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Biomedical subjects

A Stiehl

Publications and source records attributed to A Stiehl.

At least 109 records · Page 6Linked to original sources
PubMed1983

Hepatic secretion of bilirubin and biliary lipids in patients with alcoholic cirrhosis of the liver.

In patients with cirrhosis of the liver elevated bilirubin concentrations in the plasma could be the result of decreased bilirubin excretion or an overproduction of bilirubin with insufficient excretion of the increased amounts of bilirubin. Under steady state conditions with constant serum bilirubin concentrations bilirubin synthesis equals biliary and urinary bilirubin excretion. In the present study in 10 healthy volunteers and 11 patients with alcoholic cirrhosis of the liver and serum bilirubin concentrations of 7.0 +/- 1.9 mg/dl the biliary excretion of bilirubin was studied by the intestinal perfusion method and compared with the excretion of bile lipids. Biliary excretion of bilirubin in the cirrhotics was 38.7 +/- 8.8 mumol/h, the 10 healthy controls excreted 17.9 +/- 0.9 mumol/h bilirubin. Only minor amounts of bilirubin were excreted in urine. In 4 of the 11 cirrhotics 51Cr-red blood cell half-lives were studied revealing ongoing hemolysis. Bilirubin production calculated from red cell life span was identical to biliary excretion of bilirubin with an error less than 5%. The data indicate that in patients with alcoholic cirrhosis of the liver serum concentrations of bilirubin may be elevated due to overproduction of bilirubin and a concomitant decrease of the biliary transport capacity of bilirubin.

Adult↗
PubMed1983

Branched-chain amino acid-enriched elemental diet in patients with cirrhosis of the liver. A double blind crossover trial.

In 14 patients with cirrhosis of the liver and portal-systemic shunts the effect of a branched-chain amino acid-enriched elemental diet on portal systemic encephalopathy, routine laboratory parameters and plasma amino acids was investigated. In addition to the standard therapy including protein restriction (40 g/day) the patients received 44 g of an amino acid-protein mixture containing 30% of branched-chain amino acids and placebo over 3 months in a crossover regimen. Plasma valine and leucine increased significantly, whereas all other amino acids, including the ratio (formula: see text), remained unchanged. The electroencephalogram, number connection test, clinical state and laboratory parameters were not influenced by therapy with branched-chain amino acids. Thus, orally administered branched-chain amino acids probably have no influence on hepatic encephalopathy but are an adequate source of nitrogen in patients with cirrhosis of the liver.

Adult↗
PubMed1983

Biliary excretion of procollagen type III peptide in healthy humans and in patients with alcoholic cirrhosis of the liver.

Serum concentrations of procollagen type III peptide are found to be elevated in liver disease and to correlate with fibrosis activity in liver tissue. These elevated serum levels may be due to enhanced synthesis, decreased excretion, or release from deposits of the propeptide in connective tissue. To quantitatively investigate the excretion of procollagen type III peptide, we studied its presence in the bile and urine of 10 healthy controls and 11 patients with alcoholic cirrhosis of the liver. Biliary excretion rates of procollagen propeptide were determined by the duodenal perfusion method. The serum concentrations of procollagen type III peptide were 2.5 +/- 0.5 ng/ml in the healthy controls and 33.6 +/- 6.8 ng/ml in the patients with cirrhosis. Procollagen type III peptide was found in the bile; the healthy controls excreted 0.4 +/- 0.07 nmol/h and the cirrhotics excreted 0.98 +/- 0.27 nmol/h. A fragment of the procollagen propeptide, Col 1, was excreted in urine; the healthy controls excreted 0.25 +/- 0.04 nmol/h, and the cirrhotics excreted 0.11 +/- 0.03 nmol/h. These data demonstrate that the biliary excretion of procollagen type III peptide represents a quantitatively important pathway.

Bile↗
PubMed1982

[Comparative treatment of gastroduodenal haemorrhage with secretin and cimetidine].

