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Catecholamines, Fractionated, Plasma

Test Number 084152
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CPT

82384
Synonyms
  • Adrenalin®, Plasma
  • Dopamine, Plasma
  • Epinephrine, Plasma
  • Noradrenaline, Plasma
  • Norepinephrine, Plasma
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  • Updated on 04/14/2025

Test Details

Methodology

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

High-pressure liquid chromatography (HPLC) with electrochemical (EC) detection

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

Result Turnaround Time

4 - 6 days

Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.

Related Documents

Test Includes

Plasma catecholamines, fractionated (dopamine, epinephrine, norepinephrine)

Use

This test is used for measurement of fractionated catecholamines in plasma.

Diagnose pheochromocytoma and those paragangliomas which may secrete epinephrine, norepinephrine, or both. Such tumors may cause paroxysmal or persistent hypertension. Investigation of hypertensive patients, especially younger individuals, particularly when hypertension is paroxysmal, suggesting pheochromocytoma. Plasma catecholamines with urinary metanephrines and VMA are a recommended test battery for pheochromocytoma.3 Others recommend plasma catecholamines when urinary collections are not diagnostic. Work up multiple endocrine adenomatosis, type II. Used also in diagnosis of disorders related to the nervous system and in assessment of resuscitation.4

This test is used for measurement of fractionated catecholamines in plasma.

Limitations

This test was developed, and its performance characteristics determined by Labcorp. It has not been cleared or approved by the Food and Drug Administration.

As the secretion of catecholamines from pheochromocytoma and paragangliomas is episodic; a single estimation of plasma or urinary catecholamines will miss the biochemical diagnosis in about 30% of cases.1,2

Many alterations in physiologic and pathologic states can profoundly affect catecholamine concentrations. Any environmental factor that may increase endogenous catecholamine production should be avoided. These include noise, stress, discomfort, body position and the consumption of food, caffeinated beverages or nicotine. Caffeine and nicotine effects are short term, a few minutes to hours only.

Other substances and drugs that may also affect the results include:

  • Medications that inhibit reuptake of norepinephrine and epinephrine, such as serotonin-norepinephrine reuptake inhibitors (e.g., venlafaxine), selective serotonin reuptake inhibitors, and tricyclic antidepressants, result in increased concentrations of norepinephrine and epinephrine.3
  • Monoamine oxidase inhibitors block conversion of norepinephrine and epinephrine to nonfunctional metabolites raising circulating catecholamine levels.3
  • Sympathomimetic substances such as amphetamine, caffeine, nicotine and decongestants (ephedrine, pseudoephedrine, phenylephrine) increase the release of norepinephrine and epinephrine.4-6
  • Other medications such as acetaminophen, alpha-methyldopa and levodopa can also result in false-positive biochemical testing.3,4,7,8
  • Antiparkinsonian drugs (Levodopa, carbidopa) can increase plasma dopamine levels.5,9
  • Substances that reduce or increase plasma volume acutely (e.g., diuretics, radiographic contrast media, synthetic antidiuretic hormone) can artificially increase catecholamine levels.
  • The use of cocaine as well as amphetamines such as ecstasy (3,4-methylenedioxymethamphetamine or MDMA) was reported to be associated with increased plasma catecholamine concentrations in the absence of pheochromocytoma.10-12
  • Cigarette smokers may have increased plasma and urinary catecholamines and/or metanephrine levels as nicotine stimulates catecholamine release by activation of nicotinic acetylcholine receptors in the brain and the adrenal medulla.13
  • Caffeine can increase circulating catecholamines secondary to its stimulatory effects.10
  • Catecholamine-rich foods (bananas, fruit juices, nuts, tomatoes, potatoes and beans) are major sources of diet-associated FP results.14,15
  • Foodstuffs containing large amounts of tyramine such as hard cheeses and red wine can cause release of vesicular NE leading to FP test results.16

