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PubMed2002

Mice expressing the human CYP7A1 gene in the mouse CYP7A1 knock-out background lack induction of CYP7A1 expression by cholesterol feeding and have increased hypercholesterolemia when fed a high fat diet.

Cholesterol 7alpha-hydroxylase (CYP7A1) catalyzes the rate-limiting step in the pathway responsible for the formation of the majority of bile acids. Transcription of the gene is regulated by the size of the bile acid pool and dietary and hormonal factors. The farnesoid X receptor and the liver X receptor (LXR) are responsible for regulation by bile acids and cholesterol, respectively. To study the effects of dietary cholesterol and fat upon expression of the human CYP7A1 gene, mice were generated by crossing transgenic mice carrying the human CYP7A1 gene with mice that were homozygous knock-outs (CYP7A1(-/-)). The mice (mCYP7A1(-/-)/hCYP7A1) expressed the human gene at much higher levels than did the transgenics bred in the wild-type background. A diet containing 1% cholic acid reduced the expression of the human gene in mCYP7A1(-/-)/hCYP7A1 mice to undetectable levels. Cholestyramine (5%) increased the level of expression of the human gene and the mouse gene. Thus, farnesoid X receptor-mediated regulation was preserved. A diet containing 2% cholesterol increased expression of the mouse gene in wild-type mice, but it did not affect expression of the human gene in mCYP7A1(-/-)/hCYP7A1 mice. None of the diets altered the serum cholesterol or triglyceride levels in these mice; 1% cholic acid caused a redistribution of cholesterol from the high density lipoprotein to the low density lipoprotein density in the humanized mice but not in wild-type mice. A diet containing 30% saturated fat and 2% cholesterol caused a decrease in CYP7A1 levels in mCYP7A1(-/-)/hCYP7A1 mice. The serum cholesterol levels rose in all mice fed this diet. The increase was greater in the mCYP7A1(-/-)/hCYP7A1 mice. Together, these data suggest that the lack of an LXR element in the region from -56 to -49 of the human CYP7A1 promoter may account for some of the differences in response to diets between humans and rodents.

Animals↗

PubMed1991

Treating serum lipid abnormalities in high-priority patients.

Normalization of serum lipid levels should be initiated as soon as possible in patients with myocardial, cerebrovascular, or peripheral vascular disease. Clinical trials indicate that coronary artery disease and overall mortality rates can be reduced and atherosclerosis stabilized or reversed by lipid-lowering therapy. Treatment should lower low-density lipoprotein cholesterol levels to 130 mg/dL or less and total triglyceride levels to 150 mg/dL or less and increase high-density lipoprotein cholesterol levels to at least 52 mg/dL in men and 66 mg/dL in women. Nonlipid coronary risk factors should be eliminated when possible. Lipid-lowering therapy may consist of dietary modification and drug treatment with colestipol hydrochloride (Colestid), cholestyramine (Cholybar, Questran), lovastatin (Mevacor), gemfibrozil (Lopid), and nicotinic acid (Nicolar).

Anticholesteremic Agents↗

PubMed2001

Absence of dysfunctional ileal sodium-bile acid cotransporter gene mutations in patients with adult-onset idiopathic bile acid malabsorption.

BACKGROUND: A congenital form of idiopathic intestinal bile acid malabsorption (IBAM) has been associated with dysfunctional mutations in the ileal apical sodium-dependent bile acid transporter (ASBT). The aim of this study was to determine whether mutations in the ASBT gene (SLC10A2) predispose to the development of adult-onset idiopathic bile acid malabsorption and chronic watery diarrhea. METHODS: Genomic DNA was obtained from 13 adult IBAM patients previously diagnosed on the basis of clinical data, response to cholestyramine, and abnormal 75Se-homocholic acid taurine (SeHCAT) test values. The ASBT gene was screened for the presence of mutations or polymorphisms by single-stranded conformation polymorphism analysis (SSCP) and DNA sequencing. RESULTS: ASBT gene polymorphisms were detected in 5 of the 13 adult IBAM patients. Four patients were heterozygous for a common polymorphism in exon 3, leading to an alanine to serine substitution at codon 171 (A171S). An additional subject was heterozygous for a polymorphism in exon 1 that causes a valine to isoleucine substitution at codon 98 (V981). These functional polymorphisms were also found in unaffected subjects and do not appear to affect ASBT function. CONCLUSIONS: Adult-onset IBAM is not directly related to dysfunctional mutations in the coding region or intron/exon junctions of the SLC10A2 gene. In the absence of apparent ileal disease or intestinal motility defects, inappropriate down-regulation of the ileal bile acid transporter or defects in ileocyte transfer of bile acids into the portal circulation could explain this form of adult IBAM.