In a prospective multicenter study 71 patients with acute, non-arterial gastroduodenal haemorrhage from ulcers or stress lesions were treated alternately with synthetic secretin (Hoe 0690 (n = 35) or with cimetidine (n = 36). Both medications were given by infusion over 48 hours. Prior to commencement of treatment the haemorrhage was verified gastroscopically. During infusion of secretin cessation of hemorrhage was achieved without recurrence in 30 out of the 35 patients within the 48-hour infusion time and in 3 patients with recurrence within the same period. Two patients failed to obtain discontinuation of haemorrhage within the infusion period. Cimetidine led to cessation of haemorrhage without recurrence within 48 hours in 20 out of 3 patients, 3 patients had recurrences. Haemorrhages could not be arrested in 13 patients within the two-day treatment period. Differences between success of treatment among the two groups are significant (P less than 0.01) favouring secretin.

Adult↗
PubMed1982

Analysis of bile acid glucuronides in urine: group separation on a lipophilic anion exchanger.

A chromatographic separation of glucuronidated bile acids using the anion exchanger diethylaminohydroxypropyl Sephadex LH-20 (DEAP LH-20) is described. Group separation of non-sulfated, non-glucuronidated bile acids, bile acid glucuronides, bile acid monosulfates, and bile acid disulfates was obtained. The method allowed analysis of all these bile acid derivatives in the urine of 15 patients with cirrhosis of the liver and cholestasis. The patients excreted in mean 30.4 mumol/24 h non-sulfated, non-glucuronidated bile acids, 90.3 mumol bile acid monosulfates, and 10.2 mumol bile acid glucuronides. Glycine- or taurine-conjugated were 68% of the non-sulfated, non-glucuronidated bile acids, 96% of bile acid sulfates, and 81% of bile acid glucuronides.

Bile Acids and Salts↗
PubMed1982

[Hyperbilirubinemia in liver diseases].

Jaundice is often the first and sometimes the only symptom of liver disease. Besides in parenchymal liver disease jaundice is also observed in chronic non-haemolytic hyperbilirubinemias (Crigler-Najjar type I and II, Gilbert's syndrome) and in hereditary conjugated hyperbilirubinaemias (Dubin-Johnson- and Rotor-syndrome). A specific therapy is only available for Crigler-Najjar type II which is treated with phenobarbitone.

Anabolic Agents↗
PubMed1982

Estimation of biliary excretion of ureidopenicillins in healthy volunteers using marker dilution technique.

1 Aspiration of duodenal fluid and estimation of recovery by a marker dilution technique was adapted to measure the biliary excretion of two chemically related ureidopenicillins, mezlocillin and azlocillin, in healthy volunteers. 2 The drug was infused intravenously at a constant rate over a period of 6 h during which duodenal fluid was aspirated through the distal opening of a triple-lumen polyvinyl tube. 3 Drug levels in plasma, urine and duodenal fluid were determined by h.p.l.c. 4 Biliary excretion rate was calculated by multiplying the concentration in the duodenal fluid by the dilution factor resulting from the dilution of marker substance infused through the proximal opening of the triple-lumen tube. 5 Since the results obtained by the marker dilution technique are comparable to data obtained by studies in patients with t-tube drainage following biliary surgery, it can be concluded that the method is useful to measure the biliary excretion of drugs in man.

Adult↗
PubMed1982

Oral keto analogs of branched-chain amino acids in hyperammonemia in patients with cirrhosis of the liver. A double-blind crossover study.

Previous uncontrolled studies indicated a positive effect of keto analogs of amino acids on plasma ammonia in patients with cirrhosis of the liver and on portal-systemic encephalopathy. In the present double-blind study the influence of keto analogs of the branched chain amino acids valine, leucine and isoleucine on plasma ammonia and encephalopathy was investigated in 12 patients with cirrhosis of the liver and surgical portal systemic shunts. In addition to the usual therapy with lactulose and protein restriction (40 g protein/day) all patients received 15.24 g keto analogs and placebo orally over 4 weeks in a crossover regimen. In contrast to uncontrolled studies, plasma ammonia, which was elevated in all patients before the beginning of the study, was not significantly changed. In addition plasma amino acids, electroencephalogram, number connection test, clinical state and laboratory tests were not influenced by the therapy with keto analogs.

