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PubMed1997

Nonsyndromic paucity of interlobular bile ducts: clinical and laboratory findings of 10 cases.

BACKGROUND: Reports concerning nonsyndromic paucity of the interlobular bile ducts are not common. METHODS: The clinical, biochemical, and histological features of ten such children were described. RESULTS: All presented with jaundice, starting in the first month in seven and in the fourth, seventeenth, and thirtieth month in the others. Alcoholic stools were present intermittently in seven and persistently in three patients. Pruritus was a prominent symptom in five. Liver function tests were abnormal in all but one. Liver biopsies were performed at ages of 20 days to 3 years (median 5 months). In addition to a paucity of interlobular bile ducts, histology revealed intracellular cholestasis in all, portal fibrosis in four, and regenerative nodules in two patients. Complications of fat-soluble vitamin deficiency occurred in seven. Therapy consisted of supplementation of those vitamins and administration of cholestyramine, phenobarbital, prednisolone, or ursodeoxycholic acid. While one child had a successful orthotopic liver transplantation, three died. Consanguinity rate was 80% among the parents, and five of the patients had siblings with similar symptoms. CONCLUSIONS: Prognosis of these patients is variable. Differentiation from other forms of cholestasis is important especially to avoid surgery.

Bile Ducts↗

PubMed1987

Bile acids in radiation-induced diarrhea.

Radiation-induced bowel disease manifested by debilitating diarrhea is an unfortunate consequence of therapeutic irradiation for pelvic malignancies. Although the mechanism for this diarrhea is not well understood, many believe it is the result of damage to small bowel mucosa and subsequent bile acid malabsorption. Excess amounts of bile acids, especially the dihydroxy components, are known to induce water and electrolyte secretion and increase bowel motility. We have directly measured individual and total bile acids in the stool samples of 11 patients with radiation-induced diarrhea and have found bile acids elevated two to six times normal in eight of them. Our patients with diarrhea and increased bile acids in their stools had prompt improvement when given cholestyramine. They had fewer stools and returned to a more normal life-style.

Adult↗

PubMed1999

Prescribing habits in primary biliary cirrhosis: a national survey.

BACKGROUND: Primary biliary cirrhosis (PBC) is a chronic cholestatic liver disease of unknown aetiology. A number of drugs have been used in its treatment, but only ursodeoxycholic acid (UDCA) has been shown to improve survival. Our aims were to determine the current prescribing habits in PBC of all practising gastroenterologists in the UK. METHODS: A postal questionnaire was sent to 454 gastroenterologists in 1996, followed by a second questionnaire a month later to the non-responders. RESULTS: Of 454 doctors sent questionnaires, 379 (83%) replied. Of these, 58 were excluded from further analysis as they were not practising gastroenterologists. There are an estimated 4337 patients with PBC being seen by gastroenterologists in hospitals. Of these, only 1376 (32%) are being seen in liver units. Ninety-one per cent of gastroenterologists look after patients with PBC (median 10 patients, range 1-500). Ninety-five per cent of gastroenterologists prescribe UDCA but there is a large dose range (median 11.5 mg/kg/day, range 1.5-23.1). Of these, 93% also prescribe cholestyramine. Only 45 (14%) gastroenterologists prescribed other treatments for PBC (13 colchicine, 24 steroids, nine penicillamine, 13 immunosuppressants). Only 53 (17%) treat the symptoms/complications of PBC (37 fat-soluble vitamins, 15 calcium, six bisphosphonates, one hormone replacement therapy, 10 antihistamines, 10 rifampicin). CONCLUSIONS: UDCA is being prescribed for PBC by the majority of practising gastroenterologists but over a wide dose range. Very few gastroenterologists are using preventive treatment for osteoporosis in this high-risk group. Other treatments, as yet unproven in trials, are being prescribed by a minority of gastroenterologists.

Cholagogues and Choleretics↗

PubMed1987

Plasma exchange in a patient with heterozygous familial hypercholesterolaemia resistant to drug therapy.

A 40-year-old male with heterozygous familial hypercholesterolaemia was resistant to combined drug treatment with cholestyramine and nicotinic acid in adequate doses. He had angina pectoris and evidence of three vessel disease in the coronary angiogram. Repeated plasma exchange at intervals of 1-3 weeks simultaneously with combined drug treatment decreased the plasma cholesterol levels by nearly 40%. There were also signs of regression of xanthomata and some improvement of his angina pectoris. No progression of atherosclerosis was seen angiographically after two years treatment. Plasma exchange may be a therapeutic alternative in drug-resistant familial hypercholesterolaemia.