Plasma levels are useful if elevated, especially during or immediately following an episode of hypertension, but false-negatives occur when the specimen is drawn during an uneventful period. Normotensive pheochromocytoma has been reported.5 False-positive results are common. Epinephrine secretion increases in response to cold and hypoglycemia. Drugs which may affect plasma norepinephrine levels include α- and β-adrenergic blockers, vasodilators, clonidine, bromocriptine, theophylline, phenothiazine, tricyclic antidepressants, labetalol, calcium channel blockers, converting enzyme inhibitors, bromocriptine, chlorpromazine, haloperidol, and cocaine. Plasma catecholamines are less sensitive than are urinary catecholamines.6

This test was developed, and its performance characteristics determined by Labcorp. It has not been cleared or approved by the Food and Drug Administration.

As the secretion of catecholamines from pheochromocytoma and paragangliomas is episodic; a single estimation of plasma or urinary catecholamines will miss the biochemical diagnosis in about 30% of cases.1,2

Many alterations in physiologic and pathologic states can profoundly affect catecholamine concentrations. Any environmental factor that may increase endogenous catecholamine production should be avoided. These include noise, stress, discomfort, body position and the consumption of food, caffeinated beverages or nicotine. Caffeine and nicotine effects are short term, a few minutes to hours only.

Other substances and drugs that may also affect the results include:

  • Medications that inhibit reuptake of norepinephrine and epinephrine, such as serotonin-norepinephrine reuptake inhibitors (e.g., venlafaxine), selective serotonin reuptake inhibitors, and tricyclic antidepressants, result in increased concentrations of norepinephrine and epinephrine.3
  • Monoamine oxidase inhibitors block conversion of norepinephrine and epinephrine to nonfunctional metabolites raising circulating catecholamine levels.3
  • Sympathomimetic substances such as amphetamine, caffeine, nicotine and decongestants (ephedrine, pseudoephedrine, phenylephrine) increase the release of norepinephrine and epinephrine.4-6
  • Other medications such as acetaminophen, alpha-methyldopa and levodopa can also result in false-positive biochemical testing.3,4,7,8
  • Antiparkinsonian drugs (Levodopa, carbidopa) can increase plasma dopamine levels.5,9
  • Substances that reduce or increase plasma volume acutely (e.g., diuretics, radiographic contrast media, synthetic antidiuretic hormone) can artificially increase catecholamine levels.
  • The use of cocaine as well as amphetamines such as ecstasy (3,4-methylenedioxymethamphetamine or MDMA) was reported to be associated with increased plasma catecholamine concentrations in the absence of pheochromocytoma.10-12
  • Cigarette smokers may have increased plasma and urinary catecholamines and/or metanephrine levels as nicotine stimulates catecholamine release by activation of nicotinic acetylcholine receptors in the brain and the adrenal medulla.13
  • Caffeine can increase circulating catecholamines secondary to its stimulatory effects.10
  • Catecholamine-rich foods (bananas, fruit juices, nuts, tomatoes, potatoes and beans) are major sources of diet-associated FP results.14,15
  • Foodstuffs containing large amounts of tyramine such as hard cheeses and red wine can cause release of vesicular NE leading to FP test results.16

Custom Additional Information

The catecholamines (dopamine, epinephrine, and norepinephrine) are derived from tyrosine via a series of enzymatic conversions.17 All three catecholamines are important neurotransmitters in the central nervous system and play a crucial role in the autonomic regulation of many homeostatic functions, namely, vascular tone, intestinal and bronchial smooth muscle tone, cardiac rate and contractility and glucose metabolism. Their actions are mediated via alpha- and beta-adrenergic and dopamine receptors, all existing in several subforms. The three catecholamines overlap but differ in their receptor activation profile and consequent biological actions. The systemically circulating fraction of the catecholamines is derived almost exclusively from the adrenal medulla, with small contributions from sympathetic ganglia.

