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PubMed1992

Cholestyramine-induced hyperchloremic metabolic acidosis.

Cholestyramine is a nonabsorbable anion exchange resin that is used predominantly for the treatment of hypercholesterolemia in adults and the management of acute diarrhea in children. The authors report two cases of severe hyperchloremic nonanion gap metabolic acidosis associated with the use of cholestyramine therapy. The authors recommend that patients taking cholestyramine who have concomitant renal insufficiency or who are volume depleted or who are taking spironolactone be monitored carefully for the emergence of a hyperchloremic metabolic acidosis.

Acidosis↗

PubMed1996

Cholestyramine ointment to treat buttocks rash and anal excoriation in an infant.

OBJECTIVE: To describe a novel treatment for perianal excoriation in an infant receiving a promotility agent. CASE SUMMARY: A 2-month-old boy with reflux, and regurgitation was treated with cisapride. Shortly after cisapride therapy he developed a rash on his buttocks and anal irritation that progressed in severity despite the use of numerous topical products and extended diaper-free periods. A topical cholestyramine ointment compound was prepared and administered, resulting in complete resolution within 3 days. DISCUSSION: Cisapride can decrease the gastrointestinal transit time, which can lead to less time for bile acid reabsorption in the distal ileum. If high concentrations of bile acids are contained in the stool, they can irritate the anus and buttocks in a manner similar to the skin irritation experienced by patients with ostomies. Cholestyramine, a bile acid sequestrant, can irreversibly bind the bile when applied topically and bring relief to the patient. CONCLUSIONS: Topical cholestyramine ointment may be a safe and efficacious treatment option for perianal irritation due to bile acids.

Antipruritics↗

PubMed1992

Utilization of cholestyramine resin as a preventive treatment for antibiotic (clindamycin) induced enterotoxaemia in the rabbit.

Cholestyramine, an ion exchange resin shown to bind bacterial toxins, was utilized to treat rabbits with antibiotic induced enterotoxaemia. Three groups of 6 rabbits were administered 30 mg/kg clindamycin phosphate intravenously on day 1. One group was untreated; 2 groups were treated daily by gavage with 2 g cholestyramine in 20 ml water until day 21, starting on either day 1 or 3. Daily body weights, faecal output, faecal occult blood, food and water consumption, and body temperatures were determined. Four of 6 rabbits in the untreated group either died or were moribund and euthanased. There were no deaths in either treatment groups. Dramatic decreases in food consumption (86%), water consumption (62%), and faecal output (89%) were noted within 3 days after clindamycin administration in all groups. These parameters remained depressed throughout the study. There was no clear trend in body weight changes, body temperature, or faecal occult blood test results. Cholestyramine was effective in eliminating mortality associated with the intravenous administration of clindamycin and is recommended to prevent the development of enterotoxaemia when pyrogen testing or administering antibiotics known to induce the syndrome in rabbits.

Animals↗

PubMed1998

[Combined therapy with cholestyramine and HMG-CoA reductase inhibitors in secondary prevention of coronary disease].

PURPOSE: To evaluate lipid profile changes associated with cholestyramine addition in hypercholesterolemic patients with established coronary heart disease under treatment with HMG-CoA reductase inhibitors that had not achieved the ideal value of LDL-cholesterol. METHODS: Twenty patients with coronary heart disease, (12 submitted to coronary artery bypass grafts, 3 to coronary angioplasty and 5 maintained under clinical management) with mean age of 60.78 years old, who were under hypolipemic diet and were medicated with lovastatin 20 mg/d or simvastatin 10 mg/d, received cholestyramine, doses ranging from 8 to 16 g/day during 8 weeks, aiming to reduce LDL-cholesterol to values less than 100 mg/dL. RESULTS: There was a significant reduction of total cholesterol, from initial mean value of 239.52 mg/dL to final mean value of 199.00 mg/dL, with a mean reduction of 16.92%. The mean value of LDL-cholesterol was also reduced significantly from 172.73 mg/dL to 118.26 mg/dL, with a mean reduction of 31.53%. Mean triglyceridemia increased, still within the normal reference values, from 145.05 mg/dL to 162.00 mg/dL, and the mean difference was 11.69%. There was a significant increase of HDL-cholesterol fraction from an initial mean value of 38.00 mg/dL to a final mean value of 48.21 mg/dL, mean difference of 26.87%. Side effects were not frequent, and did not interfere in the duration of the study. CONCLUSION: The association of cholestyramine to HMG-CoA reductase inhibitors, both in low doses, in patients with primary hypercholesterolemia and high coronary risk is a good therapeutic option that can reach benefits on the lipid profile similar to those obtained when these drugs are used in association or separately in higher doses.