Administration, Oral↗
PubMed1982

Procollagen-type III-peptide serum concentrations in chronic persistent and chronic active hepatitis and in cirrhosis of the liver and their diagnostic value.

Until now the determination of fibrotic processes in liver disease was restricted to histological examination of liver tissue. Recently a RIA was developed to determine the procollagen-type III-peptide concentrations in biological fluids. We used this RIA to measure the serum procollagen-type III-peptide concentrations in patients with chronic liver disease. Additionally in 24 patients with chronic persistent and chronic active hepatitis the collagen content in liver biopsies was determined histomorphometrically. The serum procollagen-type III-peptide concentrations in healthy controls (n = 40) were 6.4 +/- 0.6 ng/ml, in chronic persistent hepatitis (n = 47) 8.7 +/- 0.5 ng/ml, in chronic active hepatitis (n = 53) 20.8 +/- 2.9 ng/ml, and in alcoholic cirrhosis of the liver (n = 22) 47.7 +/- 6.1 ng/ml. Thus the patients with chronic active hepatitis and cirrhosis of the liver showed significantly elevated serum procollagen-type III-peptide levels. In chronic hepatitis a highly significant correlation (p less than 0.001) could be demonstrated between collagen content in liver tissue and serum procollagen-type III-peptide concentrations. The determination of serum procollagen-type III-peptide concentrations may prove a new useful parameter in biochemical evaluation of liver disease.

Biopsy↗
PubMed1981

Biliary cholesterol saturation and weight reduction--effects of fasting and low calorie diet.

The effects of fasting or a 600-cal diet on biliary lipid composition were studied in 20 persons with overweight. With complete fasting for 20 days and a mean weight loss of 650 g/day, biliary cholesterol fell significantly from 10.1 to 6.9 mol% and the 'lithogenic index' from 1.0 to 0.7. Following fasting, the index, in 10 of the 11 patients, was in the normal range below 1.0. With a 600-cal diet, in agreement with findings by other authors, there was no significant change of individual bile lipids or of the lithogenic index. While it has been shown that lithogenicity increases up to 16 h of fasting, it obviously significantly decreases with continued fasting. Fasting, therefore, in addition to manipulation of dietary cholesterol and, possibly, fiber consumption, appears to be an effective method for rapid lowering of biliary cholesterol saturation.

Adult↗
PubMed1981

Kinetics of cholesterol gallstone dissolution by glycocheno-, glyco-ursodeoxycholic acid, and mixtures of both in vitro.

Cheno- and ursodeoxycholic acid feeding are both efficient in conservative gallstone therapy. Urso decreases biliary cholesterol excretion even more than cheno. Glyco-urso becomes dose dependent the predominant bile acid conjugate in bile under urso feeding. We therefore studied the kinetics of cholesterol gallstone dissolution in aqueous solutions of 100 mM glyco-cheno, 100 mM glyco-urso, and mixtures of both consisting of 40 mM glyco-urso plus 60 mM glyco-cheno and 80 mM glyco-urso plus 20 mM glyco-cheno in vitro. The daily dissolution rates of cholesterol achieved by these solutions were for 100 mM glyco-cheno 0.87 +/- 0.1 mg (mean +/- SEM), for 40 mM glyco-urso plus 60 mM glyco-cheno 0.28 +/- 0.003 mg, for 80 mM glyco-urso plus 20 mM glyco-cheno 0.07 +/- 0.002 mg, and for 100 mM glyco-urso 0.07 +/- 0.03 mg. Correspondingly were the weight decreases of the gallstones by 100 mM glyco-cheno 1.2 +/- 0.1 mg/day, by 40 mM glyco-urso plus 60 mM glyco-cheno 0.3 +/- 0.01 mg/day, by 80 mM glyco-urso plus 20 mM glyco-cheno 0.11 +/- 0.02 mg/day, and by 100 mM glyco-urso 0.1 +/- 0.02 mg/day. Complete gallstone dissolution occurred during the observation time of 4 months only by 100 mM glyco-cheno in 12.8 +/- 3.3 weeks. Thus glyco-urso dissolves only little cholesterol and decreases the speed of cholesterol gallstone dissolution. It is concluded that high doses of urso in gallstone therapy which lead to great amounts of glyco-urso in bile may diminish gallstone dissolution rates.

