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PubMed1980

Effects of clofibrate, cholestyramine, zanchol, probucol, and AOMA feeding on hepatic and intestinal cholesterol metabolism and on biliary lipid secretion in the rat.

Utilizing newer techniques for measuring rates of cholesterol synthesis, the effects of clofibrate, cholestyramine, zanchol, probucol, and AOMA (a copolymer of maleic acid and an alpha-olefin chain of 18 carbons) on hepatic and intestinal cholesterol metabolism and on biliary lipid secretion in the rat were examined. Uncer conditions of isocaloric feeding, female rats were administered a fixed amount of these drugs each day for 14 days. In one set of experiments the rats were killed and rates of hepatic and intestinal cholesterol synthesis and tissue cholesterol levels were measured. In a second set of studies the rats were subjected to total biliary diversion for 2 hr and rates of biliary lipid secretion were determined. Plasma cholesterol concentrations were measured in all animals. Neither AOMA nor cholestyramine had any effect on plasma cholesterol levels or biliary lipid secretion, but both markedly enhanced intestinal cholesterol synthesis. Cholestyramine also increased hepatic cholesterol synthesis. Clofibrate significantly decreased plasma cholesterol levels, whereas zanchol had the opposite effect. Both clofibrate and zanchol increased liver size and bile secretion rates but lowered biliary lipid concentrations; however, total biliary lipid output was unchanged. Total hepatic cholesterol synthesis in clofibrate-fed animals was similar to that in the controls, but in zanchol-fed animals it was approximately doubled. Neither clofibrate nor zanchol had any effect on intestinal cholesterol synthesis. Probucol dramatically lowered plasma cholesterol levels but had no effect on the other parameters measured. None of the drugs was effective in altering the molar percentage of cholesterol in bile despite the diversity of metabolic changes which occurred. These studies point up the many diverse metabolic effects of these drugs, some of which are clinically useful in lowering plasma cholesterol levels, and delineate the marked dissociations that occur between rates of cholesterol synthesis, tissue cholesterol levels, and plasma cholesterol concentrations.

Animals↗

PubMed1993

Long-term treatment (2 years) with the HMG CoA reductase inhibitors lovastatin or pravastatin in combination with cholestyramine in patients with severe primary hypercholesterolemia.

The effects of the two HMG CoA reductase inhibitors lovastatin and pravastatin in combination with 12-16 g cholestyramine on serum lipids were studied in 18 patients with severe primary hypercholesterolemia. Combined therapy of cholestyramine with lovastatin (80 mg daily) decreased low-density-lipoprotein (LDL) cholesterol by 44% (baseline 7.65 +/- 0.51 mM) and increased high-density-lipoprotein (HDL) cholesterol by 20% (baseline 1.22 +/- 0.12 mM) in 9 patients after 2 years. In 9 other patients with comparable baseline lipid values, cholestyramine plus pravastatin (40 mg daily) reduced LDL cholesterol to a comparable extent after 2 years (-43%, baseline 7.71 +/- 0.44 mM) and increased HDL cholesterol by 18% (baseline 1.06 +/- 0.11 mM). The combination with lovastatin led to a significant reduction in triglycerides level by 25% (baseline 1.63 +/- 0.24 mM), whereas the combination with pravastatin did not change triglycerides level (baseline 1.39 +/- 0.15 mM). Both drug regimens were well tolerated without serious side effects. The effects of both HMG CoA reductase inhibitors after 2 years were comparable to those after short-term intake and after 1-year therapy without loss of efficacy.

Adult↗

PubMed1994

Decreased plasma concentrations of imipramine and desipramine following cholestyramine intake in depressed patients.

The effect of cholestyramine (4 g t.i.d. for 5 days) on the steady-state plasma concentrations of imipramine and desipramine was assessed in six depressed patients receiving chronic treatment with imipramine (75-150 mg/day). Compared with baseline, cholestyramine treatment was associated with an average 23% decrease in plasma imipramine levels [from 211 +/- 95 to 159 +/- 67 nmol/L, (mean +/- SD), p < 0.05], whereas desipramine levels decreased only marginally. These data suggest that administration of cholestyramine at therapeutic doses impairs the gastrointestinal absorption of concurrently prescribed imipramine by an extent that is potentially clinically significant.