Adult↗

PubMed1995

The acceptability of resin therapy to patients attending a hospital lipid clinic.

Low dose cholestyramine ('Questran A') and colestipol ('Colestid Orange') were compared in a blinded two period crossover study of 55 patients attending a hospital lipid clinic. Colestipol was rated higher on a combined acceptability/palatability score. Both treatments reduced low density lipoprotein (LDL) cholesterol to a similar extent.

Adolescent↗

PubMed1980

Phytosterolaemia, xanthomatosis and premature atherosclerotic arterial disease: a case with high plant sterol absorption, impaired sterol elimination and low cholesterol synthesis.

A fourth case is described in which phytosterolaemia, earlier diagnosed as familial hypercholesterolaemia, was associated with normocholesterolaemia, hypersplenism and premature atherosclerotic arterial disease requiring a three-vessel coronary bypass at the age of 29 years. During a follow-up of 5 years 22-26% and 27-30% of serum and bile sterols were plant sterols, respectively. In addition to campesterol and beta-sitosterol, stigmasterol and a fourth major plant sterol, tentatively identified as avenasterol, were found in bile, and in free and esterified forms in all serum lipoproteins. Analysis of faecal steroids and measurement of biliary lipid secretion indicated that in addition to enhanced absorption of plant sterols their decreased biliary secretion contributed to the development of phytosterolaemia. Impaired biliary cholesterol secretion was compensated for by a markedly reduced cholesterol but normal bile acid synthesis and resulted in bile undersaturated with respect to cholesterol, in a reduced intestinal cholesterol pool and in a very low faecal excretion of cholesterol as neutral sterols. Cholestyramine brought about a modest increase in cholesterol elimination as bile acids, increased cholesterol synthesis as evidenced by the sterol balance value and the increased cholesterol precursors squalene and methyl sterols in plasma and bile, and reduced the plasma cholesterol by 21% and plant sterols by 16%, but had no effect on the biliary composition of main sterols.

Absorption↗

PubMed1980

Regulation of sterol synthesis in human intestinal mucosa.

The effect of dietary factors and experimental manipulations designed to perturb the enterohepatic circulation on the rate of sterol synthesis were studied in freshly isolated human jejunal mucosa from normal subjects. Fasting significantly reduced the rate of sterol synthesis from [14C]acetate in jejunal mucosa obtained from normolipaemic obese subjects. A high cholesterol diet had no consistent effect on the synthesis in normal subjects. Administration of cholestyramine resulted in a marked rise in the incorporation of [14C]acetate into sterols, while the administration of chenodeoxycholic acid did not significantly reduce basal sterol synthesis in normal subjects. These results demonstrate that in man the rate of sterol synthesis in intestinal mucosa is altered in response to physiological variables. Although these findings indicate that sterol synthesis in this tissue is subject to regulation, no difference was observed in basal sterol synthesis between normal subjects and patients heterozygous for familial hypercholesterolaemia.

Administration, Oral↗

PubMed1993

Apolipoprotein E phenotypes in familial hypercholesterolaemia: importance for expression of disease and response to therapy.

To study the possible importance of variation at the apolipoprotein (apo) E gene locus for the clinical expression of heterozygous familial hypercholesterolaemia (FH), we determined apo E phenotype and serum lipoprotein pattern in 120 patients with FH. The allele frequency of the patients studies were: epsilon 2 0.033, epsilon 3 0.733, and epsilon 4 0.233. There was no influence of apo E phenotype on the serum concentrations of total. VLDL, LDL or HDL cholesterol, triglycerides, or of apo AI, B or (a). Serum concentrations of apo E were significantly higher in patients with the apo E 3/3 phenotype compared to those with apo E 4/3 or 4/4, and the highest concentrations were found in patients carrying the epsilon 2-allele. The cholesterol-lowering response to therapy with cholestyramine or pravastatin was not related to apo E phenotype. It is concluded that variation at the apo E gene locus is not of major importance for the expression of heterozygous FH.

Apolipoproteins E↗

PubMed2004

Pharmacokinetics of flunixin in the cat: enterohepatic circulation and active transport mechanism in the liver.