Chenodeoxycholic Acid↗
PubMed1980

The synthesis of bile acid glucuronides by agarose-bound UDP-glucuronyltransferase.

Lithocholic acid, chenodeoxycholic acid and deoxycholic acid but not cholic acid or the glycine or taurine conjugates of these bile acids are glucuronidated by agarose-bound UDPglucuronyltransferase from rt liver in the presence of UDPglucuronic acid. The identification of bile acid glucuronides is based on the specific enzymatic hydrolysis, incorporation of 14C-labeled glucuronic acid into the molecule and by mass spectrometry. Mass spectrometry indicates that bile acid glucuronides formed by agarose-bound UDPglucuronyltransferase are 3-glucuronides. The glucuronidation of lithocholic acid, chenodeoxycholic acid and deoxycholic acid is linear up to 45 min and at a protein concentration between 0.5 and 2.0 mg per assay. The pH optimum of the enzyme reaction is 7.0. The Km for lithocholic acid, chenodeoxycholic acid and deoxycholic acid, which are 0.040, 0.031 and 0.037 mM, respectively, are similar to those found in microsomal preparations. The use of agarose-bound UDP-glucuronyltransferase offers the possibility to synthesize bile acid glucuronides which are needed for kinetic studies in man and animal.

Animals↗
PubMed1980

[The effect of bezafibrate on biliary lipids (author's transl)].

The effect of bezafibrate (3 x 200 mg/day) on biliary lipids was studied in 12 healthy male subjects and in 13 patients with hyperlipidemias. In normal subjects, the lithogenic index, with bezafibrate and placebo administered in a double blind cross-over design, was 1.1 and 0.77 respectively. The difference was not significant. In patients, who have been treated with bezafibrate for 6 months to 3 years the index was 0.76, and 0.64 six weeks after discontinuation of the drug. This difference, too, was not significant. It appears, therefore, that contrary to findings with clofibrate, bezafibrate may not be associated with an increased risk of cholelithiasis. This question, however, can ultimately be answered with certainty only on the basis of long-time epidemiologic evidence.

Adult↗
PubMed1980

The effect of polyunsaturated phosphatidylcholine on plasma lipids and fecal sterol excretion.

Highly polyunsaturated phosphatidylcholine (PC) was orally administered to patients with familial hypercholesterolemia and normal controls. Plasma lipid and lipoprotein composition as well as fecal sterol excretion and bile lipid composition were analyzed. Two dietary regimens were given, containing similar amounts of calories, cholesterol and polyunsaturated fatty acids in order to evaluate the specific effect of phosphorylcholine. No change in plasma lipid or lipoprotein concentration was observed. However, fecal sterol excretion was substantially increased in all subjects when PC was added to the diet. Bile acids, phospholipid and cholesterol content in bile did not vary.

Adolescent↗
PubMed1980

Passage of a large bilirubin stone through a narrow papillotomy.

Large stones in the bile are generally considered to be a contraindication for endoscopic papillotomy (EPT). In the case described a large biliary stone passed spontaneously into the lumen of the gut after EPT. It is speculated that pure pigment stones are less "rigid" than cholesterol stones and are therefore able to pass through narrower channels than cholesterol stones.

Aged↗