Adult↗

PubMedDate not supplied

Cholestyramine improves tropical-related diarrhea.

Patients exposed to the toxic dinoflagellate Pfiesteria develop an illness characterized by secretory diarrhea, conjunctival irritation, skin lesions, and varying degrees of neurologic manifestations. The anion-exchange resin, cholestyramine has been reported in one small case series to be an effective treatment of severe diarrhea associated with Pfiesteria intoxication. A 54-year-old man traveled to the Dominican Republic where he went swimming in what he describes as "dirty ocean water". Within an hour, he noted a generalized burning and itching of his skin. Later on, he noted pruritic vesicular skin lesions, intense frontal headache, and conjunctivitis. A few days later, he complained of abdominal cramping, nausea, and hourly episodes of watery, non-bloody diarrhea. Due to the constellation of symptoms, Pfiesteria intoxication was suspected. On arrival in the United States, he sought medical care for continued symptoms. Physical examination was remarkable for conjunctival injection, linear vesicular lesions (5 cm in length) over his right ankle and left orbit as well as erythema over foreskin of his penis. Mental status and memory were normal. Laboratory studies revealed an elevated serum creatinine, which eventually normalized, and stool studies were negative for leukocytes, blood, and enteric pathogens. Intense diarrhea persisted until he was started on cholestyramine (4 g PO tid). The diarrhea resolved within 2 hours of starting treatment. The headache was initially treated with narcotic agents but only resolved with IV diphenhydramine (25 mg q 4 h). Cholestyramine and diphenhydramine appear to be effective therapeutic agents for tropical-related diarrhea and headache, respectively.

Anion Exchange Resins↗

PubMed1977

A comparison of cholestyramine and nicotinic acid in the treatment of familial type II hyperlipoproteinaemia.

1 The effects of cholestyramine and nicotinic acid on plasma lipid concentration have been compared in patients with type IIa hyperlipoproteinaemia. 2 During a 3-month period, cholestyramine resulted in a mean decrease in cholesterol levels of 26%. Triglyceride levels rose in eight of the ten patients during treatment with this drug but in the majority of patients remained within the normal range. 3 During nicotinic acid therapy, cholesterol fell by a mean of 21% and triglyceride by a mean of 23%. 4 The slow release preparation of nicotinic acid used was acceptable to the majority of the patients studied and the results therefore suggest that this drug may be a useful alternative to the more widely used agent, cholestyramine.

Adolescent↗

PubMed1984

Effects of cholestyramine and colestipol on the plasma concentrations of propranolol.

The effect of equivalent hypolipidaemic doses of cholestyramine (8 g) or colestipol (10 g) on the plasma concentrations of propranolol and 4'-hydroxypropranolol was studied in 12 normal volunteers following the oral administration of 120 mg of normal release propranolol tablets. When two doses of either cholestyramine or colestipol were administered prior to the propranolol, the peak plasma concentrations and area under the curve for both propranolol and the metabolite 4'-hydroxypropranolol were reduced significantly (P less than 0.05). We conclude that the drug interaction between cholestyramine or colestipol and propranolol leads to significant reductions in plasma concentrations of propranolol and 4'-hydroxypropranolol which may cause a clinically diminished effect for a given dosage. Therefore, patients should be observed when either of these resins are added to or deleted from a therapeutic regimen.

Adult↗

PubMed1991

Effects of pravastatin and cholestyramine on gonadal and adrenal steroid production in familial hypercholesterolaemia.

