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1. Patient's age and gender are required.
2. Immediately place specimen on wet ice.
3. Centrifuge and aliquot plasma into plastic vial within 4 hours of collection.
4. If blood cannot be placed on wet ice immediately, centrifuge and aliqout plasma into plastic vial within 1 hour of collection.
5. A refrigerated centrifuge is not required if the above time restrictions are met.
Homocysteine concentration is affected by supplementation of vitamins B12, B6, or folate.
Factors that may influence and increase plasma homocysteine include:
-Poor diet/cofactor deficiencies
-Chronic kidney disease/renal disease
Medications that may increase homocysteine concentrations include:
Homocysteine is an intermediary in the sulfur-amino acid metabolism pathways, linking the methionine cycle to the folate cycle. Inborn errors of metabolism that lead to homocysteinemia or homocystinuria include cystathionine beta-synthase deficiency (homocystinuria) and various defects of methionine remethylation. Genetic defects in vitamin cofactors (vitamins B6, B12, and folate) and nutritional deficiency of vitamin B12 and folate also lead to abnormal homocysteine accumulation.
Homocysteine concentration is an indicator of acquired folate or cobalamin deficiency and is a contributing factor in the pathogenesis of neural tube defects. Homocysteine was also thought to be an independent predictor of cardiovascular disease (atherosclerosis, heart disease, thromboembolism), as early observational studies prior to the year 2000 linked homocysteine to cardiovascular risk and morbidity and mortality. However, following U.S. Food and Drug Administration mandated folic acid supplementation in 1998, homocysteine concentrations decreased by approximately 10% without a similar change in cardiovascular or ischemic events. Currently, the use of homocysteine for assessment of cardiovascular risk is uncertain and controversial. Based on several meta-analyses, at present, homocysteine may be regarded as a weak risk factor for coronary heart disease, and there is a lack of direct causal relationship between hyperhomocysteinemia and cardiovascular disease. It is most likely an indicator of poor lifestyle and diet.
This test should be used in conjunction with plasma amino acids, quantitative acylcarnitines, methylmalonic acid, and urine organic acids to aid in the biochemical screening for primary and secondary disorders of methionine metabolism.
Elevated homocysteine concentrations are considered informative in patients evaluated for suspected nutritional deficiencies (vitamin B12, foltate) and inborn errors of metabolism. Measurement of methylmalonic acid (MMA) distinguishes between B12 (cobalamin) and folate deficiencies, as MMA is only elevated in vitamin B12 deficiency. Treatment response can be evaluated by monitoring plasma homocysteine concentrations over time.