[Cholesterol esterification catalysed by LCAT and erythrocyte lipid pattern in Wilson's disease].
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Biomedical subjects
Publications and source records attributed to H Wehr.
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Antibodies directed to native and to in-vitro acetaldehyde-modified (ethylated) low-density lipoproteins (LDL) were determined in 28 alcoholic subjects divided into two groups: one with no clinical nor laboratory evidence of liver involvement and the second with histologically proven alcohol-related liver disease. The control group consisted of 18 individuals who drank alcohol socially. In the individuals with alcoholic liver disease IgG reactivity against both native and ethylated LDL was significantly higher than in alcoholic individuals without liver injury. High levels of IgG reactivity in individuals with alcoholic liver disease were also observed against malondialdehyde-modified, methylated, acetylated and carbamylated LDL. A selective high anti-ethylated LDL IgG reactivity was observed in 11% of control subjects.
In 64 individuals with dementia (26 Alzheimer type, 34 of vascular origin and 4 other types of dementia) apolipoprotein E genotype was identified. Frequency of epsilon4 allele was 36.5% in Alzheimer patients and 32.4% in vascular dementia ones. In a group of 39 nondemented individuals of the same age the epsilon4 frequency was 11.5%. In demented patients, carriers of epsilon4, a tendency to higher plasma levels of atherogenic lipids (total cholesterol and low-density lipoprotein cholesterol) as compared with noncarriers was observed. It is possible that the epsilon4 form may aggravate the course of dementia through a moderate influence on the atherogenic lipoprotein level. The results showed that both Alzheimer disease and vascular dementia shared the same risk factors which is consistent with current opinion about a link existing between these two types of dementia.
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The aim of this work was the evaluation of low density lipoprotein (LDL) susceptibility to oxidation in the survivors of ischaemic stroke. The investigations were performed in 65 individuals at least three months after the onset of acute symptoms. In 24 patients stroke was caused by alterations in main cerebral arteries, in 19 by considerable narrowing of carotid artery, in 15 by alterations in small cerebral arteries with often accompanying hypertension and/or diabetes (lacunar stroke) and in 7 by embolism of cardiac origin in individuals with cardiac arrhythmia and coronary artery disease. The control group comprised 25 age matched persons without pathological symptoms. Plasma lipids and apolipoprotein B levels were determined as well as two antioxidants: alpha-tocopherol level and superoxide dismutase activity. The evaluation of lipid peroxidation was performed by determining thiobarbituric acid reacting substances (TBARS) and lipid peroxides (LPO) increase after 5 hours oxidation of isolated LDL in vitro in the presence of copper ions. The level of IgG directed against modified LDL was also evaluated. In the patients decreased HDL cholesterol level was observed as well as increased apolipoprotein B. In the group of thrombotic strokes high triglycerides were observed. alpha-tocopherol level was decreased in the group of cerebral strokes. The amounts of oxidation products did not differ between the whole group of patients after stroke and the controls. A significant increase concerned only the group of lacunar strokes. The evaluation of LDL susceptibility to oxidation in patients after stroke by measuring absorption at 234 nm and determining the time period necessary to the onset of intensive LDL oxidation will be the subject of a separate publication.