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American Journal of Clinical Nutrition, Vol. 74, No. 2, 271-274, August 2001
© 2001 American Society for Clinical Nutrition

Letter to the Editor

Mild hyperhomocysteinemia: vitamin supplementation or not?

Roberto Cerone, Giuseppe Minniti, Antonella Piana, Ugo Armani and Renata Lorini

G Gaslini Institute, Department of Pediatrics, Largo Gaslini 5, 16148 Genova-Quarto, Italy, E-mail: cerone{at}unige.it

Dear Sir:

We read with interest the articles by Brattström and Wilcken (1) and Ueland et al (2), which raise several important questions about homocysteine and cardiovascular risk.

We studied 62 adults aged <45 y with vascular disease [20 with cerebrovascular disease (stroke or TIA; group 1), 20 with deep-vein thrombosis (group 2), and 22 with retinal vein occlusion (group 3)] and 25 healthy control subjects (3–6). We measured glucose, total cholesterol, triacylglycerol, creatinine, red blood cell folate, serum vitamin B-12, and plasma total homocysteine (tHcy) concentrations in blood samples collected at 0 h. An additional blood sample for measurement of plasma tHcy was collected 4 h after administration of oral methionine (100 mg L-methionine/g diluted in orange juice).

tHcy was determined by HPLC with fluorescence detection. In all patients, we tested for a mutation in the coding region of the MTHFR gene—a C-to-T substitution at nucleotide 677 (MTHFR 677C->T); 9.5% and 9.8% of groups 1 and 2, respectively, were homozygous for the MTHFR 677C->T polymorphism (NS compared with the control group). In group 3, 18% of the patients were homozygous for the mutation, which was significantly different from the value (10%) in control subjects (P < 0.05).

tHcy concentrations before and after the methionine load were higher in 15% of the patients in groups 1 and 2 than in the control subjects (fasting values: 12.5 ± 6.5 µmol/L compared with 7.6 ± 4.1 µmol/L; after the methionine load: 28 ± 10.1 compared with 17.4 ± 6.5 µmol/L); there was no significant increase in group 3. Values >=12 µmol/L were considered to indicate fasting hyperhomocysteinemia.

Our studies raised 2 questions: 1) Should we treat patients with mild hyperhomocysteinemia but not homozygous for the MTHFR 677C->T polymorphism or patients homozygous for the mutation but with normal tHcy concentrations? 2) Should decisions about treating mild hyperhomocysteinemia be based on absolute tHcy concentrations or on differences between tHcy concentrations measured after fasting and those measured after a methionine load?

Because homozygosity for the MTHFR 677C->T mutation is expected to increase cardiovascular risk only when tHcy concentrations are mildly elevated, we suggest that only patients with mild hyperhomocysteinemia receive folate supplementation. Finally, we believe that other risk factors that may provoke vascular lesions in patients with mild hyperhomocysteinemia must be considered before any decisions regarding folate supplementation be made.

REFERENCES

  1. Brattström L, Wilcken DEL. Homocysteine and cardiovascular disease: cause or effect? Am J Clin Nutr 2000;72:315–23.
  2. Ueland PM, Refsum H, Beresford SAA, Vollset SE. The controversy over homocysteine and cardiovascular risk. Am J Clin Nutr 2000; 72:324–32.
  3. Minniti G, Piana A, Armani U, Cerone R. Determination of plasma homocysteine by high performance liquid chromatography with fluorescence detection. J Chromatogr A 1998;828:401–5.
  4. Minniti G, Cerone R, Piana A, Armani U, Lorini R. Plasma and serum total homocysteine concentrations in paediatric patients, evaluated by high-performance liquid chromatography with fluorescence. Clin Chem Lab Med 2000;38:675–76.
  5. Piana A, Verrastro G, Minniti G, et al. Homocysteine and MTHFR genotype in young adults with retinal vein occlusion. Haematologica 2000;85:55–6.
  6. Cerone R, Minniti G, Piana A, Armani U, Susco G, Bertolini S. Screening for hyperhomocysteinemia in young adults with premature coronary artery disease. J Southeast Asian Trop Med Public Health 1999;30:145–9.




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