Anticholesteremic Agents↗

PubMed1986

The ability of antacids and cholestyramine to bind bile acids: effect of pH.

Reflux of bile into the stomach may be injurious to the gastric mucosa. The ability of antacids and cholestyramine to bind bile acids is therefore potentially valuable in the treatment of reflux gastritis. The ability of antacids and cholestyramine to remove bile acids from gastric juice, hepatic bile, and solutions of commercially available bile acids was investigated in vitro over a pH range likely to occur in the stomach. The percentage of bile acids removed by antacids decreased with decreasing initial bile acid concentration and usually decreased as the incubation pH was increased from 3.6 to 7.0. Glycine-conjugated bile acids were bound to a greater extent than taurine-conjugated bile acids and dihydroxy to a greater extent than trihydroxy bile acids. Cholestyramine bound 97-100% of all bile acids in solution at pH 3.6 and pH 7.0. The effect of pH on adsorption should therefore be considered when antacids are used to treat gastritis.

Aluminum Compounds↗

PubMed1995

Effects of an HMG-CoA reductase inhibitor, pravastatin, and bile sequestering resin, cholestyramine, on plasma plant sterol levels in hypercholesterolemic subjects.

To study exogenous sterol metabolism during the suppression or stimulation of cholesterol biosynthesis induced by treatments for hyperlipidemia, we determined plasma plant sterol concentrations before and after administration of an HMG-CoA reductase inhibitor, pravastatin, and compared these with changes in these plasma sterol levels by the bile-sequestrating resin, cholestyramine. The effects of the drugs were also studied in a sitosterolemic patient who has had increased plasma levels of plant sterols. Plasma cholesterol levels determined by the HPLC method were decreased significantly after administration of pravastatin. Plasma plant sterol (sitosterol and campesterol) as well as cholestanol concentrations were also significantly reduced. Cholestyramine administration decreased plasma levels of cholesterol, but did not change those of plant sterols in the hypercholesterolemic subjects. Pravastatin had little effect in a sitosterolemic patient on plasma levels of sterols, where cholestyramine decreased the plasma levels of both cholesterol and cholestanol. These results indicate that treatment with the HMG-CoA reductase inhibitor decreases plasma plant sterol concentrations, and suggest that the increased plasma plant sterol levels in sitosterolemia might not be due to the decreased cholesterol biosynthesis in vivo.

Acyl Coenzyme A↗

PubMed1975

In vivo effect of bile salts and cholestyramine on intestinal anaerobic bacteria.

In vitro studies have shown that some bile salts inhibit the growth of intestinal bacteria. We investigated the possibility that bile salts might have a similar action in vivo in the ileum by performing serial anaerobic cultures and bile salt analyses on postprandial ileal fluid obtained anaerobically via intestinal tube. Five subjects were studied under control conditions, and after a 1-week course of orally administered cojugated bile salts in a dose shown to increase the bile salt pool. Three of the subjects were also studied after a 1-week course of cholestyramine. The numebr of ileal anaerobic microorganisms decreased significantly after both bile salt and cholestyramine treatment. Ileal bile salt concentrations were generally high (mean 9.2 mM) and did not change significantly after either bile salt or cholestyramine treatment. The results of this study are unexplained. Although it is possible that bile salts play a role in the regulation of small intestinal anaerobic flora, the lack of a relationship between ileal bile salt concentration and population levels of anaerobic organisms is puzzling and raises further questions about such a role for bile salts.

Adult↗

PubMed2003

Vitamin K deficiency and bleeding after long-term use of cholestyramine.

Although it has been long known that in theory the use of cholestyramine can cause coagulopathy due to reduced absorption of vitamin K, only a few cases have been reported. In those cases the coagulopathy occurred within a few weeks to months after the start of therapy. We report a patient with severe pruritus due to intrahepatic cholestasis, who was on cholestyramine therapy for over 25 years before haemorrhage occurred. This case demonstrates that one should be aware of the possibility of depletion of fat-soluble vitamins during the long-term use of cholestyramine.

Adult↗

PubMed1992

[The effects of cholestyramine on pancreatic secretion].

The objective was to evaluate the effect of biliary salt depletion on morphology and function of the exocrine pancreas. Cholestyramine (15 g/day) was given during fifteen days to male Wistar rats in order to evaluate changes in pancreas weight as well as in enzymatic content of pancreatic tissue and duodenal juice (amylase, lipase and trypsinogen); in duodenal juice, bile salt concentration was also measured; Moreover ultrastructure of the exocrine pancreas was studied. Our results show an increase in pancreas weight in rats treated with cholestyramine, with a significant increase of amylase (p < 0.05) and trypsinogen in pancreatic tissue (p < 0.01), and of lipase in duodenal juice (p < 0.05). Ultrastructural changes were absent. It is concluded that cholestyramine, probably through a bile salt depletion, stimulates pancreatic function and growth, as well as lipase secretion.

