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PubMed1979

In vitro binding of various biological substances by two hypocholesterolaemic resins. Cholestyramine and colestipol.

The ability of cholestyramine and colestipol, two hypocholesterolaemic resins, to bind in vitro several compounds such as vitamin B12, vitamin B12-intrinsic factor complex, folic acid, iron citrate and calcium chloride was investigated. Both resins bound to a high extent vitamin B12-intrinsic factor complex, folic acid and iron citrate; in addition, cholestyramine also caused appreciable binding of calcium. Throughout a large range of pH, there was no change in the binding capacity; however, at pH 2, cholestyramine exhibited a marked drop in the binding of tested substances (with exception of folic acid). By increasing the molarity of the solutions, the binding to the resins of vitamin B12-intrinsic factor complex and of calcium chloride was completely inhibited. In human gastric and duodenal juices, the uptake by the resins of the studied compounds depends on the molarity of the physiological medium tested and partly confirms the results obtained with aqueous solutions. These data obtained in vitro emphasize the necessity of regular monitoring these biochemical parameters during chronic treatment of hypercholesterolaemia conducted with these two resins.

Body Fluids↗

PubMed1977

[First clinical experiences with cholestyramine for the prophylaxis of stress ulcer (author's transl)].

In a general and accident surgical intensive care ward, the possibility of prophylaxis with the exchange resin cholestyramine (which combines with bile acids) was investigated in 68 patients threatened by stress ulcers. Whereas two patients in the control group treated with an antacid (N = 24) developed deep stress ulcers, only one patient among those treated with cholestyramine alone (N=8) developed superficial erosions; no bleeding occurred at all when it was combined with an antacid (N=36). Entefal tolerance of cholestyramine was good during parenteral feeding. No side-effects were observed. The elimination of the ulcerogenic function of duodenogastric reflux in stress ulcer is discussed as a mode of action.

Adolescent↗

PubMedDate not supplied

[Cholestyramine in the treatment of acute bacterial diarrhea in infants].

32 infants admitted to Hospital "Roberto del Río" with infectious diarrhea and dehydration were assigned random to two groups, one of them receiving the usual therapeutic regimen of rehydration, refeeding and furazolidone and the other group the same treatment plus cholestyramine. The patients were studied with balance technique on days 1st, 3rd., and 5th. after admission, analyzing clinical progress, features of the stools, total digestive transit time, pH of the feces and the presence of reducing substances, volume of the stools, water excretion and sodium, potassium and chloride elimination in the feces. The patients receiving cholestyramine showed an earlier improvement in the appearance of the stools, less excretion of feces and water and diminished sodium and potassium elimination. Chloride excretion was similar in both groups. Cholestyramine tolerance was excellent. No side effects or complications were observed.

Acute Disease↗

PubMed1972

Cholestyramine and medium-chain triglyceride in prolonged management of patients subjected to ileal resection or bypass.

The pathophysiology of cholerrheic enteropathy is described and a series of patients reviewed. Of 11 patients with chronic disabling diarrhea and steatorrhea after ileal resection or bypass, two had recurrent ileitis, three had lactose intolerance and six of those operated on five years or more previously had vitamin B(12) deficiency. Cholestyramine was given alone or with medium-chain triglyceride (MCT) or Portagen (MCT and lactose). The maximal response occurred when cholestyramine was given with Portagen - significantly reduced stool frequency and weight in all patients and stool fat in five. Restudy of five patients four to 11 months later showed the same pattern of response: cholestyramine with 70% MCT abolished symptoms in four patients (ileectomy) and 100% MCT alone greatly improved the condition of the fifth (extensive small bowel resection).

Adolescent↗

PubMed1980

Effects of cholestyramine on receptor-mediated plasma clearance and tissue uptake of human low density lipoproteins in the rabbit.

This study examines the effects of cholestyramine (2 g/day) on the plasma clearance and tissue uptake of human low density lipoprotein (LDL) in rabbits. 1,2-Cyclohexanedione modification of human LDL abolishes its recognition by high affinity cell membrane receptors in vitro and delays its plasma clearance in comparison to native LDL. Consequently, the difference between the fractional rates of catabolism of simultaneously injected native and cyclohexanedione-treated LDL is an index of in vivo receptor-mediated clearance of the lipoprotein. When human 125I-LDL and 131I-cyclohexanedione-treated LDL were injected into rabbits, 44% of the lipoprotein was cleared from the plasma by the receptor mechanism. Various tissues were removed from the animals at the end of the turnover study and their relative uptakes of 125I native and 131I-cyclohexanedione-treated LDL were measured. All exhibited receptor activity to some extent, incorporating more native than cyclohexanedione-modified LDL. The greatest receptor activity per g of tissue was found in lymph nodes, spleen, and liver and, in terms of whole organ uptake, the liver played a major role in LDL catabolism. Treatment of the rabbits with cholestyramine lowered the circulating LDL cholesterol level by promoting its clearance (120%, p < 0.001) via the receptor pathway. This was associated with a virtual doubling of receptor-mediated incorporation of the lipoprotein into the liver. These results suggest that the drain which cholestyramine induces in the hepatic cholesterol pool promotes LDL receptor activity in this organ and thereby lowers the level of circulating LDL.