Catecholamines are normally present in the plasma in minute amounts, but levels can increase dramatically and rapidly in response to change in posture, environmental temperature, physical and emotional stress, hypovolemia, blood loss, hypotension, hypoglycemia and exercise. Elevation of plasma-free metanephrines less than three to four times the normal level might represent potential false-positive results.4 In many cases, this is secondary to inappropriate sampling and should be repeated with the patient in the supine position. A false-positive result commonly shows elevations in either metanephrine or normetanephrine, but not both. Very high false-positive levels (three-fold or higher) are rare, and catecholamine related disease should be suspected in such cases.1,4

Pheochromocytoma and Paragangliomas:

These rare neuroendocrine tumors arise from chromaffin cells of the adrenal medulla (pheochromocytoma) or neural crest progenitors located outside of the adrenal gland (paraganglioma).1,2,4 These tumors are derived from either sympathetic tissue in the adrenal or extra-adrenal abdominal locations or from parasympathetic tissue in the thorax or head and neck. In patients with pheochromocytoma (a potentially curable tumor of catecholamine-producing cells of the adrenal medulla) or, less commonly, paraganglioma (a tumor of the sympathetic ganglia that also produces catecholamine), plasma catecholamine levels may be continuously or episodically elevated. This results in episodic or sustained hypertension and intermittent attacks of palpitations, cardiac arrhythmias, headache, sweating, pallor, anxiety, tremor, and nausea.2,7,18

Plasma catecholamines should not be used as the first-line test for pheochromocytoma, as plasma catecholamine levels may not be continuously elevated but only secreted during a "spell." By contrast, production of metanephrines (catecholamine metabolites) appears to be increased continuously.

The recommended first-line laboratory tests for pheochromocytoma1,2,19 include:

However, plasma catecholamine measurements can be useful in patients whose plasma metanephrine or urine metanephrine measurements do not completely exclude the diagnosis.5

A dopamine-secreting paraganglioma is a very rare subtype that predominantly or exclusively secretes dopamine but not norepinephrine or epinephrine. These malignancies have been characterized by a lack of catecholamine excess symptoms, large tumor size, extra-adrenal location and high malignant potential.20-22

Neuroblastoma:

Intermittent or continuous elevations of the plasma levels of one or several of the catecholamines may be observed in patients with neuroblastoma and related tumors (ganglioneuroblastomas and ganglioneuromas) and, very occasionally, in other neuroectodermal tumors.5,23 Vanillylmandelic acid, homovanillic acid and urine catecholamine measurements are the mainstay of biochemical diagnosis and follow-up of these tumors. Plasma catecholamine levels can aid diagnosis in some cases, but diagnostic decision levels are not well established. The most useful finding is disproportional elevations in one of the three catecholamines, particularly dopamine, which may be observed in these tumors.

Autonomic Neuropathy:

Inherited and acquired syndromes of autonomic dysfunction or failure and autonomic neuropathies are characterized by either inadequate production of one or several of the catecholamines or by insufficient release of catecholamines upon appropriate physiological stimuli (e.g., change in posture from supine to standing, cold exposure, exercise, stress).24 Depending on the underlying cause and pathology, autonomic dysfunction or failure and autonomic neuropathies are associated with subnormal resting norepinephrine levels or an absent rise of catecholamine levels in response to physiological release stimuli (e.g., change in posture from supine to standing, cold exposure, exercise, stress), or both.

The adrenal medullary catecholamines (epinephrine, norepinephrine, and their precursor, dopamine) are rapidly metabolized materials with intense vasoactivity, among many other properties. They can be synthesized by extra-adrenal cells or neoplasms of the APUD system. They are pathogenic in the episodic hypertension of pheochromocytoma, and will be elevated during and immediately after such a paroxysm. However, levels may be normal during asymptomatic intervals. Urine catecholamines, metanephrines, VMA, and HVA provide additive information. A clonidine-suppression test has been described; failure to suppress plasma catecholamines with clonidine supports the diagnosis.7-9

The catecholamines (dopamine, epinephrine, and norepinephrine) are derived from tyrosine via a series of enzymatic conversions.17 All three catecholamines are important neurotransmitters in the central nervous system and play a crucial role in the autonomic regulation of many homeostatic functions, namely, vascular tone, intestinal and bronchial smooth muscle tone, cardiac rate and contractility and glucose metabolism. Their actions are mediated via alpha- and beta-adrenergic and dopamine receptors, all existing in several subforms. The three catecholamines overlap but differ in their receptor activation profile and consequent biological actions. The systemically circulating fraction of the catecholamines is derived almost exclusively from the adrenal medulla, with small contributions from sympathetic ganglia.