Amylases↗

PubMed1991

[Effects of rice bran fiber and cholestyramine on peripheral blood cells and biochemical parameters in Yusho].

To investigate clinical effects of rice bran fiber and cholestyramine therapy in Yusho, peripheral blood cells and biochemical parameters were studied before and after therapy in eleven healthy volunteers and four patients with Yusho who were treated with rice bran fiber 30 g/day and cholestyramine 12 g/day for 7 days. In healthy volunteers, a significant elevation in total leukocyte counts as well as lymphocyte counts was observed after therapy (leukocyte p less than 0.005, and lymphocyte, p less than 0.01). In lymphocyte subpopulations, significant elevations were found in CD3- and B1-positive cells (CD3, p less than 0.05 and B1, p less than 0.001). However, no significant effect of the treatment was observed in reticulocyte counts or platelet counts. In biochemical parameters, total cholesterol levels decreased significantly, from 208 +/- 36 mg/dl (mean +/- SD) to 173 +/- 30 mg/dl (p less than 0.001), after therapy. HDL-cholesterol levels were also reduced significantly after therapy (from 50 +/- 12 to 46 +/- 13/mg/dl; p less than 0.05). Serum triglyceride levels increased significantly, from 155 +/- 96 to 195 +/- 133 mg/dl (p less than 0.05), after therapy. A significant increase was observed in serum levels of alanine aminotransferase, while significant depressions were found in serum levels of total bilirubin, total protein, gamma-globulin, creatinine, and calcium. In four Yusho patients who received rice bran fiber and cholestyramine therapy twice with more than one month interval, the clinical effects of therapy in addition to biochemical effects were studied. An only significant effect was observed in serum levels of total cholesterol.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMedDate not supplied

Effects of pravastatin and cholestyramine on circulating levels of parathyroid hormone and vitamin D metabolites.

The subjects were 40 hypercholesterolemic patients (mean age, 58 years) receiving a low-fat diet and randomly assigned to treatment with placebo for eight weeks or 40 or 80 mg of pravastatin, 24 gm of cholestyramine, or 40 mg of pravastatin plus 24 gm of cholestyramine daily for 24 weeks. After eight weeks of active treatment, levels of total and low-density lipoprotein cholesterol were significantly reduced and the decline was maintained for the remaining 16 weeks. Parathyroid hormone levels and levels of the vitamin D metabolites 1,25(OH)2D3 and 25(OH)D3 did not change during treatment. The results indicate that 24 weeks of treatment with pravastatin and cholestyramine does not affect calcium metabolism.

Calcifediol↗

PubMed1990

[Experimental and clinical study of Vasosan P, a new form of pectin-enriched cholestyramine].

The bile acid sequestering agent Vasosan P is a new form of pectin-enriched cholestyramine (20%), saccharose (5%) and sorbic acid (0.18%). In comparison with cholestyramine Vasosan P has a more marked hypolipidemic effect in experiment. Vasosan P is remarkable for good organoleptic properties. It is effective in treating patients with type IIa hyperlipoproteinemia and practically has no side effects as cholestyramine.

Animals↗

PubMed1990

[Interaction of cholestyramine and chloroquine].

The plasma levels of chloroquine after an oral intake of 10 mg/kg were measured in 5 children, with or without simultaneous intake of cholestyramine. Plasma chloroquine levels measured 6 hours after intake were significantly lower in case of simultaneous administration of cholestyramine, in spite of important individual changes. These data suggest a decrease in chloroquine bioavailability in the presence of cholestyramine. However, the methodology used does not allow to assert it.

Adolescent↗

PubMed1975

Failure of cholestyramine to prevent bile salt injury to mouse gastric mucosa.

Bile salts have been implicated in the pathogenesis of gastritis and gastric ulcer. Because the bile salt binding agent cholestyramine has been suggested as a possible therapy for gastric ulcer, we studied the effects of cholestyramine, in the form of Questran, on bile salt-induced injury to mouse gastric mucosa. Solutions of taurocholate or of glycochenodeoxycholate, with or without added Questran, were instilled into the stomachs of fasted mice at pH 1, 3, 5, and 7. Taurocholate damaged the mucosa only at pH 1, whereas glycochenodeoxycholate caused injury at pH 1 and 3. Questran failed to prevent mucosal damage by either bile salt. The ineffectiveness of cholestyramine to prevent injury may be due to the nonionized fraction of bile salts at pH's below their pKa's which will not be sequestered by the anion exchange resin. This phenomenon may help explain the insignificant effect of Qestran treatment in promoting healing of gastric ulcers in a previous clinical trial.

