More advanced cases and patients submitted to physical stress (ie, infection, spontaneous or surgical trauma) also may present with abdominal pain, hyponatremia, hyperkalemia, hypoglycemia, and in extreme cases, cardiovascular shock and renal failure.

The more common causes of hypocortisolism are:

Primary adrenal insufficiency:

-Addison disease

-Congenital adrenal hyperplasia, defects in enzymes involved in cortisol synthesis

Secondary adrenal insufficiency:

-Prior, prolonged corticosteroid therapy

-Pituitary insufficiency

-Hypothalamic insufficiency