Animals↗

PubMed1976

Role of fat maldigestion in pathogenesis of steatorrhea in ileal resection. Fat digestion after two sequential test meals with and without cholestyramine.

To clarify the role of fat maldigestion in the pathogenesis of steatorrhea in patients with ileal resection the total and aqueous phase concentrations of bile acid and fatty acid were characterized in 8 such patients (5 patients with small ileal resection, bile acid diarrhea, and steatorrhea less than 20 g per day; 3 patients with large ileal resection, fatty acid diarrhea, and steatorrhea greater than 20 g per day) as well as 4 healthy control subjects after a morning and an afternoon liquid test meal. The study was then repeated with cholestyramine, 4 g being administered before each meal to induce fat maldigestion. After a conventional test meal, patients with large resections and severe steatorrhea had significantly lower aqueous phase concentrations of bile acids (and fatty acids) than patients with smaller resections or control subjects, explained in part by intraluminal precipitation of about one-half of the bile acids during digestion. When cholestyramine was administered before the meal, aqueous phase bile acid concentrations decreased in all patients, including the normal control subjects; the degree of fat maldigestion induced in the patients with small resections (and the control subjects) became similar to that present after the conventional test meal in the patients with large resections. Because steatorrhea increased little in the patients with small resections when cholestyramine was administered continuously, the data suggest that fat maldigestion per se does not induce severe fat malabsorption in patients with sufficient anatomical reserve, because such patients can absorb fat efficiently by utilizing the distal small intestine. In patients with large ileal resections, severe steatorrhea is explained in part by the combination of fat maldigestion and decreased surface area. It is also speculated that the steatorrhea occurring in patients with small resections and relatively normal fat digestion during two test meals may be explained by impaired fat digestion which occurs during the final meal of the day, which is often the largest meal.

Adult↗

PubMed1978

Oral 25-hydroxyvitain D3 in treatment of osteomalacia associated with ileal resection and cholestyramine therapy.

Severe histological osteomalacia developed in a woman with Crohn's disease 2 years after ileal resection and the start of cholestyramine therapy. Treatment with oral 25-hydroxyvitamin D3, 50 microgram daily, produced marked biochemical, radiological, and histological improvement after 6 months. It is suggested that cholestyramine, by reducing vitamin D absorption, precipitated the rapid development of osteomalacia in this patient. This case report emphasizes the importance of routine vitamin D supplementation in all patients on long term cholestyramine therapy, and indicates that even in patients with small intestinal disease or resection, oral preparations of vitamin D or its metabolities and analogues may be effective.

Administration, Oral↗

PubMed1978

High fiber diet in hyperlipemia. Comparison with cholestyramine treatment in type IIA hyperlipoproteinemia.

Fourteen patients with type IIa hyperlipoproteinemia were treated with a high fiber intake (powdered cellulose or soy hulls or both) for six months. Eight of the patients were treated with 16 g of cholestyramine resin daily without the high fiber intake for an additional six months. The cholesterol intake was comparable in both treatment programs. The mean serum cholesterol levels decreased during both, but the decrease occurred and was more pronounced in all patients treated with cholestyramine. Responsiveness to the high fiber diet was not related to an increased responsiveness to cholestyramine treatment. In most patients the serum triglyceride levels increased, and the fasting plasma glucose level did not change substantially during either treatment program. Both regimens were free of adverse side effects.

Adult↗

PubMed1984

Systemic absorption of oral cholestyramine.

A patient with Clostridium difficile -toxin colitis was treated with oral cholestyramine, but died of other causes 15 days later. At autopsy, the colitis had resolved, but cholestyramine particles were found within the vessels of most body tissues, most prominently in his ulcerated distal esophagus. Clusters of bacteria were found adjacent to some of the cholestyramine particles, suggesting a common portal of entry.

Administration, Oral↗

PubMed1976

Cholestyramine-induced inhibition of salicylazosulfapyridine (sulfasalazine) metabolism by rat intestinal microflora.

