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PubMed1989

[Diets and drugs to lower blood cholesterol].

The scope of this paper is deliberately restricted to diets and drugs devised to lower blood cholesterol levels in pure hypercholesterolaemia (ex-type II in the international classification). This treatment is twofold: (1) Diets. In all cases except cardiovascular emergencies treatment should begin with a diet. If the subject is overweight, an overall low-calorie diet should be prescribed first. This will be followed by a diet with a low cholesterol and saturated fats content and a high polyunsaturated fats content, the latter including linoleic acid (C18:12) present in sunflower margarine and sunflower, maze and soya oils or eicosapentaenoic acid (C20:5) and docosahexaenoic acid (C22:6) present in fatty fish. (2) Cholesterol-lowering drugs should then be prescribed if necessary. The most effective of these drugs are cholestyramine and fibrate derivatives. HMG CoA reductase inhibitors will shortly be available in France. This daily medicinal treatment should of course be uninterrupted, but it may be "reduced" in case of excellent therapeutic response.

Cholesterol↗

PubMed1985

Specific binding of high density lipoprotein (HDL3) is not related to sterol synthesis in rat intestinal mucosa.

There is good evidence that high density lipoprotein (HDL) is involved in the flux of cholesterol into the cells of some organs and out of the cells of other tissues. Because we have previously found that HDL is bound specifically by mucosal cells of the small intestine, we have examined the possibility that this was associated with regulation of cholesterol flux. We have, therefore, compared the specific binding of 125I-labeled HDL3 with cholesterol synthesis in mucosal cells obtained from rats that had been treated to alter intestinal cholesterol metabolism. The rate of sterol synthesis measured in tissue slices, by the incorporation of [3H]water into sterols, was altered up to fivefold by treatment with cholestyramine (to induce bile salt loss), by surformer treatment (to reduce absorption of cholesterol), and by biliary diversion. Yet the capacity of mucosal cells to bind, internalize, and degrade 125I-labeled HDL3 was unchanged. Cholesterol feeding influenced neither the interaction of 125I-labeled HDL3 with cells nor the rate of sterol synthesis. Furthermore, the interactions of 125I-labeled HDL3 with mucosal cells isolated from the proximal and distal halves of the intestine or between the upper and lower villus cells were similar, despite differences in sterol synthesis. These data suggest that, in rat intestine, the specific binding of HDL is not related to sterol synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1977

[Pharmacokinetic aspects of overdosage and intoxication with oral anticoagulant drugs (author's transl)].

Three aspects of treatment with oral anticoagulant drugs are discussed: 1. Drug interactions which can lead to changes in the elimination or distribution of oral anticoagulant drugs with special emphasis on the time course of the augmentation of the anticoagulant effect. 2. Pharmacokinetic factors responsible for inter- and intrasubject differences in the response to oral anticoagulant drugs. 3. Treatment of overdosage and intoxication with oral anticoagulant drugs. Besides symptomatic treatment with vitamin K and prothrombin complex concentrate the interruption of the enterohepatic recycling by cholestyramine is demonstrated as a useful method for enhancing the elimination of phenprocoumon and warfarin from the body.

Administration, Oral↗

PubMed1987

Granulomatous lung disease in children by aspiration of medications.

Post mortem examinations of 8 infants, 11 d to 5 months old and one 12 year old girl, demonstrated foreign bodies in the lungs which could be identified as orally administered drugs: cholestyramine (Questran) and phenobarbital (Luminal, Gardenal) or phenydantin-components. The microscopic changes caused by such deposits and the histologic methods of identifying medicines are presented. The authors point to the role of aspiration in deposit formation and to the pseudomiliary granulomatous nature of subsequent changes. It is proposed to define the alterations as a separate form of aspiratory lesion in children.

Administration, Oral↗

PubMed1977

Alkaline gastritis and alkaline esophagitis: a review.

