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Biomedical subjects

O Leiss

Publications and source records attributed to O Leiss.

51 records · Page 3Linked to original sources
PubMed1984

Biliary lipid metabolism in children with chronic intrahepatic cholestasis.

Biliary lipid composition, standard liver function tests, serum lipids and faecal fat excretion were studied in 15 children with chronic intrahepatic cholestasis (severe intrahepatic cholestasis, n = 6; paucity of intralobular bile ducts, n = 4; benign recurrent cholestasis, n = 5) and compared to 15 children without gastrointestinal diseases. Severe and benign intrahepatic cholestasis were associated with normal or moderately elevated serum lipids. Biliary lipid concentrations were extremely reduced, bile acid concentrations were below the critical micellar concentration. This may account for the high incidence of gallstone formation in these patients. Remission periods in patients with benign recurrent cholestasis were not followed by complete normalisation of biliary lipid concentrations, indicating a primary defect in hepatic excretory function. Children with paucity of intralobular bile ducts showed markedly increased serum lipids, but only a two-fold reduction in biliary lipid concentrations. Cholic acid was the predominant bile acid in bile of all cholestatic children even during remission. Neither increased levels of monohydroxy bile acids nor unusual bile acids could be identified in notable amounts.

Adolescent↗
PubMed1984

Effects of phenobarbital on biliary lipid metabolism in children with chronic intrahepatic cholestasis.

The effects of phenobarbital (5.4-7.5 mg/kg body weight) for 14 days were studied in four children with severe intrahepatic cholestasis (group I) and in four with a syndromatic type of paucity of intralobular bile ducts (group II). Phenobarbital administration resulted in a moderate improvement of pruritus in all patients. There was a significant decrease of bilirubin in serum (group I: from 4.8 to 2.7 mg/dl; group II: from 6.1 to 2.1 mg/dl); total bile acids (group I: from 416 to 337 mumol/l; group II: from 156 to 123 mumol/l) and cholesterol (group I: from 248 to 207 mg/dl; group II: from 351 to 292 mg/dl). Alkaline phosphatase activity increased from 929 to 1126 U/l in group I and from 1751 to 2360 U/l in group II. SGOT and SGPT activities remained unchanged in both groups. In group I total biliary lipid concentration and bile acid output increased from 0.09 to 0.17 g/dl and from 3.9 to 7.2 mumol/kg per 30 min, respectively. Molar percentages of cholesterol, phospholipids and bile acids in bile remained unchanged. In group II total lipid concentrations and bile acid output increased from 1.62 to 2.0 g/dl and from 27.8 to 39.1 mumol/kg per 30 min, respectively. The molar percentage of cholesterol decreased from 5.6 to 3.5 mol%. The present results indicate that short term administration of phenobarbital has only minimal effects on biliary lipid metabolism in children with chronic intrahepatic cholestasis.

Bile↗
PubMed1984

Effect of short-term treatment with bezafibrate and fenofibrate on biliary lipid metabolism in patients with hyperlipoproteinaemia.

Sixteen patients with different types of hyperlipoproteinaemia were treated with the clofibrate analogues, bezafibrate or fenofibrate. Serum lipids and lipid composition of gallbladder bile were measured before and after 3-4 weeks of treatment. Both bezafibrate and fenofibrate reduced serum lipids effectively but increased the lithogenic index of bile from 1.11 to 1.47 and 1.25 to 1.80 (P less than 0.01), respectively, by increasing molar percent of cholesterol and decreasing molar percent of bile acids. Measurements of biliary lipid secretion in three patients before and after bezafibrate administration revealed a marked and significant increase in cholesterol secretion (from 119 to 166, from 58 to 128, and from 149 to 172 mumol h-1, respectively; P less than 0.05) without altering bile acid and phospholipid output. These results indicate that bezafibrate and fenofibrate exhibit the same effect on biliary lipid metabolism as clofibrate and might therefore induce cholesterol gallstone disease.

Bezafibrate↗
PubMed1984

Differences in the effects of chenodeoxycholic and ursodeoxycholic acid on biliary lipid secretion and bile acid synthesis in patients with gallstones.

