Search PubMed⌕ Search

Biomedical subjects

G Mühlfellner

Publications and source records attributed to G Mühlfellner.

At least 19 recordsLinked to original sources
PubMed1980

[On the effect of etofylline clofibrate on serum lipids and lipoproteins in patients with hyperlipoproteinemia of various degrees (author's transl)].

Efficacy and tolerance of 1-(theophyllin-7-yl)-ethyl-2-[2-(p-chlorophenoxy)-2-methylpropionate] (etofylline clofibrate, Duolip) was investigated in 54 out-patients, 18 of whom were of Fredrickson-Types IIa, IIb and IV, over a therapeutical period of 4 months, in comparison to initial and final placebo phases of 4 weeks each. In type IIa etofylline clofibrate shows a good effect on total cholesterol and on the cholesterol fractions, both with regard to the collective treated and to the low dosage of 750 mg/d etofylline clofibrate compared to the usual dosage of 1500 mg clofibrate. The activity of etofyllineclofibrate on type IIb is inconsistent. Decreases of total cholesterol, i.e., of VLDL cholesterol along with high decreases of triglycerides in VLDL and LDL are measurable, but not significant. In type IV total cholesterol is distinctly decreased, along with high decreases of VLDL cholesterol and particularly so of the relevant VLDL triglycerides. Subjective and objective tolerability of etofylline clofibrate was most favourable.

Cholesterol↗
PubMed1980

Clinical experience with bezafibrate.

We report on 41 patients with primary hyperlipoproteinemia (type IIa, IIb and IV) treated with 450 to 600 mg of bezafibrate for 12 months. Placebo periods of 8 weeks surrounded the treatment period. In types IIa and IIb total cholesterol decreased by up to 18,7%, triglycerides to 34,6%. In type IV serum triglycerides decreased up to 48,2 and cholesterol by 12,2%. In a second investigation we differentiated the cholesterol- and triglyceride-values of 16 patients regularly controlled. We found a significant decrease during the treatment period. Bezafibrate is a potent lipid-lowering agent of the new generation.

Bezafibrate↗
PubMed1980

Creatinekinase in hyperlipoproteinemic patients treated with clofibrate.

Elevations of serum CK levels in patients treated with clofibrate have been reported in many case reports since the primary description of the acute muscular syndrome in 1968. The main point of interest in the beginning of our study were difficulties in differential diagnosis of acute heart attacks in patients treated with clofibrate. Since the rapid CK MB assays have become available, this difficulty has been eliminated. No equivocal answer was given in single case reports with regard to the prognosis of drug-induced increases of this skeletal muscular enzyme. Our experience collected in a now 5 years lasting follow-up study shows that isolated CK-elevations without clinical symptoms do not coincide with the development of skeletal muscular damage or disease.

Clofibrate↗
PubMed1979

Effect of polyenyl phosphatidyl choline on clofibrate-induced increase in LDL cholesterol.

In a double-blind, randomised, cross-over trial clofibrate and a combination of polyenyl phosphatidyl choline (PPC) plus clofibrate were tested in 67 patients with hyperlipoproteinemia. Each treatment lasted for 4 weeks and was separated by a 4 week placebo period. The daily doses were clofibrate 1.2 g and PPC 1.8 g + clofibrate 1.2 g. respectively. The results revealed that polypenyl phosphatidyl choline prevented the elevation of LDL-cholesterol induced by clofibrate treatment, and that the lipid-lowering potency of the combination did not differ significantly from that of clofibrate. Since elevation of LDL-cholesterol is considered to increase the risk of coronary heart disease, the combination appears to offer a therapeutic advantage. Despite the significance of this clinical observation, a final decision may only be obtained from a prospective, long term investigation in patients with coronary heart diseases and hyperlipoproteinemia.

Adult↗
PubMed1978

Plasma lipids, triglyceride/fatty acid pattern, and plasma insulin in fasted healthy volunteers during continuous ingestion of ethanol. Influence of lipolysis inhibited by nicotinic acid.

Healthy fasted volunteers were subjected to an acute oral ethanol load over 12 h after a diet of 3 days with high linolenic acid content. Free fatty acids, triglycerides, glycerol, phospholipids, cholesterol and insulin, as well as the fatty acid pattern of triglycerides in the plasma, were determined during the test. The test was repeated with nicotinic acid added. The lipid values obtained and the comparisons of fatty acid composition both indicate that the predominant role of peripheral lipolysis in the genesis of acute ethanol-induced hypertriglyceridemia, in spite of the possibility of enhanced synthesis of palmitic acid in the liver.

Adipose Tissue↗
PubMed1978

[Coronary artery reserve in patients with hyperlipoproteinemias (author's transl)].