Alkaline gastritis and alkaline esophagitis are now precisely defined syndromes. They occur most often after gastric surgery in which function of the pyloric and lower esophageal sphincter is compromised. Reflux of bile in these patients can then lead to severe inflammation of the gastric and lower esophageal mucosa. Epigastric pain, nausea and bilious vomiting are characteristic symptoms. Gastroscopy with biopsy is, therefore, the definitive diagnostic test; during endoscopy bile is seen in the lower esophagus or stomach, and the mucosa is red, friable and contains acute erosions. Conservative therapy including the administration of cholestyramine has not been helpful. Surgery consisting of diversion of the duodenal contents away from the stomach and lower esophagus is the treatment of choice. The Roux-en-Y procedure has been used most often and has resulted in the amelioration of the symptoms and signs in most patients.

Animals↗

PubMed1987

[Value of percutaneous blind liver biopsy in preoperative diagnosis of atresia of the extrahepatic bile ducts].

During a period of 7 years the case histories of 60 infants with direct hyperbilirubinaemia were prospectively evaluated. At presentation the majority of infants had an age below 1 month. By close clinical follow-up of all infants including the observation of acholic stools (21 infants), quantitative estimations of lipoprotein X during cholestyramine therapy (17 infants), cholescintigraphy (20 infants) and percutaneous liver biopsy (17 infants) the efficiency of the preoperative diagnostic work-up reached 96.6%. Liver biopsies were carried out selectively in only 29.3% of all infants (47.6% in infants with acholic stools and 17.9% in infants with normal stools); their efficiency in the differential diagnosis of extrahepatic biliary atresia was 88.2%.

Bile Ducts↗

PubMed1988

Cholesterol metabolism during ketoconazole treatment in man.

Ketoconazole, an antifungal antibiotic, inhibits cholesterol synthesis by blocking demethylation of lanosterol. Effects of this inhibition were studied on serum cholesterol, lipoproteins and cholesterol precursors, biliary lipid composition, and fecal steroid elimination in five patients with prostate cancer treated with large doses of ketoconazole. The serum level of total cholesterol fell by 27%, that of LDL cholesterol by 41% and that of LDL apoB by 32% with ketoconazole alone; the fall in the total cholesterol level of a patient treated with ketoconazole-cholestyramine was 65%. Serum contents of free lanosterol and dihydrolanosterol increased up to 250 times, yet the total concentrations remained less than 2 mg/dl. Of the other cholesterol precursor sterols only those with delta 8-double bond increased several times, indicating that in addition to 14 alpha-demethylation, ketoconazole also interfered with metabolism of later intermediary sterols to some extent. Compared with serum sterols, lanosterols were enriched in biliary and fecal sterols up to 10-20 times. Fecal lanosterol output increased from 12 to 247 mg/day, and comprised over 20% fecal steroids of endogenous origin. Bile acid synthesis was significantly decreased, the proportion of chenodeoxycholic acid being markedly reduced in both biliary and fecal bile acids. Cholesterol absorption appeared to decrease yet fecal neutral sterol output and cholesterol synthesis were unchanged and the overall sterol synthesis was increased. It thus appears that ketoconazole inhibits cholesterol elimination as bile acids. However, by blocking 14 alpha-demethylation, it results in effective drainage of sterol nucleus as lanosterols into bile and feces, which, in turn, is associated with a marked reduction in low density lipoprotein (LDL) cholesterol level probably through activation of hepatic LDL apoB receptors.

Aged↗

PubMed1986

Rates of sterol synthesis in the liver and extrahepatic tissues of the SHR/N-corpulent rat, an animal with hyperlipidemia and insulin-independent diabetes.

