Abstract-Oxidation of low density lipoproteins (LDL) obviously plays an important role in the pathogenesis of atherosclerosis. The purpose of the study was to determine whether antibodies against oxidized LDL are associated with coronary artery disease (CAD). We determined the serum levels of antibodies against copper-oxidized LDL by enzyme-linked immunosorbent assay in 58 patients with angiographically verified CAD and 34 controls without CAD. The mean antibody level, expressed in optical density units, was significantly higher in patients than in controls (0.150Ϯ0.088 versus 0.094Ϯ0.054, respectively; Pϭ0.00089). In logistic regression analysis, high antibody level against oxidized LDL was associated significantly with CAD (Pϭ0.0114), independent of age (Pϭ0.00137), gender (Pϭ0.0021), body mass index (Pϭ0.5947), triglyceride concentration (Pϭ0.9813), and total cholesterol-high density lipoprotein (HDL) cholesterol (Pϭ0.0080) group. Similar analysis in nondiabetic subjects (nϭ79) and in men only (nϭ75) showed analogous results, with only minor changes in P values. The antibody level against oxidized LDL differed significantly between nonsmokers and smokers in CAD patients (PϽ0.00197) but not in controls (PϭNS). In addition, the antibody level against oxidized LDL differed significantly between nonsmokers and smokers in subjects with low HDL cholesterol (Յ0.9 mmol/L) but not in subjects with high HDL cholesterol (Ͼ0.9 mmol/L). In conclusion, elevated levels of antibodies against oxidized LDL were associated with CAD. The data suggest that oxidized LDL plays a role in the pathogenesis of atherosclerosis and suggest a protective function for HDL against LDL oxidation.

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Chitosan (CAS 9012-76-4) is derived by alkaline deacetylation from chitin, an abundant polymeric product of natural biosynthesis especially in crustaceans. It is available in a primary, unorganised structure, but also in a microcrystalline form. As a dietary supplement, chitosan has been claimed to control obesity and to lower serum cholesterol. A variety of chitosan products have been freely available worldwide in health stores and pharmacies. This review summarises the current knowledge about cholesterol-lowering and safety properties of chitosan and focuses its possible application for the treatment of hypercholesterolaemia. Chitosan behaves as a polycationic(+) cellulose-like fibrillar biopolymer that forms films with negatively charged surfaces. It is not specifically hydrolysed by digestive enzymes in man, but limited digestion of chitosan due to bacterial flora and to the unspecific enzymes might occur. Negatively charged molecules in stomach attach strongly to the positive charged tertiary amino group (-NH3+) of chitosan. Therefore, chitosan reduces fat absorption from gastrointestinal tract by binding with anionic carboxyl groups of fatty and bile acids, and it interferes with emulsification of neutral lipids (i.e., cholesterol, other sterols) by binding them with hydrophobic bonds. In short-term animal studies the safety of chitosan has been good. There are only few studies with chitosan in humans. In man, dietary chitosan has been reported to reduce serum total cholesterol levels by 5.8-42.6% and low-density lipoprotein levels by 15.1-35.1%. In short-term trials up to 12 weeks, no clinically significant symptoms have been observed with chitosan compared to placebo. Mild and transitory nausea and constipation have been reported in 2.6-5.4% of subjects. Although chitosan has been clinically well tolerated, it cannot be recommended to people allergic to crustaceans.

ApoE allele epsilon4 may speed up the rate of decline of the GFR in patients with progressive diabetic renal disease.

Apolipoprotein (apo)E gene epsilon4 allele carrier status modulates the responses of lipoprotein metabolism to hormone-replacement therapy (HRT). We investigated the effect of long-term HRT on the progression of atherosclerosis in postmenopausal women with or without apoE epsilon4 allele. One hundred forty-one nonsmoking postmenopausal women, 45-71 yr old, were divided into 3 groups based on the use of HRT. The HRT-EVP group (n = 61) used sequential estradiol valerate (EV) plus progestin (P), the HRT-EV group used EV alone (n = 40), and a control group had no HRT. Of these 141 women, 93 participated in a 5-yr follow-up study in 1998. In addition to serum lipid concentration and apoE genotype, the atherosclerosis severity score of the abdominal aorta and carotid arteries was determined by sonography. In apoE4-negative subjects, the progression of atherosclerosis severity score was significantly faster in control than in the HRT groups (genotype-by-time interaction P = 0.0026); whereas in apoE4-positive subjects, there were no significant differences in atherosclerosis severity score progression between the control and HRT groups. The effects of HRT on atherosclerosis progression in subjects with no apo epsilon4-allele seems to be especially beneficial, compared with controls with same phenotype status but without HRT. These results may help us to understand, in more detail, the benefit and possible risk of HRT on atherosclerotic diseases.