1. Adrenal and gonadal steroids are derived from cholesterol, which may be derived from plasma lipoproteins or de novo synthesis. 2. Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, the rate limiting enzyme in cholesterol synthesis, may therefore affect steroidogenesis when used as lipid-lowering agents in hypercholesterolaemia. 3. We have assessed gonadal and adrenal function in subjects with heterozygous familial hypercholesterolaemia (FH) before and after 12 weeks treatment with pravastatin, an HMG CoA reductase inhibitor, or cholestyramine as a control in maximal recommended doses. 4. No changes in measured plasma cortisol responses to tetracosactrin injection were seen in 11 patients on cholestyramine or 12 on pravastatin. 5. No changes were seen in testosterone, sex hormone binding globulin, androstenedione, dehydroepiandrosterone sulphate, oestradiol or 17 alpha-hydroxyprogesterone. 6. Gonadotrophin levels were unaffected in 10 male subjects on cholestyramine and 7 on pravastatin. 7. Measurements on a subset of subjects continuing to 24 weeks treatment also showed no changes. 8. No adverse effect on adrenal or gonadal function could be demonstrated in patients with familial hypercholesterolaemia on maximal recommended doses of pravastatin.

Adrenal Glands↗

PubMed1980

Treatment of dermatitis herpetiformis with cholestyramine.

Two patients with clinically and histologically typical dermatitis herpetiformis showed a dramatic clearing of their skin lesions in association with an oral dose of 4 g of cholestyramine three times a day. Reappearance of the lesions occurred on the discontinuance of the therapy, followed by remission on resumption of cholestyramine. It is postulated that the non-absorbable anion exchange resin, cholestyramine, may have bound and hence blocked absorption of an unidentified compound (possibly gluten, iodine, or endotoxin) critical to the pathogenesis of dermatitis herpetiformis.

Aged↗

PubMed1987

A combination of phototherapy and cholestyramine for the relief of pruritus in primary biliary cirrhosis.

A patient with primary biliary cirrhosis is reported in whom UV phototherapy alone was repeatedly effective in controlling severe pruritus. Symptomatic relief was sustained by introducing cholestyramine at a low dosage, despite previous failure of the drug alone to produce any therapeutic benefit, even in large doses. Bile acid concentrations were measured in sera, urine and suction blister fluid from skin exposed to ultraviolet light before, during and following treatment. The findings suggest that phototherapy reduces cutaneous bile acid levels which can subsequently be maintained by low dose cholestyramine. Routine liver function tests remained unaltered. This combination of phototherapy and cholestyramine may be useful in controlling severe pruritus in primary biliary cirrhosis when the drug alone is not tolerated or is ineffective.

Adult↗

PubMed1991

Gemfibrozil in familial combined hyperlipidaemia: effect of added low-dose cholestyramine on plasma and biliary lipids.

Gemfibrozil is frequently used for lipid-lowering in familial combined hyperlipidaemia (FCHL) and in other forms of combined hyperlipidaemia. This therapy increases biliary cholesterol saturation, enhancing the risk for gallstone formation. Furthermore, in hypertriglyceridaemia, LDL cholesterol levels often tend to rise. We have explored the possibility that addition of a low dose of cholestyramine to gemfibrozil therapy obliterates these phenomena. Eighteen gallstone-free patients with definite (n = 5) or probable (n = 10) FCHL, or combined hyperlipoproteinaemia (n = 3) were randomized to a 6 week treatment with gemfibrozil, 600 mg b.i.d., or gemfibrozil 600 mg b.i.d. plus 4 g cholestyramine o.d. After 6 weeks the patients were crossed over to the alternative treatment. Plasma lipoproteins and biliary lipids were determined at baseline and at the end of each period. Institution of gemfibrozil treatment resulted in a decrease in plasma cholesterol by 15% (P less than 0.05) and in plasma triglycerides by 47% (P less than 0.05); HDL cholesterol increased by 18% (P less than 0.05). Addition of cholestyramine further decreased plasma and LDL total cholesterol by 9% (P less than 0.05). Total triglycerides and HDL cholesterol did not change. Gemfibrozil treatment was associated with a rise in the relative biliary concentration of cholesterol from 5.6 +/- 0.4 to 6.9 +/- 0.5 molar percent (P less than 0.01), and a parallel decrease in the relative concentration of bile acids, resulting in an increased cholesterol saturation of the bile, from 77 +/- 5 to 90 +/- 6% (P less than 0.05). This change was not observed during the combined therapy (mean cholesterol saturation, 82 +/- 4%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Decreased sensitivity to adenosine in platelets from patients with familial hypercholesterolaemia--a change reversed by cholestyramine treatment.