The SHR/N-corpulent rat is a new genetically obese strain that exhibits both insulin-independent diabetes and hyperlipidemia. The present studies were undertaken to characterize various parameters of cholesterol metabolism in this model. At 11 weeks of age, the obese animals had markedly elevated plasma cholesterol, triglyceride, glucose, and insulin concentrations and elevated hepatic triglyceride concentrations compared to their lean littermates. The additional cholesterol in plasma was carried in the fractions of density less than 1.006, 1.020-1.055, 1.055-1.095, and 1.095-1.21 g/ml. In the obese rats the level of free cholesterol in the liver was decreased significantly while that of cholesteryl ester showed little change. Hepatic sterol synthesis was markedly suppressed in the obese animals. However, the rate of sterol synthesis in the small intestine and other extrahepatic tissues generally remained unchanged. Although hepatic synthesis was suppressed, whole animal sterol synthesis in the obese rats was similar to that in the lean controls. This resulted because, in the obese animals, not only was the reduced rate of hepatic synthesis partly balanced by a greater than 70% increase in liver mass, but the mass of the small intestine and adipose tissue was also increased more than 30% and 4-fold, respectively, thereby making these tissues quantitatively more important sites of sterol synthesis. When obese rats were pair-fed to the intake of their lean littermates for 10 weeks, there was only a modest reduction in body weight and plasma cholesterol concentration, and the rate of hepatic sterol synthesis remained very low. The suppression of synthesis in the liver also persisted when the obese rats were fed surfomer, a drug that specifically blocks cholesterol absorption. In contrast, feeding cholestyramine restored the rate of hepatic sterol synthesis to that found in lean animals. Bile acid pool size in the obese males and females was 2.5-fold greater than in their lean controls. The suppression of hepatic sterol synthesis in this model may be due to a change in the entero-hepatic circulation of bile acids arising from an expanded pool or, alternatively, it may represent a compensatory response to overproduction of sterol and its precursors in the intestinal and adipose compartments.

Adipose Tissue↗

PubMed1987

Primary bile acid malabsorption. Histologic and immunologic study in three patients.

Three patients are presented with a history of chronic watery diarrhea due to bile acid malabsorption, proved by the tauro-23[75Se]selena-25 homocholic acid test and an unequivocal response to cholestyramine therapy. Fecal fat tests, Schilling tests, and barium studies of the small intestine and colon were all normal. Jejunal biopsies were normal but multiple biopsies of the terminal ileum, performed by retrograde ileoscopy, showed uniform crypt hyperplastic villous atrophy and features of colonic metaplasia with increased mononuclear infiltration of the lamina propria. All 3 patients demonstrated evidence of abnormal immune function, including the presence of serum autoantibodies, circulating immune complexes, and hypocomplementemia. One patient had Sjögren's syndrome. This disorder, which might be immunologically mediated, should be called primary bile acid malabsorption and should be distinguished from other ileal disorders.

Adult↗

PubMed1987

Bile acid-mediated postcholecystectomy diarrhea.

Diarrhea that develops after cholecystectomy may be due to increased amounts of bile acids presented to the large bowel, a "cholerheic enteropathy." We have studied eight patients to determine the cause for chronic diarrhea after cholecystectomy and found no abnormality other than elevated bile acids in the stool of six of them. All patients with bile acid malabsorption had daily stool weights greater than 200 g and total fecal bile acids three to ten times greater than normal. Patients responded dramatically to treatment with cholestyramine resin.

Adult↗

PubMed1986

Efficacy of mevinolin as adjuvant therapy for refractory familial hypercholesterolaemia.

Mevinolin, a potent inhibitor of cholesterol synthesis, was used as a therapeutic adjuvant in patients with refractory familial hypercholesterolaemia for an average period of 13 months. Sustained decreases in serum cholesterol of 23 and 31 per cent were achieved by doses of 20 mg and 40 mg/day respectively in 13 heterozygotes already on cholestyramine or after partial ileal bypass. Administration of 80 mg/day to three patients undergoing plasma exchange reduced peak serum cholesterol levels by 11.5 per cent in two homozygotes and by 17 per cent in a double heterozygote for familial hypercholesterolaemia and type III hyperlipoproteinaemia. The decrease in cholesterol was largely confined to low-density lipoprotein and no significant changes occurred in serum triglyceride or high-density lipoprotein cholesterol. Mevinolin was well-tolerated except in one patient who developed myositic symptoms; asymptomatic, transient elevations of serum enzymes were observed in five others. Short and long Synacthen tests showed no evidence that the drug impaired adrenocortical response to ACTH. These results indicate that mevinolin provides a safe and highly effective means of reducing LDL levels in patients with heterozygous familial hypercholesterolaemia refractory to conventional treatment but is less useful in homozygotes.