Catecholamines are normally present in the plasma in minute amounts, but levels can increase dramatically and rapidly in response to change in posture, environmental temperature, physical and emotional stress, hypovolemia, blood loss, hypotension, hypoglycemia and exercise. Elevation of plasma-free metanephrines less than three to four times the normal level might represent potential false-positive results.4 In many cases, this is secondary to inappropriate sampling and should be repeated with the patient in the supine position. A false-positive result commonly shows elevations in either metanephrine or normetanephrine, but not both. Very high false-positive levels (three-fold or higher) are rare, and catecholamine related disease should be suspected in such cases.1,4

Pheochromocytoma and Paragangliomas:

These rare neuroendocrine tumors arise from chromaffin cells of the adrenal medulla (pheochromocytoma) or neural crest progenitors located outside of the adrenal gland (paraganglioma).1,2,4 These tumors are derived from either sympathetic tissue in the adrenal or extra-adrenal abdominal locations or from parasympathetic tissue in the thorax or head and neck. In patients with pheochromocytoma (a potentially curable tumor of catecholamine-producing cells of the adrenal medulla) or, less commonly, paraganglioma (a tumor of the sympathetic ganglia that also produces catecholamine), plasma catecholamine levels may be continuously or episodically elevated. This results in episodic or sustained hypertension and intermittent attacks of palpitations, cardiac arrhythmias, headache, sweating, pallor, anxiety, tremor, and nausea.2,7,18

Plasma catecholamines should not be used as the first-line test for pheochromocytoma, as plasma catecholamine levels may not be continuously elevated but only secreted during a "spell." By contrast, production of metanephrines (catecholamine metabolites) appears to be increased continuously.

The recommended first-line laboratory tests for pheochromocytoma1,2,19 include:

However, plasma catecholamine measurements can be useful in patients whose plasma metanephrine or urine metanephrine measurements do not completely exclude the diagnosis.5

A dopamine-secreting paraganglioma is a very rare subtype that predominantly or exclusively secretes dopamine but not norepinephrine or epinephrine. These malignancies have been characterized by a lack of catecholamine excess symptoms, large tumor size, extra-adrenal location and high malignant potential.20-22

Neuroblastoma:

Intermittent or continuous elevations of the plasma levels of one or several of the catecholamines may be observed in patients with neuroblastoma and related tumors (ganglioneuroblastomas and ganglioneuromas) and, very occasionally, in other neuroectodermal tumors.5,23 Vanillylmandelic acid, homovanillic acid and urine catecholamine measurements are the mainstay of biochemical diagnosis and follow-up of these tumors. Plasma catecholamine levels can aid diagnosis in some cases, but diagnostic decision levels are not well established. The most useful finding is disproportional elevations in one of the three catecholamines, particularly dopamine, which may be observed in these tumors.

Autonomic Neuropathy:

Inherited and acquired syndromes of autonomic dysfunction or failure and autonomic neuropathies are characterized by either inadequate production of one or several of the catecholamines or by insufficient release of catecholamines upon appropriate physiological stimuli (e.g., change in posture from supine to standing, cold exposure, exercise, stress).24 Depending on the underlying cause and pathology, autonomic dysfunction or failure and autonomic neuropathies are associated with subnormal resting norepinephrine levels or an absent rise of catecholamine levels in response to physiological release stimuli (e.g., change in posture from supine to standing, cold exposure, exercise, stress), or both.

Specimen Requirements

Specimen

Plasma, frozen

Volume

1.5 mL (plasma)

3 mL (plasma)

1.5 mL (plasma)

Minimum Volume

0.7 mL plasma (Note: This volume does not allow for repeat testing.)

2.2 mL (plasma)

0.7 mL plasma (Note: This volume does not allow for repeat testing.)