The plasma and urine pharmacokinetics of flunixin-meglumine (FNX) in cats were examined using a total of 12 adult animals. After an intravenous injection of FNX (2 mg/kg), the plasma concentration time curves showed a profile of a two-compartment open model with an elimination half-life of 6.6 h. In spite of high plasma protein binding (>99%), the V(d)beta was unusually large, 0.7 L/kg. Although the recovery of FNX from urine was only 0.4% of the dose, the estimated inherent renal clearance closely corresponded to the renal plasma flow rate, indicating that a renal active tubular secretion was involved in the pharmacokinetics of FNX. Cholestyramine (ChSA), an anion exchanger, was orally administered immediately before the FNX injection in order to determine the involvement of enterohepatic circulation in FNX pharmacokinetics. The elimination phase of the profile of FNX was prevented by the concomitant administration of ChSA, so it was concluded that the drug undergoes enterohepatic circulation in cats. Pravastatin (PV) is a specific substrate of the type-2 organic anion transporting polypeptide transporter (OATP-2) in human liver cells. The effect of a concomitant intravenous injection of PV with FNX was examined in order to determine the involvement of OATP-2 like transporter in the pharmacokinetics. The V1 and total body clearance were decreased after the injection of PV. In conclusion, at least two active transport mechanisms are involved in the pharmacokinetics of FNX in cats. One pathway is renal tubular secretion and the other is sinusoidal active uptake by liver cells. The latter may be responsible for the enterohepatic circulation of FNX in cats.

Animals↗

PubMed1981

Cytochromes P-450 LM3b and LM4 in biosynthesis of bile acids.

Cytochromes P-450 LM3b and LM4 were prepared from untreated and cholestyramine-treated rabbits. The catalytic properties of these cytochrome P-450 fractions towards substrates in bile acid biosynthesis were studied in reconstituted systems containing NADPH -- cytochrome P-450 reductase and phospholipid. Cytochrome P-450 LM3b showed no hydroxylase activity towards cholesterol and only low activity towards some other C27-steroids whereas it catalyzed efficient hydroxylation of testosterone and demethylation of ethylmorphine. Preparations of cytochrome P-450 LM4 catalyzed hydroxylation of cholesterol and other C27-steroids more efficiently than microsomes. Cytochrome b5 had no stimulatory effect on the C27-steroid hydroxylase activities.

Animals↗

PubMed1989

Biosynthesis of dolichol by rat liver peroxisomes.

The ability of peroxisomes and microsomes to synthesize dolichol from [3H]mevalonate, [3H]isopentenyl-P2 or [3H]farnesyl-P2 in vitro was investigated. It was found that isoprenoid biosynthesis also occurs in peroxisomes and that this process demonstrates properties differing from those of isoprenoid biosynthesis by microsomes. The pH optimum in peroxisomes was 8.0 and, in contrast to microsomes, the peroxisomal biosynthesis was largely insensitive to detergents. After treatment with proteolytic enzymes, microsomes lost their capacity to incorporate [3H]mevalonate into dolichol, whereas proteolysis of intact peroxisomes did not influence their corresponding rate of incorporation. The soluble content of peroxisomes was separated from the membranes and found to demonstrate half of the biosynthetic capacity of the intact organelle. Fasting and cholestyramine treatment decreased only the microsomal incorporation of [3H]mevalonate into dolichol, while treatment with clofibrate, di-2-ethylhexyl phthalate or phenobarbital increased microsomal, but decreased peroxisomal labeling. After injection of [3H]mevalonate into the portal vein of rats, high initial labeling of dolichol was recovered both in isolated microsomes and peroxisomes, whereas when [3H]glycerol was administered, peroxisomal phospholipids became labeled later than the corresponding microsomal constituents. These results support the conclusion that dolichol is synthesized both in peroxisomes and the endoplasmic reticulum, but that the biosynthetic processes at these two locations have different properties.

Animals↗

PubMed1994

7 alpha hydroxylation of 25-hydroxycholesterol in liver microsomes. Evidence that the enzyme involved is different from cholesterol 7 alpha-hydroxylase.