Adult↗

PubMed1997

Perioperative anti-endotoxin strategies.

Lipopolysaccharides from the outer membrane of Gram-negative bacteria are potent stimuli for the production of numerous cytokines by the immune cells. The systemic inflammatory response to these gut-derived endotoxins is therefore dependent on the responsiveness of the immune system. This paper presents results on anti-endotoxin strategies and the responsiveness to endotoxin in animal models of liver failure. Following partial hepatectomy in the normal rat, anti-endotoxin treatment using the enteral endotoxin binder cholestyramine and the bactericidal permeability-increasing protein showed beneficial effects in terms of reducing the exaggerated metabolic and inflammatory responses. Similar beneficial effects of gut endotoxin restriction were found in bile duct ligated rats subjected to a laparotomy. The beneficial effects of anti-endotoxin strategies in these models were explained by completely different mechanisms. In partial hepatectomized rats the effects were explained by the direct inhibition of the stimulatory action of endotoxin on immune cells preventing an exaggerated inflammatory response. In contrast, in postoperative BDL rats the effects of anti-endotoxin therapy were explained by the restoration of endotoxin sensitivity of the immune cells resulting in an inflammatory response necessary for an adequate reaction to surgery. These different mechanism will be discussed in the light of the phenomenon of endotoxin tolerance.

Animals↗

PubMed1999

Benign recurrent intrahepatic cholestasis in a Saudi child.

We report a case of benign recurrent intrahepatic cholestasis (BRIC) in an 11-year-old Saudi girl who developed three episodes of pruritus and jaundice at the ages of 4, 8, and 9 years. These episodes were almost stereotypic and lasted 5-8 weeks. Although she had elevated liver enzymes and serum bile acids in her blood during the attacks, they returned to normal between attacks. Thorough investigation excluded other causes of liver disease and her recurrent attacks were shortened by cholestyramine therapy. A diagnosis of BRIC should be kept in mind in patients with cholestasis.

Bile Acids and Salts↗

PubMed2001

Low-density lipoprotein apheresis in a patient aged 3.5 years.

UNLABELLED: A 3.5 y-old girl carrying a severe mutation of the LDL-receptor gene known as "FH Pavia", affected by homozygous familial hypercholesterolaemia (FH), and at high risk of developing coronary artery atherosclerosis was treated with selective dextran sulphate cellulose (DSC) column low-density lipoprotein apheresis (LDL-a). This is the youngest patient ever treated with LDL-a. Plasma total cholesterol (982 mg/dl) and LDL-cholesterol (939 mg/dl) (T-Chol, LDL-Chol) levels at baseline showed a transient decrease: -13.4%, and -16.8%, respectively, after 9 mo of combined treatment with a diet, cholestyramine (max. 12 g/d) and atorvastatin (max. 30 mg/d). However, the drugs were discontinued because of intolerance and an increase in aminotransferases and creatine phosphokinase in the plasma. Moreover, after 9 mo of this therapy, the mean plasma T-Chol and LDL-Chol levels were still high (930 mg/dl and 869.5 mg/dl, respectively). Therefore, 9 consecutive treatments with LDL-a were carried out every 15 d (plasma volumes treated: 1000-1700 ml). Mean plasma T-Chol, LDL-Chol, triglycerides (TG), and Lp(a) decreased significantly: -75.5%, -77.2%, -67.5% and -50.8%, respectively. HDL-cholesterol (HDL-Chol) concentration was considerably decreased immediately after apheresis because of haemodilution (X: -45.1%). CONCLUSION: LDL-a treatment improved the plasma apo B 100-containing lipoproteins--LDL, Lp(a)--profile in a homozygote with a severe inherited disorder in which coronary artery atherosclerosis frequently has its clinical onset before 10 y of age. At the time of this report, no significant side effects had been observed.

Blood Component Removal↗

PubMed2005

Intravenous immunoglobulin for resistant Clostridium difficile infection.