Container

Lavender-top (EDTA) tube or green-top (heparin) tube

Collection Instructions

Draw blood in chilled lavender-top (EDTA) tube. Invert to mix with preservatives. Centrifuge and transfer the plasma to a labeled plastic transport tube. Place on-ice immediately (do not refrigerate) and freeze separated plasma within four hours of collection. Important: The patient should be in a fully recumbent position (lying down) for at least 20 minutes before and during sample collection. To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested.

Draw blood in lavender-top (EDTA) tube or green-top (heparin) tube. Invert to mix with preservatives. Centrifuge and transfer the plasma to labeled plastic transport tube. Freeze immediately (within one hour after collection) at -20°C and ship frozen. The time between blood collection and the preparation of plasma is quite critical; if the time exceeds one hour, catecholamine values increase (when blood is kept at 4°C) or decrease (when left at 20°C).1 To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested.

For more information, refer to the Preservative Quick Reference Chart in Specimen Collection: Urine Specimens.

Draw blood in chilled lavender-top (EDTA) tube. Invert to mix with preservatives. Centrifuge and transfer the plasma to a labeled plastic transport tube. Place on-ice immediately (do not refrigerate) and freeze separated plasma within four hours of collection. Important: The patient should be in a fully recumbent position (lying down) for at least 20 minutes before and during sample collection. To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested.

Stability Requirements

TemperaturePeriod
Room temperatureUnstable
RefrigeratedUnstable
Frozen14 days
Freeze/thaw cyclesStable x2
Temperature Period
Room temperature Unstable
Refrigerated Unstable
Frozen 14 days
Freeze/thaw cycles Stable x2

Reference Range

Analyte

Adults, ≥18 years

(Supine)

Dopaminea0.0–36.7 pg/mL
Epinephrineb0.0–55.4 pg/mL
Norepinephrinea115–524 pg/mL

• Norepinephrine, plasma:

− 0 to 1 year: 0−659 pg/mL

− 1 to 18 years: 0−611 pg/mL

− 18 years and older: 0−874 pg/mL

• Epinephrine, plasma:

− 0 to 1 year: 0−34 pg/mL

− 1 to 18 years: 0−80 pg/mL

− 18 years and older: 0−62 pg/mL

• Dopamine, plasma:

− 0 to 1 year: 0−42 pg/mL

− 1 to 18 years: 0−32 pg/mL

− 18 years and older: 0−48 pg/mL
Analyte

Adults, ≥18 years

(Supine)
Dopaminea 0.0–36.7 pg/mL
Epinephrineb 0.0–55.4 pg/mL
Norepinephrinea 115–524 pg/mL

Storage Instructions

Freeze. After centrifugation, the plasma must be frozen immediately.

Freeze. After centrifugation, the plasma can be stored up to two hours at room temperature. Sample can be kept for up to two weeks at -20°C.

Freeze. After centrifugation, the plasma must be frozen immediately.

Patient Preparation

Patient should discontinue drugs and other substances that may affect measured catecholamine results for at least one week before obtaining the specimen (see Limitations for details).

Patient should not be smoking for four to six hours. Walnuts, bananas, and α-methyldopa (Aldomet®) should be avoided for a week prior to sampling. Other drug interference may occur, including epinephrine and epinephrine-like drugs (eg, nosedrops, sinus and cough preparations, bronchodilators, appetite suppressants). Test is unreliable in subjects on levodopa or methenamine mandelate. Avoid patient stress.2 See Limitations. An indwelling heparinized venous catheter is advocated, since venipuncture can cause an increase in the substances for which testing is being done. Patient should remain supine in quiet surroundings for at least 30 minutes.

Patient should discontinue drugs and other substances that may affect measured catecholamine results for at least one week before obtaining the specimen (see Limitations for details).