Platelet-rich plasma was obtained from patients with untreated heterozygous familial hypercholesterolaemia (FH), from FH patients treated with cholestyramine and from control subjects. Responsiveness of platelets to the aggregation inhibitors adenosine, its analogue N-ethylcarboxamidoadenosine (NECA) and prostaglandin I2 was decreased in FH. Patients on cholestyramine therapy showed normal responsiveness to adenosine and NECA. There were only minor changes in the binding of [3H]NECA to high-affinity binding sites on platelet membranes from untreated FH or cholestyramine-treated FH patients. The initial rate of cyclic AMP formation in response to a high concentration of NECA was severely decreased in platelets from FH patients. By contrast, the rate of cyclic AMP formation in response to forskolin or a high concentration of prostaglandin I2 was unchanged. These data point to a defect in the coupling of the platelet A2 adenosine receptor to adenylyl cyclase in untreated FH patients.

Adenosine↗

PubMed1989

Simvastatin and cholestyramine in the long-term treatment of hypercholesterolaemia.

After 6 weeks on a lipid-lowering diet, 20 outpatients with type II hyperlipoproteinaemia (18 type IIa) were randomized to treatment with cholestyramine 12 g b.i.d. (5 patients) or simvastatin (a new HMG-CoA reductase inhibitor) 40 mg q.p.m. (15 patients) for 12 weeks. From week 13 to week 20 nine patients in the simvastatin group and all patients in the cholestyramine group were treated with the combination of the two drugs. From week 21 to week 52 all patients were on monotherapy with simvastatin. Simvastatin treatment reduced low-density lipoprotein (LDL) cholesterol by 40% after 12 weeks, compared with 33% in the cholestyramine group. This difference was not significant. The total reductions of LDL-cholesterol on combination therapy were respectively 60% and 56% in each group. After 52 weeks LDL-cholesterol was still reduced by 36% (P less than 0.001) on monotherapy with simvastatin. Simvastatin also reduced triglycerides (TG) by 17% (P less than 0.05) and high-density lipoprotein (HDL) cholesterol was increased by 19% (P less than 0.01). No serious side effects were observed, and the new HMG-CoA reductase inhibitors may offer a new approach to the treatment of hypercholesterolaemia.

Adult↗

PubMed1984

Cholestyramine induced hyperchloremic metabolic acidosis.

The first reported case, in an adult, of cholestyramine induced hyperchloremic metabolic acidosis is a 70 year old female with a two year history of primary biliary cirrhosis confirmed by histologic and immunologic criteria. After taking cholestyramine II sachets twice daily for two months she presented with lethargy, confusion and drowsiness. Examination revealed confusion, jaundice, signs of chronic liver disease, portal hypertension and hepatic encephalopathy. Laboratory investigations confirmed a metabolic acidosis (pH 7.15) and hyperchloremia. Multiple cultures failed to reveal sepsis and a urinary pH of 4.85 together with tests of renal acidification, excluded renal tubular acidosis. She received 600 mEq of sodium bicarbonate intravenously over 36 hours by which time her mentation, electrolytes and pH were normal. It is presumed that her hyperchloremic metabolic acidosis was secondary to cholestyramine because of the similarity to pediatric reports; the rapid and lasting response to intravenous sodium bicarbonate; the absence of another etiology; normal serum potassium, chloride and bicarbonate despite continued spironolactone therapy after recovery.

Acidosis↗

PubMed1988

Combination treatment with cholestyramine and bezafibrate for heterozygous familial hypercholesterolaemia.

