[Therapy of hypercholesteremia with apple pectin].
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Biomedical subjects
Publications and source records attributed to P Weisweiler.
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Six female patients with a primary hyperlipoproteinemia type IIa received 40 mg/day etiroxate for 2 months. Serum lipids, low density and high density lipoprotein cholesterol, the apolipoproteins B and A-I, and cholesterol and apolipoprotein A-I in ultracentrifuged HDL2 and HDL3 were analysed before and after the treatment. Etiroxate caused a significant reduction in serum cholesterol, LDL-cholesterol, and serum apolipoprotein B. Concerning the HDL, there was a significant decrease in HDL-cholesterol. The analysis of HDL subfractions revealed a uniform fall in HDL2-cholesterol and HDL2-apolipoprotein A-I. It is concluded that detailed information about lipoproteins leads to a better understanding of the relationships between drug treatment and the possible prevention of atherosclerotic diseases.
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Serum lipids, lipoproteins and apolipoproteins were measured in 16 obese female subjects before and after a short-term fast of four days. The mean body weight loss was 2.9 +/- 0.8 kg. Serum triglycerides decreased, serum, LDL, and HDL cholesterol increased significantly. Furthermore there was a significant reduction of the serum apolipoprotein B concentration, while apolipoprotein A I did not change. The atherogenic ratio apo B/apo A I were significantly lowered by the fasting period.
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The effect of 3 months' treatment with D-thyroxine on the lipoprotein lipids and apolipoproteins AI and B was investigated in 12 patients with type IIa hyperlipoproteinemia. VLDL, LDL and HDL were separated by preparative ultracentrifugation. Both apolipoproteins were measured in serum by electroimmunoassay procedures with monospecific antisera. There was a significant decrease of cholesterol, phospholipids and apolipoprotein B in serum and of all lipids in the LDL class. VLDL and HDL lipids and apolipoprotein AI showed no significant alterations. The atherogenic ratios LDL/HDL lipids and apolipoprotein B/apolipoprotein AI were lowered with the most pronounced effect on the ratio between the two apoliopoproteins. It is concluded that there is an effective reduction of LDL particles by D-thyroxine. Further investigations are necessary to evaluate whether lipoprotein lipids or apolipoproteins are a better discriminator of the influence on atherosclerotic risk in type IIa hyperlipoproteinemia.
The effect of a six-month treatment with bezafibrate on HDL2 and HDL3, measured as cholesterol and apolipoprotein A-I, was studied in 10 hypertriglyceridemic patients. The significant increase of total HDL-cholesterol and HDL-apolipoprotien A-I was due to an increase of HDL2-cholesterol and HDL2-apolipoprotein A-I. The lowered ratio of cholesterol to apolipoprotein A-I in HDL, HDL2, and HDL3 remained unaltered. It is concluded that bezafibrate raises the possibly antiatherogenic HDL2, whereas the disturbed cholesterol/apolipoprotein A-I ratio is not changed.
Cholesterol as well as phospholipids in high-density lipoproteins (HDL) have been measured in 60 serum samples after heparin-manganese chloride precipitation of the apolipoprotein B containing lipoproteins. The values obtained correlated well with values from ultracentrifugal separation (slope 1.11 for cholesterol, 0.92 for phospholipids). Furthermore, there was a significant correlation between the low-density lipoprotein (LDL) cholesterol estimated by the formula of Friedewald et al. and the ultracentrifugally separated LDL cholesterol (slope 1.02). By the additional determination of HDL phospholipids with a precipitation procedure, further information about the "antiatherogenic" is easily available.
The effect of long-term treatment over 6 months with beta-pyridylcarbinol on the lipoprotein lipids was investigated in 12 patients with primary type IIa hyperlipoproteinemia. VLDL, LDL and HDL were separated by preparative ultracentrifugation. There was a significant decrease of serum cholesterol and phospholipids. The normal serum triglycerides were unaffected. While VLDL and HDL lipids showed no signicant alterations, the LDL lipids decreased. The atypical lipid composition of the LDL was changed towards normal. Though there was a significant decrease of the "atherogenic" LDL/HDL-lipid ratios after 6 months treatment, beta-pyridylcarbinol did not result in a normalization of this ratio.