Causes for Rejection

Specimen not drawn in correct tube; plasma not received frozen

Specimen not drawn in correct tube; plasma not received frozen; thawed specimen; inadequate patient preparation

Specimen not drawn in correct tube; plasma not received frozen

References

Bergmann ML, Schmedes A. Highly sensitive LC-MS/MS analysis of catecholamines in plasma. Clin Biochem. 2020 Aug;82:51-57. PubMed 32201304

Dunand M, Gubian D, Stauffer M, Abid K, Grouzmann E. High-throughput and sensitive quantitation of plasma catecholamines by ultraperformance liquid chromatography-tandem mass spectrometry using a solid phase microwell extraction plate. Anal Chem. 2013 Apr 2;85(7):3539-3544. PubMed 23432705

Neumann HPH, Young WF Jr, Eng C. Pheochromocytoma and Paraganglioma. N Engl J Med. 2019 Aug 8;381(6):552-565. PubMed 31390501

Smith MD, Maani CV. Norepinephrine. 2023 May 8. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan. 2024 Dec 11. PubMed 30725944

Bergmann ML, Schmedes A. Highly sensitive LC-MS/MS analysis of catecholamines in plasma. Clin Biochem. 2020 Aug;82:51-57. PubMed 32201304

Dunand M, Gubian D, Stauffer M, Abid K, Grouzmann E. High-throughput and sensitive quantitation of plasma catecholamines by ultraperformance liquid chromatography-tandem mass spectrometry using a solid phase microwell extraction plate. Anal Chem. 2013 Apr 2;85(7):3539-3544. PubMed 23432705

Neumann HPH, Young WF Jr, Eng C. Pheochromocytoma and Paraganglioma. N Engl J Med. 2019 Aug 8;381(6):552-565. PubMed 31390501

Smith MD, Maani CV. Norepinephrine. 2023 May 8. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan. 2024 Dec 11. PubMed 30725944

Footnotes

1. Lenders JW, Duh QY, Eisenhofer G, et al. Pheochromocytoma and paraganglioma: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2014 Jun;99(6):1915-1942. PubMed 24893135

2. Pacak K, Tella SH. Pheochromocytoma and Paraganglioma. 2018 Jan 4. In: Feingold KR, Anawalt B, Blackman MR et al, editors. In: Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000. 2018 Jan 4. PubMed 29465938

3. Neary NM, King KS, Pacak K. Drugs and pheochromocytoma--don't be fooled by every elevated metanephrine. N Engl J Med. 2011 Jun 9;364(23):2268-2270. PubMed 21651412

4. Jain A, Baracco R, Kapur G. Pheochromocytoma and paraganglioma-an update on diagnosis, evaluation, and management. Pediatr Nephrol. 2020 Apr;35(4):581-594. PubMed 30603807

5. Grouzmann E, Lamine F. Determination of catecholamines in plasma and urine. Best Pract Res Clin Endocrinol Metab. 2013 Oct;27(5):713-723. PubMed 24094641

6. Westfall TC, Westfall DP. Adrenergic agonists and antagonists. In: Brunton LL, Chabner BA, Knollmann BC, editors. Goodman and Gilman’s the pharmacological basis of therapeutics. 12th ed. McGraw Hill Companies; 2011. p. 277-334.

7. Lenders JWM, Eisenhofer G. Update on Modern Management of Pheochromocytoma and Paraganglioma. Endocrinol Metab (Seoul). 2017 Jun;32(2):152-161. PubMed 28685506

8. Mazzaglia PJ. Hereditary pheochromocytoma and paraganglioma. J Surg Oncol. 2012 Oct 1;106(5):580-585. PubMed 22648936

9. Zendron L, Fehrenbach J, Taverna C, et al. Pitfalls in the diagnosis of phaeochromocytoma. BMJ. 2004 Mar 13 328(7440):629-630. PubMed 15016696

10. Pacak K, Lenders JW, Eisenhofer G. Current trends in biochemical diagnosis of pheochromocytoma. In: Pacak K,Lenders JW, Eisenhofer G, editors. Pheochromocytoma: diagnosis, localization and treatment. 1st ed. Oxford: Blackwell; 2007. p. 72-92.