Rat, pig and human liver microsomes were found to catalyze 7 alpha-hydroxylation of 25-hydroxycholesterol. In contrast to cholesterol 7 alpha-hydroxylase activity, the 7 alpha-hydroxylase activity towards 25-hydroxycholesterol in rat liver was not stimulated by cholestyramine treatment. After transfection with cDNA for human cholesterol 7 alpha-hydroxylase, COS cells showed a significant activity towards cholesterol but not towards 25-hydroxycholesterol. During purification of cholesterol 7 alpha-hydroxylase from pig liver microsomes, about 99% of the 7 alpha-hydroxylase activity towards 25-hydroxycholesterol and 27-hydroxycholesterol was clearly separated from 7 alpha-hydroxylase activity for cholesterol. The small amount of 25-hydroxycholesterol 7 alpha-hydroxylase activity retained in a partially purified preparation of cholesterol 7 alpha-hydroxylase was not inhibited by addition of cholesterol, indicating that the oxysterol binding site is different from the cholesterol binding site, presumely due to the presence of two different enzymes. It is concluded that different enzymes are involved in 7 alpha-hydroxylation of cholesterol and 7 alpha hydroxylation of side-chain-oxidized cholesterol in rat, pig and human liver. Inhibition experiments with a partially purified fraction of the oxysterol 7 alpha-hydroxylase from pig liver gave results consistent with the contention that the same enzyme is responsible for 7 alpha hydroxylation of both 25-hydroxycholesterol and 27-hydroxycholesterol. It has been suggested that cholesterol 7 alpha-hydroxylase can preferentially use oxysterols, in particular 25-hydroxycholesterol, as substrates and by this means inactivate important physiological regulators of cholesterol homeostasis. Such a mechanism would explain the unique property of the liver to resist down-regulation of the low-density-lipoprotein receptor [Dueland, S., Trawick, J.D., & Davies, R.A. (1993) J. Biol. Chem. 267, 22695-22698]. The present results do not support the contention that the important coupling between cholesterol 7 alpha-hydroxylase activity, the low-density-lipoprotein receptor activity and hydroxymethylglutaryl coenzyme A reductase activity in liver cells is due to inactivation of 25-hydroxycholesterol or 27-hydroxycholesterol by the action of cholesterol 7 alpha-hydroxylase.

Animals↗

PubMed2005

Successful treatment of a leg ulcer occurring in a rheumatoid arthritis patient under leflunomide therapy.

OBJECTIVE: We report the case of a leg ulcer in a rheumatoid arthritis (RA) patient under treatment with leflunomide, discuss the influence of the drug on the aetiopathogenesis of the ulcer and describe its successful treatment. CASE SUMMARY: A 68-year-old woman with a 12-year history of RA developed a leg ulcer after 4 months of leflunomide treatment. Other ulcerogenic factors were ruled out. There were some clinical hints for rheumatoid vasculitis. The ulcer was resistant to ambulant conservative phase adapted wound bed preparation and a split skin transplantation failed. After omission of leflunomide and washout procedure with cholestyramine a second split skin transplantation resulted in complete healing. DISCUSSION: Leflunomide inhibits the division of activated T cells and thus inhibits among others the production of proinflammatory cytokines and the adhesion of cells to the endothelium. These mechanisms may partly explain the possible influence of leflunomide on the perpetuation of the ulcer. Until now, occurrence of vasculitis and leg ulcers has been described in one case each for the novel immunomodulator leflunomide. No successful treatment of a leg ulcer under leflunomide has been described yet. Omission of leflunomide and a washout treatment in our case led to a complete healing. This may indicate a critical role of leflunomide in the maintenance of this slow healing ulcer. CONCLUSIONS: An association between leflunomide intake, occurrence of leg ulcers in RA patients and delayed wound healing should be considered.

Aged↗

PubMed1991

Pharmacologic and surgical treatment of dyslipidemic children and adolescents.

A wide variety of treatment modalities have been used in children with dyslipidemias to reduce the concentrations of atherogenic lipoprotein particles. Most of the published experience has focused upon children with familial hypercholesterolemia (FH). A variety of pharmacologic regimens have been utilized with variable degrees of success. The bile acid sequestrants colestipol and cholestyramine, lovastatin, pantethine, paraminosalicylic acid, and fenofibrate have all been successful in reducing total blood cholesterol concentrations by 18-24% in hypercholesterolemic children. Of these medications, only the bile acid sequestrants are not absorbed into the circulation. This theoretic advantage is paralled by long-term safety studies which indicate the absence of serious adverse effects with bile acid sequestrant therapy. Therefore, the bile acid sequestrants represent the drugs of choice in treating severely dyslipidemic children. In selected cases of profoundly dyslipidemic children, other therapeutic strategies have been utilized. Most of these efforts have been directed in the treatment of the child homozygous for FH. Despite the lipid lowering effects of partial ileal bypass surgery in hypercholesterolemic adults, homozygous familial hypercholesterolemic children are not adequately treated by this approach. Portacaval shunt has reduced the total cholesterol concentrations by 20-35% in homozygous FH children without having a negative impact on growth and development. These children have, however, gone on to develop atherosclerotic cardiovascular disease despite therapy. Liver transplantation has led to virtual normalization of the plasma lipoprotein concentrations in 3 children homozygous for familial hypercholesterolemia, and there is evidence for regression of vascular lesions in the coronary arteries in one of these children. However, considering the expense, the difficulty in posttransplantation management, and the irreversible nature of the therapy, liver transplantation should be reserved as the therapy of last resort for homozygous FH. The best therapy for FH homozygotes is the frequent removal of the atherogenic lipoproteins by one of the several apheresis procedures currently available. Total plasma exchange, immunoadsorption, membrane filtration, dextran sulfate adsorption, and heparin extracorporeal precipitation have all been used successfully in significantly reducing the concentrations of total and low-density lipoprotein cholesterol. Studies currently under way will more extensively evaluate the long-term safety as well as the efficacy of apheresis procedures.