The effect of multiple oral administration of the hypocholesterolemic agent cholestyramine (a strongly basic anion-exchange resin) on the metabolism of salicylazosulfapyridine by microflora present in the colon and cecum was assessed in conventional rats by following the time course of salicylazosulfapyridine and its metabolites in the urine and feces. The intestinal metabolism of salicylazosulfapyridine (a single 100 mg/kg oral dose), which involves reduction of the azo linkage by bacterial azo reductases and the liberation of sulfapyridine and 5-aminosalicylic acid (potential active metabolites of the drug), was markedly inhibited by the resin (250 mg/kg oral doses at -2, +2 and +6 hours), resulting in an enhanced fecal excretion of intact salicylazosulfapyridine. The existence of a rank-order correlation between the in vitro binding of salicylazosulfapyridine, sulfapyridine and 5-aminosalicylic acid to the resin and their fecal excretion pattern in resin-treated animals suggests that a direct cholestyramine-salicylazosulfapyridine interaction occurred within the intestinal tract and that in the bound state, the azo bond of the drug was inaccessible to bacterial azo reductases. These findings suggest that chronic oral administration of cholestyramine to patients with ulcerative colitis who are receiving salicylazosulfapyridine could result in a significant reduction in the absorption and metabolism of the drug and hence, in its therapeutic efficacy.

Aminosalicylic Acids↗

PubMed1978

Treatment of antibiotic-associated pseudomembranous colitis with cholestyramine resin.

Pseudomembranous colitis (PMC) is an infrequent but serious complication of oral and intravenous antibiotic therapy. Twelve patients with antibiotic-associated PMC, documented by sigmoidoscopy and rectal biopsy, were treated with cholestyramine resin. The mean time from the institution of therapy to cessation of diarrhea was 2.1 days. The response interval bore no relationship to the time symptoms were present prior to therapy. Complete resolution of sigmoidoscopic and histologic evidence of PMC usually accompanied or followed cessation of diarrhea. Obstipation was reported in 5 of 12 patients as a side effect of cholestyramine treatment. Therapy should be continued for up to five days after cessation of diarrhea to prevent recurrence of active PMC. Cholestyramine resin is shown to be an effective treatment for antibiotic-associated PMC.

Adolescent↗

PubMedDate not supplied

[Cholestyramine in the treatment of refractory diarrhea of the newborn].

Eleven infants with severe protracted diarrhea were studied. All of them were treated with cholestyramine, 2 g/kg/day in three or four doses. Feces became normal in two to four days in ten out of eleven infants. Tolerance to cholestyramine was good. Fat balance was performed in five patients showing steatorrhea in all of them, ranging from 15 to 42%. Reduction in resin doses was followed by normal fat excretion. Three infants died. One of them did not show improvement with cholestyramine therapy and developed Salmonella typhimurium sepsis. The other two, even though they normalized their stools, died because of Salmonella typhimurium and bacteroides sepsis respectively.

Cholestyramine Resin↗

PubMed1982

Effects of neomycin alone and in combination with cholestyramine on serum methyl sterols and conversion of acetate and mevalonate to cholesterol.

Serum free methyl sterols (cholesterol precursors) and the acetate-mevalonate test (the 14C/3H ratio in serum cholesterol after an intravenous injection of a 14C-acetate-3H-mevalonate mixture) were studied in hypercholesterolaemic patients treated with neomycin, cholestyramine or their combination so as to show whether the two tests could detect changes in cholesterol synthesis (measured with faecal steroids). During a 2-week neomycin treatment the ratio increased (+55%) proportionately with the increase in faecal steroids (+29%), the decrease in serum cholesterol (-20%) being negatively correlated with the change in serum methyl sterols. After 1 to 2 years on neomycin, faecal steroids were still high and serum cholesterol low. The ratio had fallen, however, below the initial level, the respective proportionate decrease in methyl sterols being insignificant. In cholestyramine-treated patients a marked increase in cholesterol synthesis (171% increase in faecal steroids) was reflected in a proportionate increase in the ratio (+196%) and serum methyl sterols (+134%). Inclusion of neomycin in the cholestyramine treatment increased faecal steroids (overall increase 206%) and further decreased serum cholesterol (from -25% to -38%) but tended to reduce the ratio and serum methyl sterols. The findings suggest that neomycin activates the pre- and post-mevalonate steps of cholesterol synthesis.

Acetates↗

PubMed1978

Influence of cholestyramine on synthesis of cholesterol and bile acids in germfree rats.