11. Stuerenburg HJ, Petersen K, Bäumer T, et al. Plasma concentrations of 5-HT, 5-HIAA, norepinephrine, epinephrine and dopamine in ecstasy users. Neuro Endocrinol Lett. 2002 Jun;23(3):259-261. PubMed 12080289

12. Devlin RJ, Henry JA. Clinical review: major consequences of illicit drug consumption. Crit Care. 2008;12 (1):202. PubMed 18279535

13. Haass M, Kübler W. Nicotine and sympathetic neurotransmission. Cardiovasc Drugs Ther. 1997 Jan;10(6):657-665. PubMed 9110108

14. de Jong WH, Eisenhofer G, Post WJ, Muskiet FAJ, de Vries EGE, Kema IP. Dietary influences on plasma and urinary metanephrines: implications for diagnosis of catecholamine-producing tumors. J Clin Endocrinol Metab. 2009 Aug;94(8):2841-2849. PubMed 19567530

15. de Jong WH, Post WJ, Kerstens MN, de Vries EGE, Kema IP. Elevated urinary free and deconjugated catecholamines after consumption of a catecholamine-rich diet. J Clin Endocrinol Metab. 2010 Jun;95(6):2851-2855. PubMed 20382681

16. Goldstein DS, Eisenhofer G, Kopin IJ. Sources and significance of plasma levels of catechols and their metabolites in humans. J Pharmacol Exp Ther. 2003 Jun;305(3):800-811. PubMed 12649306

17. Eisenhofer G, Kopin IJ, Goldstein DS. Catecholamine metabolism: a contemporary view with implications for physiology and medicine. Pharmacol Rev. 2004 Sep;56(3):331-349. PubMed 15317907

18. Guerrero MA, Schreinemakers JM, Vriens MR, et al. Clinical spectrum of pheochromocytoma. J Am Coll Surg. 2009 Dec;209(6):727-732. PubMed 19959041

19. Darr R, Kuhn M, Bode C, et al. Accuracy of recommended sampling and assay methods for the determination of plasma-free and urinary fractionated metanephrines in the diagnosis of pheochromocytoma and paraganglioma: a systematic review. Endocrine. 2017 Jun;56(3):495-503. PubMed 28405881

20. Miyamoto S, Yoshida Y, Ozeki Y et al. Dopamine-Secreting Pheochromocytoma and Paraganglioma. J Endocr Soc. 2021 Oct 29;5(12):bvab163. PubMed 34870059

21. Dubois LA, Gray DK. Dopamine-secreting pheochromocytomas: in search of a syndrome. World J Surg. 2005 Jul;29(7):909-913. PubMed 15951922

22. Foo SH, Chan SP, Ananda V, Rajasingam V. Dopamine-secreting phaeochromocytomas and paragangliomas: clinical features and management. Singapore Med J. 2010 May;51(5):e89-93. PubMed 20593136

23. Eisenhofer G, Peitzsch M, Bechmann N, Huebner A. Biochemical Diagnosis of Catecholamine-Producing Tumors of Childhood: Neuroblastoma, Pheochromocytoma and Paraganglioma. Front Endocrinol (Lausanne). 2022 Jul 26;13:901760. PubMed 35957826