Adult↗

PubMed1987

Cholesterol synthesis in rat liver peroxisomes. Conversion of mevalonic acid to cholesterol.

The key regulatory enzyme of cholesterol, dolichol, and isopentenyl adenosine biosynthesis, 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase) is a 97-kilodalton transmembrane glycoprotein which was believed until recently to reside exclusively in the endoplasmic reticulum of mammalian cells. However, several recent publications have shown that the enzyme in liver cells is present not only in the endoplasmic reticulum but also within peroxisomes. In an effort to clarify the role of peroxisomal HMG-CoA reductase, highly purified (95%) rat liver peroxisomes from cholestyramine-treated rats were incubated with RS-[2-14C]mevalonic acid plus cytosolic proteins and then tested for the presence of newly synthesized cholesterol. For comparison, highly purified microsomes from the same liver preparation were incubated at several protein concentrations under the same conditions. A three-step procedure was employed to resolve the newly synthesized cholesterol from the complex mixture of sterol intermediates in cholesterol biosynthesis. After termination of the reaction and addition of a [3H]cholesterol standard, the incubation products were extracted and separated by thin layer chromatography into a number of fractions. The fraction containing C-27 sterols was further resolved by reverse-phase high pressure liquid chromatography. After acetylation, the products were then separated by silicic acid high pressure liquid chromatography. Confirmation of the identity of newly synthesized cholesterol was obtained by recrystallization with added non-radioactive cholestenyl acetate standard. The results indicate that highly purified rat liver peroxisomes are able to convert mevalonic acid to cholesterol in the presence of cytosolic fraction in vitro. An abstract of these results has been published (Krisans, S. K., Thompson, S. L., Burrows, R., and Laub, R. J. (1986) J. Cell Biol. 103, 525 (abstr.).

Animals↗

PubMed1986

Lipoprotein-X.

Jaundice can occasionally present a medical dilemma. Is the jaundice due to a surgically correctable or medical condition? One method to resolve this problem is the determination of levels of serum lipoprotein-X. A review of the literature concerning lipoprotein-X and pertinent clinical trials suggests that the determination of levels of serum lipoprotein-X, by itself, is of little value, but measurement after a two-week course of cholestyramine therapy can provide significant information regarding the presence of extrahepatic obstruction.

Cholestasis, Extrahepatic↗

PubMed1986

Bile acid synthesis in man: assay of hepatic microsomal cholesterol 7 alpha-hydroxylase activity by isotope dilution-mass spectrometry.

The present work describes an accurate assay of the rate-limiting enzyme in bile acid synthesis, the cholesterol 7 alpha-hydroxylase, in human liver. The assay is based on isotope dilution-mass spectrometry, and endogenous microsomal cholesterol is used as the only substrate for the enzyme. Operative liver biopsies were obtained from patients undergoing elective cholecystectomy under highly standardized conditions. In ten gallstone patients, the enzyme activity of the microsomal fraction averaged 9.6 +/- 1.4 (mean +/- SEM) pmol X min-1 X mg protein-1 corresponding to a daily synthesis of about 0.5 mmol of bile acids. Three cholestyramine-treated patients displayed a four-fold higher enzyme activity. No evidence was obtained supporting the concept that the cholesterol 7 alpha-hydroxylase is modulated by phosphorylation-dephosphorylation.

Bile Acids and Salts↗

PubMed1985

Antibiotic-associated pseudomembranous colitis.

All antibiotics, except parenteral aminoglycosides, sulfonamides and vancomycin, can induce pseudomembranous colitis. The worst offenders are clindamycin, ampicillin, amoxicillin and the cephalosporins. The cytotoxin produced by Clostridium difficile has been identified as the cause of pseudomembranous colitis. Treatment includes an antimicrobial to eradicate the organism and cholestyramine or colestipol to bind the toxin.