Clostridium difficile (CD)-associated diarrhoea and colitis may relapse in up to 20% of treated patients. We present a patient who failed to respond over a 6-month period to treatment either singly or in combination with metronidazole, vancomycin, rifampicin, cholestyramine and probiotics. Her diarrhoea rapidly resolved after a 3-day course of intravenous immunoglobulin. This treatment may compensate for a failed immune response to CD toxin and should be considered for relapsing CD-associated diarrhoea where there is no response to conventional treatment strategies.

Clostridioides difficile↗

PubMed1979

Dietary fiber and blood lipids: reduction of serum cholesterol in type II hyperlipidemia by guar gum.

Guar gum, a storage polysaccharide galactomannan and a form of dietary fiber, was administered to 10 patients with type II a or b hyperlipidemia for 2 weeks. Five grams of gum was given before each of three meals daily, either in a specially prepared soup or mixed with fruit juice or milk. No other deliberate change of diet was made. Three patients had been taking 12 to 16 g/day of cholestyramine for more than 2 years and one had been taking 1000 mg of clofibrate daily. These drugs were continued throughout the trial. Serum cholesterol levels of all 10 patients had been stable for 6 to 18 months before the trial at the start of which the mean level was 345 +/- 15 mg/dl. After 2 weeks of guar gum the mean was 308 +/- 16 mg/dl, a fall of 10.6% (P less than 0.01). Serum triglyceride was not changed significantly. Guar gum, which can be incorporated into foods, merits further study as a potential hypocholesterolemic agent.

Anticholesteremic Agents↗

PubMed1979

Clindamycin-induced colitis.

The hamster model of enterocolitis after the administration of clindamycin was used to study various drugs used in treatment of the disease in humans. Current evidence strongly suggests toxigenic, clindamycin-resistant Clostridium difficile is a cause of the disease in hamster and man. This organism is susceptible to vancomycin and metronidazole, and the disease could be prevented in the hamster so long as the antibiotics were given orally. A fatal colitis almost invariably ensued once they were discontinued. Administration of cholestyramine significantly prolonged survival of hamsters, but did not pervent death or colitis. Corticosteroids or atropine-diphenoxylate (Lomotil) did not alter the disease. The hamster model may be useful in studying other kinds of treatment of this disease.

Animals↗

PubMed1980

Effects of dietary saponins on fecal bile acids and neutral sterols, plasma lipids and lipoprotein turnover in the pig.

Four young mature male pigs, 110 to 120 kg of body weight, were maintained on a low (0.01%) cholesterol diet. A double changeover design was used so that at any time two pigs received additionally 20 g/day of saponins as a 0.33% solution in drinking water. Saponins raised concentrations of fecal bile acids and neutral sterols and increased the contribution of primary acids to excretion. Neither the concentration of total plasma cholesterol nor low-density and high-density lipoprotein cholesterol were affected by saponins. There was also no change in either absolute or fractional catabolic rate of low-density or high-density lipiproteins. The data are discussed in relation to the effects of cholestyramine on plasma cholesterol and bile acid excretion in the pig and to the possible role of saponin-containing foods in the control of plasma cholesterol in man.

Animals↗

PubMed1984

A commentary on the Rationale of the Diet-Heart Statement of the American Heart Association.

The objective of the Rationale of the Diet-Heart Statement of the American Heart Association was to restate the diet-heart recommendations of the American Heart Association and to quote the original publications on which they are based. Examination of those publications reveals that for the most part, they are obsolete or misquoted. The last section of the Rationale concerns the role of genetics and very briefly reviews the epidemiological and dietary intervention trial evidence. The latter discussion may be summarized as meaning that risk levels are in the 90 percentile group of plasma cholesterol levels and that those levels are due to genetic factors which "dietary changes alone cannot normalize." It admits that "all" dietary intervention trials "were flawed in one or another aspect of experimental design." Hope is expressed that the Multiple Risk Factor Intervention Trial and the Lipid Research Clinics Primary Prevention Trial will support the diet-heart theory. The former did not and the latter was designed to test cholestyramine and not diet.

American Heart Association↗

PubMed1992

Retinyl palmitate hydrolase activity in human liver.