Measurements of biliary lipid secretion rates were performed in 10 patients with radiolucent gallstones before and after 4 wk of administration of chenodeoxycholic acid and ursodeoxycholic acid (1 g/day) in a randomized crossover study. The results of both bile acid feeding periods were similar in many respects: expansion of the bile acid pool, increase in bile acid and phospholipid secretion, reduction in cholesterol output, and decrease in percent saturation of hepatic bile, which was more pronounced with ursodeoxycholic than chenodeoxycholic acid therapy. Despite these similarities, the mechanisms by which these two litholytic bile acids induced these changes were quite different. Ursodeoxycholic acid, in contrast to chenodeoxycholic acid, only partially suppresses bile acid synthesis. During chenodeoxycholic acid feeding, the ratio of phospholipids to bile acids increased from 0.264 to 0.307 (p less than 0.05), indicating an increased coupling of phospholipids by chenodeoxycholic acid, whereas ursodeoxycholic acid did not alter this ratio. The molar ratio of cholesterol to bile acid during the chenodeoxycholic- and ursodeoxycholic-acid periods decreased significantly from 0.073 to 0.058 and 0.041, respectively. However, this ratio during the ursodeoxycholic-acid period was unchanged when the amount of ursodeoxycholic acid was subtracted from total bile acid (0.069), indicating that UDCA has little, if any, effect on the mobilization of hepatic cholesterol into bile.

Adult↗
PubMed1984

Effect of three different dihydroxy bile acids on intestinal cholesterol absorption in normal volunteers.

Measurements of cholesterol absorption were performed by an intestinal perfusion technique before and after 4 wk of administration of three different dihydroxy bile acids [ursodeoxycholic acid (1 g/day), chenodeoxycholic acid (1 g/day), and deoxycholic acid (0.4 g/day)] in 6 normal volunteers. Mean hourly absorption of cholesterol declined from 41 mumol/h in the control period to 31 mumol/h (-22%) during feeding of chenodeoxycholic acid (NS). During deoxycholic acid administration, mean cholesterol absorption decreased from 46 to 28 mumol/h (-28%; p less than 0.05). Ursodeoxycholic acid feeding was associated with a reduction of cholesterol absorption from 38 to 13 mumol/h (-70%; p less than 0.05), even though the input of cholesterol from bile was reduced significantly (from 123 to 86 mumol/h). The results suggest that the hydroxy groups at different positions on the bile acid nucleus of these three dihydroxy bile acids differ in their potential for cholesterol absorption.

Adult↗
PubMed1983

[Relation between serum lipoprotein metabolism and biliary lipid metabolism].

This review concern with recent results regarding interrelationships between serum lipoprotein and bile acid metabolism. First, changes in bile acid metabolism in primary hyperlipoproteinaemia type II and type IV are described. In addition, influences of lipid-lowering drugs such as sitosterol, cholestyramine/colestipol, neomycin, nicotinic acid, clofibrate and thyroxin on serum lipoproteins and biliary lipid metabolism are discussed. Changes in lipoprotein metabolism in disorders of bile acid metabolism and effects of primary and secundary bile acids on lipoprotein metabolism, hepatic cholesterol metabolism and intestinal cholesterol absorption are described. In the final discussion interrelationships between very low density lipoprotein - triglycerides and cholic acid metabolism as well as low density lipoprotein and chenodeoxycholic acid metabolism are stressed. The positive correlation between serum triglycerides and lithogenicity of bile is underlined and the possible significance of high density lipoprotein-cholesterol as precursor of biliary cholesterol is discussed.

Bile↗
PubMed1983

Lipid composition of human aqueous humor.

The lipid composition of human aqueous humor was determined in ten samples from patients undergoing cataract surgery. The mean concentration was 16.4 mg/dl for total lipids, 2.5 for phospholipids, 1.1 for free fatty acids, 1.7 for unesterified cholesterol 2.0 for triglycerides, and 9.0 mg/dl for cholesterol esters, respectively. The presence of lipids in aqueous humor suggests that lipids are transported through the human aqueous humor.

Aged↗
PubMed1982

Different effects of chenodeoxycholic acid and ursodeoxycholic acid on serum lipoprotein concentrations in patients with radiolucent gallstones.

