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Angiology
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*Peripheral Arterial Disease
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Plasma Homocysteine and Lipoprotein Profile in Patients with Peripheral Arterial Occlusive Disease

Volker Richter, PhD

Christian Janke, MD

Kathrin Purschwitz, MS

Bernd Klötzer, MD

Jürgen Geisel, MD

Wolfgang Herrmann, MD, PhD

F. Rassoul, PhD

Department of Clinical Chemistry and Pathobiochemistry University of Leipzig Paul-List-Straße 13 04103 Leipzig Germany

Several studies have identified moderate hyperhomocysteinemia (HCy) as an indepen dent risk factor for atherosclerosis. The purpose of this case control study was to determine lipoprotein profile and homocysteine concentration in serum of 85 male patients with peripheral arterial occlusive disease (PAOD) and in 51 normolipidemic age- matched male controls. Cholesterol, triglycerides, and high-density lipoprotein (HDL) cholesterol as well as subfractions HDL2 and HDL3 cholesterol, low-density lipoprotein (LDL) cholesterol, apo B, apo A-I, and lipoprotein particles LpA-I and LpA-I:A-II were measured in serum. Homocysteine, folic acid, and vitamins B6 and B 12 were determined with the help of high-pressure liquid chromatography. The 677 C -> T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene was analyzed in PAOD patients. Patients with peripheral arterial occlusive disease showed a significantly higher mean concentration of homocysteine than control subjects (p< 0.001). There was a negative correlation between the levels of homocysteine and vitamin B12 as well as folic acid (for vitamin B12: r=-0.40 and for folic acid: r=-0.38). The prevalence of hyperhomocys teinemia (Hcy > 16 µmol/L) in the patients was 45% in contrast to 8% in controls. HDL cholesterol, HDL3 cholesterol, Apo A-I, and Lp A-I were significantly reduced in patients and triglycerides were elevated. The elevated plasma homocysteine concentra tion is frequently seen in homozygous carriers of a point mutation (677 C -> T) in the methylenetetrahydrofolate reductase gene, as the product of this gene is an enzyme, participating in homocysteine remethylation. The homozygous state for the 677 C -> T mutation was found in 13.3% of PAOD patients.

Angiology, Vol. 51, No. 3, 189-196 (2000)
DOI: 10.1177/000331970005100302


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