CPT: 83090
Print Share

Expected Turnaround Time

1 - 2 days

Related Information

Specimen Requirements


Plasma (preferred); serum is acceptable.


2 mL

Minimum Volume

1 mL


Lavender-top (EDTA) tube, green-top (heparin) tube, red-top tube, or gel-barrier tube


Plasma: It is important to centrifuge blood samples for plasma collection immediately after collection to separate the plasma from the blood cells. If immediate centrifugation is not possible, collected blood specimens should be kept on ice and centrifuged within an hour.

Serum:Allow 45 minutes for serum to clot and centrifuge to separate serum from cells immediately thereafter.

Storage Instructions

Room temperature. Stable at room temperature or refrigerated for 14 days. Stable frozen for six months.

Patient Preparation

A fasting specimen is preferred to establish baseline values or monitor treatment.

Causes for Rejection

Specimen received not separated from cells (do not respin a gel-barrier tube to harvest additional serum); gross hemolysis (eg, bright red or cherry red); whole blood tube without a gel separator; plasma from a light blue-top (sodium citrate) tube or yellow-top (ACD) tube used for coagulation studies (liquid citrate tubes have a dilutional effect of approximately 1.2 on this assay and are not approved for use); gross lipemia

Test Details


Screen patients who may be at risk for heart disease and stroke


This test is not intended for use in the diagnosis of folate or vitamin B12 deficiency.



Reference Interval

See table.


Male (µmol/L)

Female (µmol/L)

0 to 6 m



7 m to 1 y



2 to 12 y



13 to 17 y



18 to 60 y



61 to 70 y



71 to 80 y



>80 y



Additional Information

Severe homocysteinemia is typically caused by a rare inborn error of metabolism.1,2 The most common defect that can produce levels >100 μmol/L is homozygous cystathionine-β-synthase (CS) deficiency, which occurs with an incidence of 1 per 300,000 live births. About 1% of the population has heterozygous CS deficiency, a condition that typically results in moderate to intermediate hyperhomocysteinemia. Individuals with CS deficiency are at increased risk for occlusive vascular disease.1,2 Individuals with a thermolabile variant of the enzyme methylene-tetrahydrofolate reductase can have high normal to moderately elevated levels of homocysteine.1,2 Homocysteine can be considered to be an independent risk factor for the development of cardiovascular disease.1-3 Patients with cardiovascular disease, including heart disease, stroke, peripheral vascular disease, and thromboembolic disease generally have higher homocysteine levels than matched controls. The results of a large number of epidemiological studies have been analyzed through a meta-analysis.1 The increased risk, or odds ratio (OR), for coronary artery disease in patients with increased homocysteine levels was estimated to be 1.7. The OR for stroke was estimated to be 2.5 and the OR for peripheral vascular disease was estimated to be 6.8. Several conditions, other than specific genetic defects or cardiovascular disease, have been associated with hyperhomocysteinemia.1 These include vitamin deficiency, advanced age, hypothyroidism, impaired kidney function, and systemic lupus erythematosus. Medications including nicotinic acid, theophylline, methotrexate, and L-dopa have been reported to cause elevated homocysteine levels.


1. Malinow MR, Bostom AG, Krauss RM. Homocyst(e)ine, diet, and cardiovascular diseases: A statement for healthcare professionals from the nutrition committee, American Heart Association. Circulation. 1999; 99(1):178-182. 9884399
2. Clarke R, Stansbie D. Assessment of homocysteine as a cardiovascular risk factor in clinical practice. Ann Clin Biochem. 2001; 38(Pt 6):624-632. 11732645
3. Herrmann W. The importance of hyperhomocysteinemia as a risk factor for diseases: An overview. Clin Chem Lab Med. 2001; 39(8):666-674.11592431


Fortin LJ, Genest J Jr. Measurement of homocyst(e)ine in the prediction of arteriosclerosis. Clin Biochem. 1995; 28(2):155-162 (review). 7628074
Kang SS, Wong PW, Malinow MR. Hyperhomocyst(e)inemia as a risk factor for occlusive vascular disease. Annu Rev Nutr. 1992; 12:279-298. 1503807
Malinow MR. Plasma homocyst(e)ine and arterial occlusive diseases: A mini review. Clin Chem. 1995; 41(1):173-176 (review). 7813076
Robinson K, Mayer E, Jacobsen DW. Homocysteine and coronary artery disease. Cleve Clin J Med. 1994; 61(6):438-450 (review). 7828335
Ueland PM, Refsum H, Stabler SP, et al. Total homocysteine in plasma or serum: Methods and clinical applications. Clin Chem. 1993; 39(9):1764-1779 (review). 8375046
Verhoef P, Stampfer MJ, Buring JE, et al. Homocysteine metabolism and risk of myocardial infarction: Relation with vitamins B6, B12, and folate. Am J Epidemiol. 1996; 143(9):845-859. 8610698


Order Code Order Code Name Order Loinc Result Code Result Code Name UofM Result LOINC
706994 Homocyst(e)ine 13965-9 707009 Homocyst(e)ine umol/L 13965-9

For Providers

Please login to order a test

Order a Test

© 2021 Laboratory Corporation of America® Holdings and Lexi-Comp Inc. All Rights Reserved.

CPT Statement/Profile Statement

The LOINC® codes are copyright © 1994-2021, Regenstrief Institute, Inc. and the Logical Observation Identifiers Names and Codes (LOINC) Committee. Permission is granted in perpetuity, without payment of license fees or royalties, to use, copy, or distribute the LOINC® codes for any commercial or non-commercial purpose, subject to the terms under the license agreement found at https://loinc.org/license/. Additional information regarding LOINC® codes can be found at LOINC.org, including the LOINC Manual, which can be downloaded at LOINC.org/downloads/files/LOINCManual.pdf