The coronary reserve was measured in 119 patients with different types of primary hyperlipoproteinemia. Cardiovascular diseased with clinical manifestation were excluded. 90 patients of same age with normal serum lipids served as controls. The groups did not differ in other risk factors as blood pressure or overweight (the latter excluded in hyperlipoproteinemia type IV). The controls showed decreased coronary reserve in 8%, type IIa patients in 36%, IIb patients in 18% and type IV patients in 23%. The frequency of restriction in coronary flow increased with age: in hyperlipoproteinemic patients of 50 years and more it was found in nearly 40%. Further interesting results were the significantly higher systolic and diastolic blood pressures reached during exercise in our hyperlipoproteinemic patients.

Adolescent↗
PubMed1977

[Beta-sitosterin in the treatment of essential type II hyperlipoproteinemias].

The effect of Beta-Sitosterol (Sitosterin Delalande) on plasma lipids in 20 pretreated patients with type IIa and IIb familial hyperlipoproteinemia is reported. 6-18 g of the drug were given for a time of two to twelve months. In 11 patients the plasma cholesterol level decreased between 10 and 30%. Since Beta-Sitosterol has no effect on plasma triglycerides, an additional hypertriglyceridemia must be taken care of and treated if necessary. Beta-Sitosterol can be called an effective substance in the treatment of hypercholesterinemia. In addition the diet cure becomes easier.

Adult↗
PubMed1977

Studies on the metabolic defect in Broad-beta disease (hyperlipoproteinaemia type III).

The apoprotein composition of the main lipoprotein fractions (VLDL, LDL-1, LDL-2 and HDL) was studied initially in 15 patients with Broad-beta disease. Analytical isoelectric focusing of urea-soluble apo-VLDL and apo LSL-1 demonstrated a variant pattern of the polymorphic Apoprotein E with a deficient Apo E-III band in all patients. The Apo E-III deficiency pattern was seen in only six out of 304 hyperlipidaemic controls. These six Apo E-III deficient controls had characteristic signs of Broad-beta disease, and thus represented patients not previously recognized as having the disorder. The Apo E focusing patterns were constant on repeated examinations and were stable under different metabolic conditions. The data show that Apo E-III deficiency in VLDL is a specific qualitative marker for Broad-beta disease, allowing an unequivocal diagnosis that had not been possible previously. Indirect evidence suggests that Apo E-III deficiency is the basic lipoprotein abnormality underlying the familial dyslipoproteinaemia.

Adult↗
PubMed1976

[Changes of triglycerid-fatty acids in healthy volunteers during acute ethanol ingestion with and without blocking peripheral lipolysis (author's transl)].

This investigation decided to answer the question of the origin of fatty acids for the increased synthesis of triglycerides in acute ethanol-induced hyperlipoproteinemia. Healthy persons ingested 0.5 g of ethanol/kg body weight initially and 0,15 g of ethanol/kg and hour for 12 hours. The fatty acids of plasma triglycerides were determined before and after ingestion of ethanol in persons fasting and nourished isocaloricaly, with and without blocking peripheral lipolysis by nicotinic acid and with addition of glucose. The fasting persons triglycerides fatty acids increased to 165.7 % of the initial value after 12 hours of ethanol ingestion, with a preferential increase in palmitic-, oleic- and stearic acid. When lipolysis in adipose tissue was blocked by 0.5 g of nicotinic adic/hour the triglyceride-fatty acids reached only 116.2% after 12 hours, with a decrease in oleic acid, which is present in adipose tissue to a higher degree than in plasma triglycerides. When nourished isocaloricaly, the enhancement of plasma triglyceride-fatty acids could not be suppressed by nicotinic acid. The changes in concentration and pattern of triglyceride-fatty acids announce that the fatty acids used for increased synthesis of triglycerides in fasting persons come from adipose tissue preferentially. In contrast ethanol-ingested hyperlipoproteinemia during ingestion of a food which cannot be suppressed by nicotinic acid, seems to orginate from fatty acids of the food and for de novo synthesis of fatty acids in the liver.

Adipose Tissue↗
PubMed1976

[Beta-sitosterin in unsuccessfully pretreated patients with hypercholesteremia. Simultaneously, a contribution to dose dependence].

To 9 patients with hyperlipoproteinemia type II and treated with different hypolipidemic drugs without success, sitosterol was given for a period of 4 to 16 months. The effective dose was 10.56 to 21.12g beta-sitosterol corresponding to 12 to 24g granulate. One patient developed a serious diarrhoe and dropped out. 4 patients showed an impressive decrease of serum cholesterol levels.

Adult↗