Amoxicillin↗

PubMed1985

Biochemical diagnosis and monitoring therapeutic modulation of disease activity in an unusual case of congenital erythropoietic porphyria.

We describe the methodology used for quantifying and characterizing porphyrins in various tissues and in excreta, in the diagnosis and monitoring of the therapeutic modulation of biochemical disease activity in a 53-year-old white man who has a rare form of familial porphyria cutanea tarda with bone marrow rather than hepatic expression of the disease. Liquid-chromatographic and thin-layer chromatographic analyses of the patients's urine and skin showed predominantly heptacarboxylic porphyrin and uroporphyrin, whereas his stool and bile contained isocoproporphyrin and coproporphyrin as the major products. The data reflect defective uroporphyrinogen decarboxylation. Both analytical methods gave quantitatively similar results for urinary and fecal porphyrins. A triple-lumen perfusion study of samples procured both at the ampulla of Vater and 15 cm downstream provided data for porphyrins excreted in the bile and their reabsorption in the small intestine. We evaluated: suppression by hypertransfusion of bone marrow overproduction of porphyrins and reduction of enteral absorption of porphyrins by orally administered charcoal (Acta Char) and cholestyramine.

Bile↗

PubMed1974

Effect of alterations of the specific activity of the intracellular acetyl CoA pool on apparent rates of hepatic cholesterogenesis.

We have previously shown significant dilution of the specific activity of the intracellular acetyl CoA pool when radiolabeled acetate is used as the precursor in liver slice experiments. In the present study, using liver from animals subjected to various manipulations known to alter the rate of cholesterogenesis, the specific activity of the intramitochondrial acetyl CoA pool was 27-49% of the theoretical specific activity expected if no endogenous dilution occurred. Because the cytosolic acetyl CoA pool that gives rise to cholesterol is not in equilibrium with the intramitochondrial pool, these values cannot be used to correct the flux of labeled carbon from [(14)C]acetate into cholesterol. However, because [(14)C]octanoate is rapidly oxidized intramitochondrially to acetyl CoA, which feeds both the intra- and extramitochondrial metabolic pathways, [(14)C]octanoate can be utilized to determine true flux rates of C(2) units into cholesterol and other products. Using this substrate in liver slices from animals subjected to a variety of experimental manipulations, the specific activity of the intracellular acetyl CoA pool was 54-71% of the expected specific activity. After correction for endogenous dilution, the C(2) flux into cholesterol varied from 335 to 459 nmoles.g(-1).hr(-1) in control animals, was suppressed 10-40-fold in animals subjected to fasting and cholesterol feeding, and increased into the range of 1500 nmoles.g(-1).hr(-1) after derepression with cholestyramine feeding or biliary diversion. Data also are presented that show very good agreement between the corrected C(2) flux rate from octanoate into cholesterol and microsomal HMG CoA reductase activity in the same liver under conditions in which the synthetic rates were varied over a 100-fold range.

Acetates↗

PubMedDate not supplied

Pathogenesis and therapy of liver disease in protoporphyria.

Protoporphyria is an inherited disorder in man characterized by the overproduction of protoporphyrin, a compound that is excreted by the liver. Hepatobiliary disease may occur in protoporphyria, and several cases have been reported in which death was due to liver disease. Based on the histological evaluation of liver biopsy specimens from 18 patients, 6 of whom died with cirrhosis and liver failure, we speculate that liver disease in this condition is caused by protoporphyrin deposits in hepatobiliary structures. These deposits are composed of crystals and have a characteristic birefringence when examined by polarization microscopy.One patient with early liver damage was given cholestyramine and vitamin E in an attempt to reduce the amount of protoporphyrin which the liver excreted daily. Liver function tests returned to normal, and red cell and plasma protoporphyrin levels decreased. A repeat liver biopsy after one year of therapy showed healing, with decrease of the protoporphyrin deposits.Liver disease in protoporphyria may be treated by directing therapy toward the metabolic abnormality.

5-Aminolevulinate Synthetase↗