24. Goldstein DS, Cheshire WP. Roles of catechol neurochemistry in autonomic function testing. Clin Auton Res. 2018 Jun;28(3):273-288. PubMed 29705971
1. Boomsma F, Alberts G, van Eijk L, Man in 't Veld AJ, Schalekamp MA. Optimal collection and storage conditions for catecholamine measurements in human plasma and urine. Clin Chem. 1993 Dec; 39(12):2503-2508. 8252722
2. Sheps SG, Jiang NS, Klee GG, van Heerden JA. Recent developments in the diagnosis and treatment of pheochromocytoma. Mayo Clin Proc. 1990 Jan; 65(1):88-95. 1967325
3. Knight JA, Wu JT. Catecholamines and their metabolites: Clinical and laboratory aspects. Lab Med. 1987; 18:153-158.
4. D'Alesandro MM, Reed HL, Robertson R, et al. Simplified method of collecting and processing whole blood for quantitation of plasma catecholamines. Lab Med. 1990; 26-29.
5. Feldman JM, Blalock JA, Zern RT, et al. Deficiency of dopamine-beta-hydroxylase. A new mechanism for normotensive pheochromocytomas. Am J Clin Pathol. 1979 Aug; 72(2):175-185. 474494
6. Rumley A. The in vitro stability of catecholamines in whole blood. Ann Clin Biochem. 1988 Sep; 25(Pt 5):565-586. 3232962
7. Bravo EL, Tarazi RC, Fouad FM, Vidt DG, Gifford RW Jr. Clonidine-suppression test: A useful aid in the diagnosis of pheochromocytoma. N Engl J Med. 1981 Sep 10; 305(11):623-626. 7266587
8. Landsberg L, Young JB. Pheochromocytoma. In Braunwald E, Isselbacher KJ, Petersdorf RG, et al, eds.Harrison's Principles of Internal Medicine. New York, NY: McGraw-Hill Book Co;1987:1775-1778.
9. Bravo EL, Gifford RW Jr. Current concepts. Pheochromocytoma: Diagnosis, localization, and management. N Engl J Med. 1984 Nov 15; 311(20):1298-1303 (review). 6149463

1. Lenders JW, Duh QY, Eisenhofer G, et al. Pheochromocytoma and paraganglioma: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2014 Jun;99(6):1915-1942. PubMed 24893135

2. Pacak K, Tella SH. Pheochromocytoma and Paraganglioma. 2018 Jan 4. In: Feingold KR, Anawalt B, Blackman MR et al, editors. In: Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000. 2018 Jan 4. PubMed 29465938

3. Neary NM, King KS, Pacak K. Drugs and pheochromocytoma--don't be fooled by every elevated metanephrine. N Engl J Med. 2011 Jun 9;364(23):2268-2270. PubMed 21651412

4. Jain A, Baracco R, Kapur G. Pheochromocytoma and paraganglioma-an update on diagnosis, evaluation, and management. Pediatr Nephrol. 2020 Apr;35(4):581-594. PubMed 30603807

5. Grouzmann E, Lamine F. Determination of catecholamines in plasma and urine. Best Pract Res Clin Endocrinol Metab. 2013 Oct;27(5):713-723. PubMed 24094641

6. Westfall TC, Westfall DP. Adrenergic agonists and antagonists. In: Brunton LL, Chabner BA, Knollmann BC, editors. Goodman and Gilman’s the pharmacological basis of therapeutics. 12th ed. McGraw Hill Companies; 2011. p. 277-334.

7. Lenders JWM, Eisenhofer G. Update on Modern Management of Pheochromocytoma and Paraganglioma. Endocrinol Metab (Seoul). 2017 Jun;32(2):152-161. PubMed 28685506

8. Mazzaglia PJ. Hereditary pheochromocytoma and paraganglioma. J Surg Oncol. 2012 Oct 1;106(5):580-585. PubMed 22648936

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LOINC® Map

Order Code Order Code Name Order Loinc Result Code Result Code Name UofM Result LOINC
084152 Catecholamines, Plasma 34551-2 081471 Norepinephrine, Pl pg/mL 2666-6
084152 Catecholamines, Plasma 34551-2 081489 Epinephrine, Pl pg/mL 2230-1
084152 Catecholamines, Plasma 34551-2 081497 Dopamine, Pl pg/mL 2216-0
Order Code084152
Order Code NameCatecholamines, Plasma
Order Loinc34551-2
Result Code081471
Result Code NameNorepinephrine, Pl
UofMpg/mL
Result LOINC2666-6
Order Code084152
Order Code NameCatecholamines, Plasma
Order Loinc34551-2
Result Code081489
Result Code NameEpinephrine, Pl
UofMpg/mL
Result LOINC2230-1
Order Code084152
Order Code NameCatecholamines, Plasma
Order Loinc34551-2
Result Code081497
Result Code NameDopamine, Pl
UofMpg/mL
Result LOINC2216-0