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HelpTest Code CIVC Cortisol, Inferior Vena Cava, Serum
Reporting Name
Cortisol, IVCUseful For
Testing cortisol levels in the inferior vena cava
Second-order testing wen cortisol measurement by immunoassay gives results that are not consistent with clinical symptoms, or if patients are known to, or suspected of, taking exogenous synthetic steroids
An adjunct in the differential diagnosis of primary and secondary adrenal insufficiency
An adjunct in the differential diagnosis of Cushing syndrome
Method Name
Liquid Chromatography Tandem Mass Spectrometry (LC-MS/MS)
Performing Laboratory
Mayo Clinic Laboratories in Rochester
Specimen Type
SerumOrdering Guidance
For confirming the presence of synthetic steroids, order SGSS / Synthetic Glucocorticoid Screen, Serum.
Specimen Required
Collection Container/Tube: Red top
Specimen Volume: 1.5 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
0.5 mL
Specimen Stability Information
| Specimen Type | Temperature | Time | Special Container |
|---|---|---|---|
| Serum | Refrigerated (preferred) | 28 days | |
| Ambient | 28 days | ||
| Frozen | 28 days |
Reject Due To
| Gross hemolysis | OK |
| Gross lipemia | Reject |
| Gross icterus | OK |
Special Instructions
Reference Values
Not established
Day(s) Performed
Monday through Friday
CPT Code Information
82533
LOINC Code Information
| Test ID | Test Order Name | Order LOINC Value |
|---|---|---|
| CIVC | Cortisol, IVC | 2143-6 |
| Result ID | Test Result Name | Result LOINC Value |
|---|---|---|
| 6347 | Cortisol, IVC | 2143-6 |
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
For more information see Steroid Pathways.