Adolescent↗

PubMed1994

The cost-effectiveness of different blood-cholesterol-lowering strategies in the prevention of coronary heart disease.

We aimed to compare the cost-effectiveness of two screening strategies and a population strategy for lowering blood cholesterol to prevent coronary heart disease. Census data, known risk-factor profiles, known coronary heart disease event rates and costs in 1988-89 Australian dollars for all men aged 35 to 64 in the Lower Hunter region of New South Wales (n = 67,651) were used to compare a high-risk strategy identifying and treating men with cholesterol levels above 6.5 mmol/L with diet and drug (cholestyramine), a moderate/high-risk strategy where in addition diet counselling was offered to those with levels 5.5 to 6.5 mmol/L, and a population strategy where the diet of the whole population was changed regardless of blood cholesterol. Costs of implementing strategies, heart disease events saved, discounted and undiscounted cost-effectiveness ratios and savings in initial treatment costs over five years were measured. For the high-risk, moderate/high-risk and population strategies, the costs of implementation were $50.1m, $53.1m and $5.4m respectively; the numbers of events saved were 104, 144, 116 respectively; cost-effectiveness ratios were $482,224, $369,098, $46,667 (per event saved) respectively. Cost savings for each strategy were approximately half a million dollars. The moderate/high-risk strategy was more cost-effective than the high-risk strategy but the population strategy cost one-tenth that of the two screening strategies per event saved. More research is required to design and test strategies that alter the eating habits of the whole population.

Adult↗

PubMed1972

Bile salt and non-bile salt components in bile affecting micellar cholesterol uptake by rat intestine in vitro.

1. The uptake of micellar cholesterol was measured in sacs of the upper half of everted rat intestine. Sacs of 20 cm length were incubated 1 hr in 25 ml. phosphate buffer containing fatty acid, monoglyceride and (3)H-labelled cholesterol in micellar form with the bile salt, sodium taurocholate, as the dispersing agent.2. Sacs obtained from bile fistula rats (bile duct cannulated 48 hr previously) took up more than twice as much cholesterol as did sacs obtained from untreated control rats.3. In experiments utilizing bile-deficient sacs increasing the sodium taurocholate concentration caused an increase in cholesterol uptake. Conversely, adding a small amount of whole bile caused a decrease in cholesterol uptake.4. The inhibitory effects of the bile were greatly enhanced if the bile was pre-treated with cholestyramine to remove the bile salts.5. It is concluded that bile has a variable effect on intestinal cholesterol absorption depending upon its relative concentration of bile salt and a non-bile salt component having opposite actions.6. It is suggested that the variable effect may be related to the physico-chemical dispersion of cholesterol and that the non-bile salt component may be lecithin.

Animals↗

PubMed1978

Case of congenital nonobstructive, nonhaemolytic jaundice. Successful long-term phototherapy at home.

Use of cholestyramine made it possible to shorten the daily duration of phototherapy in a case of congenital nonobstructive, nonhaemolytic jaundice. Treatment at home was therefore possible, allowing normal parental care. Development and neurological examinations were normal at the age of 27 months. Frequent determinations of reserve bilirubin binding capacity may be useful in controlling such management.

Bilirubin↗

PubMed1995

Response to drugs and diet in a compound heterozygote for familial hypercholesterolaemia.

A boy with a total plasma cholesterol concentration of 20.9 mmol/l which fell significantly with a low fat diet, cholestyramine and simvastatin, was shown to have two different mutations in the low density lipoprotein receptor gene, demonstrating that some patients with homozygous familial hypercholesterolaemia show a good lipid lowering response to treatment.

Base Sequence↗