The effect on serum lipoprotein concentrations of chenodeoxycholic acid (CDCA) and ursodeoxycholic acid (UDCA) was examined in eight normolipemic patients with radiolucent gallstones during constant liquid formula infusion into the duodenum. Every patient received each bile acid (1000 mg/day) during two consecutive randomized 4-week periods. During treatment with CDCA but not UDCA, the serum triglycerides decreased by an average of 26%. Mean HDL cholesterol decreased by 46% during CDCA therapy and remained unchanged during UDCA administration. Simultaneous measurements of biliary lipid secretion showed a significant negative correlation between HDL cholesterol concentration and hepatic secretion of CDCA (r = -0.652) and a positive correlation between the LDL cholesterol/HDL cholesterol ratio and hepatic secretion of CDCA (r = 0.840). Despite their close chemical relationships and similar effects on biliary lipids, CDCA and UDCA differ markedly in their effects on serum lipoproteins. Because of this and minor side effects, UDCA seems to be a safer agent than CDCA for cholesterol gallstone dissolution.

Adult↗
PubMed1979

[The microanalysis of serum lipoprotein lipids (author's transl)].

A method is described which allows the determination of phospholipids, free and esterified cholesterol, triglycerides and free fatty acids in lipoprotein fractions starting from 50 microliter of serum. Lipoproteins were separated by successive precipitation: VLDL with Heparin/Mg++, LDL with Dextran sulfate/Mg++ and finally HDL with Dextran sulfate/Mn++. Lipids extracted from the precipitated lipoproteins were determined gravimetrically and by densitometry after thin layer chromatography and charring (van Gent, C.M. (1968), Z. Anal. Chem. 236, 344--350; Egge, H. et al. (1970) Z. Klin. Chem. Klin. Biochem. 8, 488--491). The results obtained from the serum of 12 adult healthy persons were compared with those from lipoprotein fractions separated by preparative ultracentrifugation (Havel, R. J. et al. (1955) J. Clin. Invest. 34, 1345--1353). The distribution of lipids in beta-lipoproteins (d less than 1.063 g/ml) and HDL (1.063 less than d less than 1.21 g/ml) prepared by both methods showed good agreement. Some differences were observed between VLDL (d less than 1.006 g/ml) and VHDL (d greater than 1.21 g/ml) prepared either by precipitation or ultracentrifugation. Compared to the total lipid of the sera, recovery rates were 95--105%. Variation coefficients were in the range of 15--20% for VLDL lipids, 5--10% for LDL and HDL lipids and 10--15% for VHDL lipids. Gravimetrically determined total lipids had a variation coefficient of 4 and 6% for LDL and HDL respectively.

Cholesterol↗
PubMed1976

[Metabolic degradation of cartilage by leucocyte enzymes under the influence of antirheumatic drugs (author's transl)].

Lately the importance and participation of leucocytes in rheumatoid arthritis have been discussed. In order to study catabolic reactions in connective tissue we investigated the autolytic liberation of mucopolysaccharides in cartilage alone and in the presence of leucocyte enzymes. Factors of optimal experimental conditions, such as pH and constituents of incubation medium, incubation time and the number of leucocytes, were determined. In further experiments we studied the influence of antirheumatic drugs, such as sodium salicylate, phenylbutazone, pentosanpoly-sulfate and gold thiopolypeptide, on cartilage degradation. In our experiments only phenylbutazone and pentosanpoly-sulfate exerted an inhibitory effect on leucocyte-stimulated degradation of cartilage. The relevance of this finding for the therapeutic use of these drugs is evaluated.

Animals↗
PubMedDate not supplied

[Clinico-pharmacologic considerations in Helicobacter pylori eradication therapy].

Problems and pitfalls of treatment regimens for eradication of Helicobacter pylori (Hp) are discussed from a clinical, pharmacological and microbiological point of view. Problems concerning the physician who treats the patient consists mainly in inappropriate indication and suboptimal knowledge of drugs, doses and duration of therapy against Hp. For successful triple therapy with complicated dosage protocols cooperation with and compliance by the patient is stressed. Physicochemical, pharmacological and pharmacokinetic properties of bismuth salts and antibiotics as well as physiological aspects of pH and motility in the stomach must be considered in order to achieve optimal antibactericidal concentrations in the special micro milieu of Hp in the mucus/on the mucosa of the stomach. In addition, present pretreatment resistance of Hp against antibiotics and possible acquired resistance during antibiotic treatment are important aspects. Successful eradication of Hp mainly depends on the physician's clinical and pharmacological knowledge of bismuth salts and antibiotics, on considerations of microbiological aspects of Hp, on good doctor-patient-relationship and compliance by the patient.

Anti-Bacterial Agents↗