The present investigation describes the influence of partial, pharmacologic interruption of bile acid enterohepatic circulation on cholesterol and bile acid synthesis in germfree rats. Seven rats received a basal, semisynthetic diet and five rats received the basal diet supplemented with 5% cholestyramine. After 6 weeks, feces were collected in one 3- and one 4-day pool for analysis of bile acids and cholesterol. When the sampling period was concluded, the rats were killed and the liver microsomal fractions were isolated. The activities of HMG CoA reductase and 7alpha-hydroxylase were determined. The main fecal bile acids in the untreated rats were cholic acid and beta-muricholic acid. During cholestyramine treatment cholic acid increased from 4.4 +/- 0.7 to 39.5 +/- 5.6 mg/kg body weight/day and beta-muricholic acid from 4.5 +/- 0.6 to 7.7 +/- 0.9 mg/kg body weight/day. Chenodeoxycholic acid became a major bile acid averaging 10.4 +/- 1.6 mg/kg body weight/day. The total amount of bile acids increased about 6-7 times and the percentage of cholic acid increased from 49.4 +/- 2.0 to 68.6 +/- 1.1%. The 7alpha-hydroxylase activity increased 4-5 times. During cholestyramine treatment the fecal excretion of cholesterol was increased from 12.0 +/- 1.4 to 68.0 +/- 5.0 mg/kg body weight/day. The endogenous formation of cholesterol was increased 6 times and the HMG CoA reductase activity was increased about 20 times. In conclusion, germfree rats, like conventional rats, have the ability to increase the endogenous formation of bile acids and cholesterol during interruption of the enterohepatic circulation of bile acids, which is also reflected in a stimulation of the activities of the rate-determining enzymes.

Animals↗

PubMedDate not supplied

[Cholestyramine activating effect on lipoprotein biosynthesis in the rat liver].

The cholestyramine effect on the biosynthesis of lipids and lipoproteins in the rat liver was investigated in order to elucidate the mechanisms of serum triglyceride concentration increase. Cholestyramine feeding produces an increase in the biosynthesis of neutral lipids by the liver and a considerable rise in specific radioactivity of serum free cholesterol and triglycerides. Cholestyramine intensifies the biosynthesis of apoproteins of very low density lipoproteins (VLDL), formation of lipoproteins and their secretion into the blood. Increased secretion of newly synthesized VLDL, the major component of which are triglycerides, leads to hypertriglyceridemia.

Animals↗

PubMed1980

Beneficial effect of cholestyramine in sclerosing cholangitis.

Cholestyramine exerted a beneficial effect on the course of a patient with sclerosing cholangitis associated with ulcerative proctitis. Over a 6.5-yr period, discontinuation of cholestyramine resulted in episodes of RUQ pain and/or appearance of abnormalities in liver tests. Readministration of the resin was followed by disappearance of symptoms and normalization of test resuls. The mechanism of the beneficial effect of cholestyramine was not elucidated.

Adolescent↗

PubMed1979

Use of cholestyramine resin in the treatment of digitoxin toxicity.

Two case reports describing the treatment of digitoxin toxicity with cholestyramine resin are presented. Both female patients were receiving 100 microgram/day of digitoxin when toxicity occurred. In both patients, digitoxin was discontinued and hypokalemia was corrected. In patient 1, lidocaine hydrochloride and phenytoin sodium also were administered. Serum digitoxin levels were decreased from 43 ng/ml to 21.8 ng/ml and from 42 ng/ml to 29 ng/ml in patients 1 and 2, respectively, following administration of three 4-g doses of cholestyramine resin over a one-day period. Previous studies on the treatment of digitoxin intoxication with potassium chloride, phenytoin sodium, lidocaine hydrochloride, digitoxin-specific antibodies, colestipol hydrochloride and cholestyramine resin are discussed. Ion-exchange resins may be valuable adjuncts in the treatment of digitoxin intoxication but further studies of their utility are needed.

Aged↗

PubMed1993

[Therapeutic trials for promotion of faecal excretion of PCDFs by the administration of rice bran fiber and cholestyramine in Yusho patients].

It is well-known that Yusho disease was caused by polychlorinated dibenzofurans (PCDFs), and that 2, 3, 4, 7, 8-Pentachlorodibenzofuran (PnCDF), 1, 2, 3, 4, 7, 8- and 1, 2, 3, 6, 7, 8-Hexachlorodibenzofurans (HxCDFs) still retain in the patient bodies. As patients usually suffer from various chronic syndrome, an effective treatment is extremely needed. In order to assess the rice bran fiber (RBF) and cholestyramine on stimulating faecal excretion of PCDFs, two clinical trials were carried out in 1990 and 1991. In the first trial in 1990, 10 g of RBF (dietary fiber content was 50%) and 4 g of cholestyramine were administered to four Yusho patients three times a day for a week. The stool from patients were collected a week before and during the administration. These were pooled respectively, and then two samples for measurement. In the second trial in 1991, 10 g of dietary fiber rich RBF (refined-RBF, dietary fiber content was 85%) and 4 g of cholestyramine were administered to four Yusho patients three times a day for two weeks. In this trial, three stool samples were obtained from each patient, ie., a week before administration, and first and second week during administration. Level of PCDFs was determined by high resorption GC/MS and the following results were obtained. 1) In the first trial (1990) the faecal excretion of PnCDF and HxCDFs increased at the rates of 42-88% and 7-47%, respectively, in three out of four patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Benzofurans↗