The effect of 3 months' treatment with cholestyramine on lipoprotein lipids was investigated in 12 patients. VLDL, LDL and HDL were separated by preparative ultracentrifugation. There was a significant decrease of serum cholesterol and phospholipids and an increase of serum triglycerides. All the VLDL-lipids increased by nearly 30%. The LDL-lipids decreased with a tendency for normalisation of their atypical lipid composition. The small but significant alterations of HDL triglycerides and cholesterol are correlated with the corresponding alterations of the other lipoproteins; the HDL-phospholipids were unchanged. The LDL/HDL-lipid ratios were decreased but not normalised. The 30% decrease of LDL-cholesterol is negatively correlated with an increase in all the VLDL-lipids.
The cholesterol in high density lipoproteins (HDL) has been determined in 140 serum samples after dextran sulfate-magnesium chloride precipitation of the apolipoprotein B-containing lipoproteins. The values correlated well with simultaneously measured values from preparative ultracentrifugation (slope 0.98, r = 0.93). Furthermore, there was a significant correlation in 60 specimen between the dextran sulfate-MgCl2 and heparin-MnCl2-precipitation method.
The changes of serum lipoprotein lipids including the phospholipids of twelve hyperlipoproteinemic patients were studied after a four weeks treatment with 1200 mg/day gemfibrozil. There was a decrease of all VLDL lipids as well as of LDL and HDL triglycerides and an increase of HDL cholesterol. The phospholipids were influenced in different directions, particularly their concentration in the HDL was constant. The LDL/HDL lipid ratios remained elevated after gemfibrozil. To evaluate the effect of a hypolipidemic drug in more detail, the analysis of the complete lipoprotein lipid moiety and the ratios within and between the lipoproteins would be helpful.
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Cholesterol, triglyceride and phospholipid concentrations of VLDL, LDL and HDL were studied in 20 patients with primary type IIb, 25 patients with primary type IV and in 18 controls. Both types are not only characterized by different concentrations of lipoprotein lipids, but also by their different lipid composition. Type IIb had more triglycerides in the LDL, type IV in the LDL and HDL. The HDL cholesterol content of type IV was decreased. The percent phospholipid concentration of HDL was identical in the 3 groups, demonstrating the constant role of this lipid fraction. The lipid relationships between the lipoproteins showed that the LDL/HDL lipid ratio of type IIb exceeded type IV ratio in spite of normal HDL lipid concentration in type IIb.
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The effect of clofibrate treatment (1.5 g/day for four weeks) on triglycerides, cholesterol and phospholipids in very low density lipoproteins (VLDL), low density lipoproteins (LDL) and high density lipoproteins (HDL) was investigated in 12 patients with type IV hyperlipoproteinaemia. The decrease of serum triglycerides was due to the reduction of VLDL-triglycerides. Furthermore, LDL-hypertriglyceridemia was normalised by clofibrate. -- There existed a significant decrease of VLDL- und HDL-cholesterol as well as of VLDL-phospholipids. The changes in LDL-cholesterol and LDL-phospholipids by clofibrate depended on their initial concentrations which were negatively correlated to the serum triglycerides before treatment. -- The normalisation of lipid concentrations in VLDL and LDI could be explained by a stimulated delipidation of the apo B-lipoproteins.
21 patients with primary hyperlipoproteinemias of type IIb and IV were treated for 8 weeks with placebo, 8 weeks with 0.3 g butylbiguanide and 1.5 g clofibrate/day and then for 8 weeks with 1.5 g clofibrate/day. In 12 patients a second placebo phase of 8 weeks followed. After 8 weeks of combined treatment with butylbiguanide and clofibrate the serum triglycerides decreased from 725 mg to 269 mg/100 ml. During the following period of clofibrate treatment the serum triglycerides increased after 4 and 8 weeks to 326 mg and 306 mg/100 ml respectively. The combined treatment with 0.3 g butylbiguanide and 1.5 g clofibrate/day is more effective in lowering elevated serum triglycerides and cholesterol than 1.5 g clofibrate alone.