Animals↗

PubMed1989

Lipid and carbohydrate metabolism in cholestyramine-fed rats.

In rats fed semipurified diets, increasing amounts of dietary cholestyramine counteracted the effects of dietary cholesterol on plasma and liver cholesterol concentrations. These effects were associated with increasing rates of fecal bile acid excretion. Cholestyramine caused an increase in plasma triglyceride concentrations, and increased the ratio of triglycerides to cholesterol in plasma. The anion resin did not influence plasma glucose concentrations and blood concentration of acetoacetate, beta-hydroxybutyrate and lactate. Thus cholestyramine specifically affects cholesterol metabolism and plasma triglyceride concentrations without influencing other metabolites of fatty acid and carbohydrate metabolism.

Animals↗

PubMed1989

Contrasting effects of lovastatin and cholestyramine on low-density lipoprotein cholesterol and 24-hour urinary mevalonate excretion in patients with heterozygous familial hypercholesterolemia.

To further validate the usefulness of quantitative measurements of urinary mevalonic acid excretion as an indicator of rates of cholesterol biosynthesis, we have determined the 24-hour urinary excretion of mevalonic acid in patients with heterozygous familial hypercholesterolemia treated with drugs that have opposing effects on cholesterol biosynthesis. In patients with familial hypercholesterolemia treated with the bile acid sequestrant cholestyramine (16 gms/day), urinary mevalonate excretion increased by 28%, whereas low-density lipoprotein cholesterol concentrations decreased by 21%. In patients with familial hypercholesterolemia treated with the 3-hydroxy 3-methyl glutaryl coenzyme A reductase inhibitor lovastatin (80 mg/day), concentrations of low-density lipoprotein cholesterol and the urinary excretion of mevalonate both decreased (by 40% and 34%, respectively). When cholestyramine was used in combination with lovastatin, low-density lipoprotein cholesterol levels decreased by an additional 14% as compared to monotherapy with lovastatin; urinary mevalonate excretion rose by (25%), but the magnitude of this increase was not statistically significant. We conclude that rates of excretion of urinary mevalonic acid (which may reflect rates of whole body cholesterol biosynthesis) in patients with FH decrease on therapy with lovastatin and increase in response to cholestyramine treatment. When used in combination, these drugs counteract each other's effects on cholesterol synthesis, but low-density lipoprotein cholesterol concentrations decrease further. Measurement of urinary mevalonate excretion affords a practical means of assessing the comparable effects of different dietary or pharmaceutical manipulations on cholesterol biosynthesis in human beings.

Adult↗

PubMed1977

Effect of cholestyramine on the symptoms of reflux gastritis. A randomized, double blind, crossover study.

Bile acids have been proposed to be important in the pathophysiology of the syndrome of "bile reflux gastritis" after surgery. To examine the role of cholestyramine, an ion exchange resin that binds bile acids, on symptoms of this syndrome, we did a randomized, double-blind crossover study on 16 patients. No differences in frequency of abdominal pain, nausea, vomiting, or bitter taste were observed among cholestyramine (4 g, three times daily for 3 weeks), placebo, and routine (dietary restriction and ad libitum antacid) treatment periods. We conclude that this regimen of cholestyramine was ineffective in symptomatic treatment of bile reflux gastritis.

Adult↗

PubMed1987

Adsorption of bile acids by sucralfate, antacids, and cholestyramine in vitro.

Sucralfate, one of the newer drugs shown to be effective in the treatment of peptic ulcer and esophagitis; cholestyramine, a known bile acid binder; and commercial antacid preparations of pure aluminum hydroxide, pure magnesium hydroxide, and a combination of aluminum hydroxide, magnesium hydroxide, and magnesium carbonate were tested in vitro for bile acid-binding capacity. Cholestyramine was found to be the most effective bile acid binder, with more than 90% of bile acids adsorbed at all of the pH values studied. Sucralfate proved efficacious at pH 4, 6, and 8, adsorbing about 50% of the bile acids, but its binding capacity decreased at pH 2. Pure aluminum hydroxide was the most effective of the various antacid preparations; it adsorbed about 90% of bile acids at pH 2, although this percentage was significantly reduced at pH 6 and 8. Sucralfate was significantly more effective as a bile acid absorbent at pH 4 than either the magnesium hydroxide or aluminum-magnesium hydroxide plus magnesium carbonate antacids, as effective as the aluminum hydroxide antacid, and significantly less effective than cholestyramine.

Adsorption↗