Cholestyramine and bezafibrate were compared individually and in combination in the treatment of 18 patients with heterozygous familial hypercholesterolaemia. The study used a double blind, placebo controlled block design with a placebo run in period of two months followed by three phases of active treatment, each of two months' duration. Patients were randomly allocated to one of the six possible sequences of medication so that three patients would be treated with each sequence. Two patients withdrew from the study before completion. The median concentration of total cholesterol decreased from 9.65 mmol/l (interquartile range 8.62 to 8.72) to 7.24 mmol/l (6.70 to 7.52) with cholestyramine, to 8.09 mmol/l (7.18 to 8.68) with bezafibrate, and to 6.31 mmol/l (5.84 to 7.27) with the combination. This fall was due almost entirely to a decrease in the low density lipoprotein cholesterol concentration, and the combination was significantly more effective than either drug alone. The 98% confidence intervals for the median differences between the combination and cholestyramine and the combination and bezafibrate were 0.04 to 1.49 mmol/l and 0.51 to 2.18 mmol/l respectively. These results suggest that this combination is an effective and useful treatment in heterozygous familial hypercholesterolaemia.

Adult↗

PubMed1971

Combined use of clofibrate and cholestyramine or DEAE sephadex in hypercholesterolaemia.

A comparison was made of the effect of DEAE (diethylaminoethyl) Sephadex (an anion exchange resin) and cholestyramine (Questran) with and without the addition of clofibrate in normal and hypercholesterolaemic patients. DEAE Sephadex (12-15 g/day) alone appeared to be as effective as cholestyramine in lowering the plasma cholesterol by 12-15%. Clofibrate acted synergistically with DEAE Sephadex and increased the activity of the latter by over twofold. This combination proved superior to that of clofibrate and cholestyramine and has the greatest potential use in the treatment of type II pattern hyperlipoproteinaemia.

Anticholesteremic Agents↗

PubMed1977

Double-blind trial of cholestyramine in post-vagotomy diarrhoea.

The effect of cholestyramine in post-vagotomy diarrhoea has been assessed under double-blind conditions. Cholestyramine produced a significant improvement in frequency, urgency, and consistency of stool as well as episodic diarrhoea. Faecal bile acid excretion was significantly higher in the post-vagotomy group when compared with normal controls. These findings confirm the effectiveness of cholestyramine and support the concept of a bile acid mediated aetiology in post-vagotomy diarrhoea.

Bile Acids and Salts↗

PubMed1979

Cholestyramine in the peritoneal cavity of the rat.

The effects of cholestyramine in the peritoneal cavity of the rat are described. Cholestyramine causes mild peritonitis with adhesion formation between the liver and the omentum. In the management of biliary peritonitis, a lavage solution containing a suspension of cholestyramine would appear to be contra-indicated by these experimental studies.

Animals↗

PubMed2002

Light symptoms following a high-dose intentional L-thyroxine ingestion treated with cholestyramine.

Adult exposure to L-thyroxine has a wide range of presentations: most adults either do not develop symptoms or only become minimally symptomatic. Appropriate treatments after exposure to L-thyroxine have yet to be established. A 26-year-old woman with a suicidal intention was witnessed to ingest approximately 50 L-thyroxine tablets, each containing 0.1 mg L-thyroxine (total dose 5 mg). Cholestyramine was administered (4 g every 8 h p.o.). Vital signs were monitored every 6 h and the hormone levels (L-thyroxine and thyroid-stimulating hormone) every 24 h. The thyroxine levels increased, and the thyroid-stimulating hormone levels decreased, with a normalization of the L-thyroxine level on postingestion day 6. Hypertension, dysrhythmias, and delusions did not appear in our patient. Only distal tremor and diaphoresis appeared on day 1 after ingestion. Cholestyramine has been used in cases of iatrogenic hyperthyroidism, in patients with Graves' disease, and in patients with digoxin intoxications, with good responses in all cases and a low incidence of side effects. This case illustrates the potential utility of cholestyramine to treat L-thyroxine intoxications.

Adult↗