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Biomedical subjects

A Stiehl

Publications and source records attributed to A Stiehl.

At least 19 recordsLinked to original sources
PubMed1979

[The effect of lipid level lowering diets on bile lipids and plasma lipoproteins in normal persons].

The effects of two fat-modified diets, one rich in polyunsaturated and the other in oleic acids, were studied in 10 healthy young males with regard to bile lipid composition, plasma lipids and lipoproteins. The two experimental diets were given for 2 weeks each and findings compared with those from the subject's normal diet. The fat-modified diets had marked but comparable effects on plasma total cholesterol (decreases by 23% and 16% respectively), on LDL-cholesterol (decreases by 27% and 17% respectively) and on HDL-cholesterol (decreases by 26% and 27% respectively). HDL apolipoproteins A-I and A-II were unaffected. Therefore, the apo A-I/HDL-cholesterol and apo A-II/HDL-cholesterol ratios significantly increased. The "lithogenic index" as a measure for the relationship of cholesterol to bile acids and phospholipids, and thus for the solubility of cholesterol in gallbladder bile, was not affected by the lipid lowering diets, which therefore should not increase the risk of cholelithiasis.

Adult↗
PubMed1979

A bile-acid-rich high-density lipoprotein (HDL) in acute hepatitis.

Severe liver dysfunction is often associated with alterations of plasma lipids and lipoproteins. In this study the high-density lipoprotein (HDL) class has been further investigated. HDL from patients with acute, cholestatic hepatitis (n = 10) was isolated and compared with that of normals. Lipid and protein analyses were performed during the acute stage of the disease, with consequent follow-up studies. It was found that (1) only apo A-I was decreased by 50% in the isolated HDL fractions, whereas apo A-II remained unchanged; apo A-I in total plasma was normal; (2) immunoelectrophoresis of hepatitis HDL against monospecific anti-A-II revealed one precipitin line but two or more bands against anti-A-I; (3) concomitant with an increase of phospholipids and a decrease of triglycerides and the total cholesterol fraction, hepatitis HDL contained 10--12 times more bile acid than normal HDL. Chenodeoxycholic acid was the predominant bile acid. These alterations were fully reversible when patients recovered. These parameters seem to be sensitive markers for the degree of disturbance and restoration of liver function. The structural-functional implications of the observed compositional changes of HDL during cholestasis are discussed.

Acute Disease↗
PubMed1978

[Successful gastric ulcer treatment of a patient with primary hyperparathyroidism with cimetidine (author's transl)].

Case report on the successful gastric ulcer treatment of a patient with primary hyperparathyroidism with the H2-receptor antagonist cimetidine. After four weeks of therapy with 0.8 g/d cimetidine stomal ulcerations were seen by x-rays and endoscopy to be healed. The patient was discharged on a regimen of 400 mg daily of oral cimetidine. Peptic ulcer did not recur after 1/2 year of treatment with this H2-receptor antagonist, although the signs of primary hyperparathyroidism were still present.

Aged↗
PubMed1978

Human colonic adenylate cyclase: effects of bile acids.

Three different bile acids--deoxycholic acid, chenodeoxycholic acid and ursodeoxycholic acid--were tested for their capacity to stimulate the adenylate cyclase in human colonic mucosa. This enzyme system was found to be sensitive towards vasoactive intestinal polypeptide and prostaglandin E2. These three bile acids were ineffective in activating the human cyclase system over a wide concentration range tested. Concentrations above 1 X 10(-5) mmol/l induced a dose-dependent inhibition of basal enzyme activity. These results suggest that bile-acid induced diarrhoea is not associated with activation of the membrane-bound adenylate cyclase system at least in man.

Adenylyl Cyclases↗
PubMed1978

Pool size, synthesis, and turnover of sulfated and nonsulfated cholic acid and chenodeoxycholic acid in patients with cirrhosis of the liver.