Retinyl palmitate hydrolase (RPH) activity was studied in human liver after the optimal conditions of the assay in normal human liver homogenates were determined. The mean activity was 118 +/- 66 nmol.min-1.g-1 (mean +/- SD) protein in liver homogenates from six children and seven adults; no correlation was found between liver hydrolase activity and the enzyme endogenous substrate, ie, liver vitamin A concentrations. RPH activity was also studied in a human model of vitamin A deficiency represented by 22 children with biliary atresia: 11 patients with vitamin A deficiency (liver vitamin A concentration less than 70 nmol/g wet wt of liver) and 11 patients with normal vitamin A status after vitamin A treatment. The enzymatic assay had to be conducted after the removal of endogenous bile salts by cholestyramine because bile salts are accumulated in the liver of children with biliary atresia. No correlation was found between RPH activity and vitamin A status.

Adolescent↗

PubMed1979

Serum glycine-conjugated bile acids in pediatric hepatobiliary disorders.

Measurements of serum bile acids (glycine conjugates of cholic, chenodeoxycholic, deoxycholic, and lithocholic acids) by radioimmunoassay in a variety of pediatric hepatobiliary disorders showed elevations in neonatal hepatitis syndromes, cholestasis, and hepatitis of extrahepatic or intrahepatic origin. Measurements of individual serum bile acids failed to differentiate between the various neonatal hepatitis syndromes. In one patient with cholestasis, the increased levels of bile acids observed returned to normal following therapy with cholestyramine and phenobarbital. In chronic active hepatitis the serum bile acid values correlated well with the bilirubin and SGOT in response to therapy with corticosteroids. These data confirm suggestions that serum cholylglycine and chenodeoxycholylglycine levels are a sensitive indicator of disturbed hepatic function and can be used in monitoring the course, activity, and therapeutic response in various hepatitis syndromes. In Reye's syndrome and protracted diarrhea of infancy, elevations in serum bile acids were detected without associated hyperbilirubinemia and provided additional evidence of disturbed hepatic function.

Adolescent↗

PubMed1996

Uremic pruritus.

Uremic pruritus and its treatment are reviewed. Pruritus affects 50-90% of patients undergoing peritoneal dialysis or hemodialysis; symptoms usually begin about six months after the start of dialysis and range from localized and mild to generalized and severe. The mechanism underlying uremic pruritus is poorly understood; possibilities include secondary hyperparathyroidism and divalent-ion abnormalities; histamine, allergic sensitization, and proliferation of skin mast cells; hypervitaminosis A; iron-deficiency anemia; neuropathy and neurologic changes; or some combination of these. The cornerstone of therapy for uremic pruritus is regular, intensive, efficient dialysis. Other nonpharmacologic measures consist of the use of non-complement-activating dialysis membranes, compliance with dietary restrictions, electric-needle (acupuncture) therapy, and ultraviolet light therapy. Pharmacologic treatments that have been used include activated charcoal, antihistamines, capsaicin, cholestyramine, emollients and topical corticosteroids, epoetin, pizotyline, ketotifen, and nicergoline. Treatment results have been highly variable, and many of the clinical trials have been flawed. Phosphate-binding agents appear to be the most effective. Although enough is known to determine a reasonable set of steps in approaching a patient's uremic pruritus, more research is needed to understand the pathophysiology of this condition and to establish more reliable treatments. Pruritus is a common and sometimes severe complication of chronic renal failure. Efficient dialysis, dietary restrictions, phosphate-binding therapy, and phototherapy are the most effective treatments currently available.

Humans↗

PubMed1998

Antidiarrheal agents for the management of treatment-related diarrhea in cancer patients.

The efficacy and use of antidiarrheal agents in patients who diarrhea associated with cancer treatments are reviewed. Diarrhea is common in cancer patients and may interfere with cancer treatment. Diarrhea may be induced by chemotherapy, radiation therapy, surgery, graft-versus-hot disease (GVHD) or infection after bone marrow transplantation, and other causes. The general goal of antidiarrheal therapy is to reduce fluid loss in the stool by inhibiting intestinal secretion, promoting absorption, and decreasing intestinal motility. Antidiarrheal agents may be classified as intestinal transit inhibitors, intraluminal agents, proabsorptive agents, and antisecretory drugs. Opiate agonists are the most commonly used intestinal transit inhibitors; they can be effective in treating cancer treatment-related diarrheas but must be used cautiously. Intraluminal agents include clays, activated charcoal, and cholestyramine; these adsorbents and other binding resins can interfere with the absorption of orally administered antidiarrheals and other drugs and are unlikely candidates for use in most cases of diarrhea in cancer patients. Clonidine, a proabsorptive agent, should be used only in patients with secretory diarrhea refractory to opiate agonist treatment. Octreotide is an antisecretory drug that has shown considerable efficacy in clinical trails as a treatment for diarrhea caused by chemotherapy of GVHD; its use for radiation therapy-induced diarrhea, although not studied clinically, is nevertheless an option. In general, opiate agonists and octreotide appears to offer the most efficacy and flexibility. Opiate agonists and octreotide are effective agents for cancer treatment-related diarrhea.

Antidiarrheals↗

PubMedDate not supplied

Recent advances in management of bacterial diarrhea.

The number of recognized infectious causes of diarrhea potentially treatable with specific antibiotics has markedly increased within the past ten years. Laboratories are developing and expanding their abilities to deal with these new pathogens. Neither prophylaxis nor specific treatment of diarrhea in travelers is simple, practical, and safe. Although enterotoxigenic Escherichia coli is the most important cause of diarrhea in U.S. travelers to tropical areas, Campylobacter jejuni causes acute diarrhea in persons in the United States about as often as do Salmonella and Shigella. Vibrio parahemolyticus is an important cause of outbreaks of gastroenteritis following ingestion of improperly cooked shellfish; Bacillus cereus is important in outbreaks of diarrhea after ingestion of improperly cooked and stored rice in Chinese restaurants. Although Yersinia enterocolitica is probably an important cause of severe enteritis in the United States, imperfect techniques for its isolation and lack of good serologic tests have hampered recognition of its importance. Practical means for diagnosing antibiotic-associated colitis and the role of Clostridium difficile toxins in this disease are now available. Vancomycin, metronidazole, bacitracin, and cholestyramine are useful in treatment of antibiotic-associated colitis.

Adult↗

PubMed1990

Review of clinical trials: proving the lipid hypothesis.

The Lipid Hypothesis, which states that lowering blood cholesterol levels should significantly reduce the incidence of coronary heart disease (CHD), has been repeatedly tested in primary and secondary intervention trials. Viewed as a whole, it is apparent that the incidence of CHD in treated groups decreased in proportion to the degree of plasma cholesterol reduction. An early study at the Wadsworth Hospital in Los Angeles showed that a diet high in polyunsaturated fat and low in cholesterol reduced the incidence of CHD. The Oslo study of diet and smoking intervention demonstrated a significant decrease in CHD concomitant with a 13% reduction in serum cholesterol achieved through a low saturated-fat diet and cessation of smoking. In the World Health Organization primary prevention trial, clofibrate reduced serum cholesterol by 9% and first clinical episodes of myocardial infarction by 20%. There was a 37% rise in total mortality, but no causal link with clofibrate has been found, and this was not significant when corrected for age at death. A secondary trial, the Coronary Drug Project, demonstrated that oestrogen and dextrothyroxine were clearly toxic. In this trial, niacin produced a 10% fall in serum cholesterol and mortality was 11% lower than in the placebo group after long-term follow-up. The Lipid Research Clinics-Coronary Primary Prevention Trial (LRC-CPPT) found an 8% reduction in plasma cholesterol and a 19% reduction in the incidence of CHD in the group treated with cholestyramine compared with placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1977

Bile acids, diarrhea, and antibiotics: data, speculation, and a unifying hypothesis.

The primary bile acid, chenodeoxycholic acid, and the secondary bile acid, deoxycholic acid, when present at a concentration of greater than 3 mM, induce salt and water secretion from the human colon and cause a marked increase in the permeability of the human colon to molecules of a molecular weight of 200-500 daltons. Scanning electron microscopy indicates that this action may be associated with tissue damage in some species. In the healthy individual, the primary bile acids, cholic and chenodeoxycholic acid, are dehydroxylated in the colon and are simultaneously precipitated from solution; at pH less than 7, deoxycholic and lithocholic acid are insoluble. In patients with bile acid diarrhea resulting from bile acid malabsorption, dehydroxylation is decreased, and the concentration of bile acids in the colon is markedly elevated. The major secretory bile acid in solution is chenodeoxycholic acid. Administration of cholestyramine, a resin that binds bile acid, reduces the elevated concentration of chenodeoxycholic acid and abolishes the diarrhea. These facts can be used to develop a unifying hypothesis which proposes that elevated concentrations of primary bile acids in the colon play a role in diarrhea and pseudomembranous colitis induced by clindamycin.

Anti-Bacterial Agents↗