In 5 patients with cirrhosis of the liver sulfated and nonsulfated [14C]cholic acid and [14C]chenodeoxycholic acid were administered intravenously and the specific activity curves were determined. Specific activities declined exponentially and pool sizes, synthesis rates, and turnover rates of bile acids were calculated on the basis of a one-pool system. The biological half-life of cholic acid was 4.3 +/- 1.6 days (mean +/- SEM) and of chenodeoxycholic acid was 2.8 +/- 1.2 days. The half-life of cholic acid sulfate was 0.7 +/- 0.5 day and of chenodeoxycholic acid sulfate was 0.8 +/- 0.5 day. The pool size of cholic acid was 513 +/- 103 mg, of chenodeoxycholic acid, 477 +/- 77 mg, of cholic acid sulfate, 4.7 +/- 1.0 mg, and of chenodeoxycholic acid sulfate, 38.7 +/- 4.0 mg. The daily synthesis of cholic acid was 90 +/- 14 mg, of chenodeoxycholic acid, 118 +/- 6 mg, of cholic acid sulfate, 7.2 +/- 2.1 mg, and of chenodeoxycholic acid sulfate was 32.6 +/- 3.2 mg. The data indicate that sulfate esters of bile acids are significantly more rapidly excreted than are unsulfated bile acids. More than one-fourth of the chenodeoxycholic acid but less than one-tenth of the cholic acid formed was sulfated. The preferential sulfation of chenodeoxycholic acid is responsible for the more rapid turnover of chenodeoxycholic acid in comparison to cholic acid. Sulfation enhances the excretion and thereby prevents the accumulation of hepatotoxic concentrations of chenodeoxycholic acid in patients with cirrhosis of the liver.

Alkaline Phosphatase↗
PubMed1978

[Methods for serum bile acid analysis and their diagnostic inpact (author's transl)].

Various hepatic disorders lead to elevated serum bile acid concentrations. Determination of serum bile acids is helpful for screening and follow up of liver diseases, it gives however only little support in the differentiation of various hepatic diseases. Besides the enzymatic method which has been shown to be good for routine analysis of serum bile acids, also radioimmunological methods seem to be useful.

Bile Acids and Salts↗
PubMed1977

[Treatment of intrahepatic cholesterol stones by chenodeoxycholic acid (author's transl)].

Intrahepatic gallstones were demonstrated by operative cholangiography in two men, aged 34 and 46 years, respectively. The cholesterol stones were dissolved in both patients within eight and two months, respectively, by retrograde instillation of chendeoxycholic acid via a T-drain. Additional endoscopic papillotomy was performed because of a papillary stenosis in one instance, and extrahepatic occlusion during treatment in the other. During treatment there was a rise of transaminases of 5-fold levels, of gamma-glutamyl transferase up to 10-fold of normal. Since chenodeoxycholic-acid instillations both patients have been receiving the drug orally to prevent recurrence of gallstones. So far all biochemical values are within the normal range, the patients are without symptoms and have a normal exercise tolerance.

Adult↗
PubMed1977

[Morphologic studies on the toxicity of sulfated and nonsulfated lithocholic acid in the isolation-perfused rat liver].

The isolated liver of male Sprague-Dawley rats was perfused by means of media containing lithocholic acid, taurolithocholic acid, lithocholic acid sulfate and taurolithocholic acid sulfate. 150 minutes later the tissue was being examined light- and electrone microscopically. After LC and TLC perfusion considerable alterations were found in the bile capillaries, in the ergastoplasm and minor ones in mitochondria. After perfusion with sulfate esters the tissue was unchanged. Our investigations have shown that sulfation provides a highly effective mechanism of detoxication in rats; but detoxication results not only in a decrease of reabsorption of excreted lithocholic acid sulfate esters but sulfation tenders the very lithocholic acid untoxic for the liver cell. The primary point of action of lithocholic acid seems to be the lipoprotein membrane.

Animals↗
PubMed1976

Induction and activation of rat liver microsomal bile salt glucuronyltransferase.

In vivo induction and in vitro activation of the recently described bile salt glucuronyltransferase were investigated in rat. A radioactive assay for the determination of glucuronyltransferase activity was used. 14C-Labeled bile salts served as substrates, and the glucuronides were separated by thin layer chromatography. Lithocholate glucuronyltransferase activity was determined in liver microsomes of phenobarbital- and 3-methylcholanthrene-treated rats and of untreated controls. Pretreatment with phenobarbital induced lithocholate glucuronyltransferase activity to 150.5% of controls. In contrast, 3-methylcholanthrene treatment decreased activity to 29.6% of controls. In vivo activation of lithocholate glucuronyltransferase by Triton X-100 was observed in controls and in the 3-methylcholanthrene group, but not in the phenobarbital group. Substrate activation of the enzyme by lithocholate was demonstrated in microsomes of untreated controls. Pretreatment with 3-methylcholanthrene, but not phenobarbital, increased the latency of lithocholate glucuronyltransferase. The results indicate that rat liver microsomal bile salt glucuronyltransferase activity is increased by in vivo induction with phenobarbital and by in vitro activation with detergents like Triton X-100. The induction of bile salt glucuronide formation by phenobarbital is most likely one of the factors contributing to the increased biliary and fecal excretion of bile salts in patients with cholestasis following phenobarbital therapy.

Animals↗