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PubMed1970

Cholesteryl ester turnover in human plasma lipoproteins during cholestyramine and clofibrate therapy.

The effects of cholestyramine and of clofibrate on the turnover rates of individual cholesteryl esters in whole human plasma and in each of the three classes of plasma lipoproteins have been studied. Four hyperlipidemic patients (two under treatment with each of the two drugs) were injected intravenously with cholesterol-(14)C, and serial plasma samples were collected after 3-4 hr, 8 hr, 24 hr, and 4-5 days. The plasma samples were separated into three classes of lipoproteins by ultracentrifugation. The cholesteryl esters and free cholesterol were isolated from each sample, and the specific radioactivity of the free and esterified cholesterol was determined. The specific radioactivity of each individual cholesteryl ester was then determined for each sample, by separately measuring the distribution of cholesterol mass and of radioactivity among four different cholesteryl ester groups, namely the saturated, mono-, di-, and tetra-unsaturated esters. In all subjects the plasma cholesteryl esters were metabolically heterogeneous, and could be divided into three pools corresponding to the three classes of plasma lipoproteins. High density lipoprotein (d > 1.063) cholesteryl esters showed the greatest fractional turnover rate, and low density lipoprotein (d 1.019-1.063) cholesteryl esters showed the smallest fractional turnover rate. In each subject the cholesteryl ester composition of the three classes of plasma lipoprotein was almost identical. Within each lipoprotein, and in whole plasma, all the different individual cholesteryl esters were found to turn over at the same fractional rate. In all respects these results were similar to those previously obtained with normal subjects. The results suggest that neither drug has a strongly selective effect on the turnover of one particular cholesteryl ester, or on the turnover or composition of the cholesteryl esters in one particular plasma lipoprotein.

Aged↗

PubMed1971

Extraction of bile acids from rat feces containing cholestyramine.

The fecal extraction procedure described by Evrard and Janssen (1) was inadequate for the complete extraction of conjugated bile acids from feces containing the bile acid sequestrant, cholestyramine. As judged by gas-liquid chromatographic analysis, substitution of 0.5 n HCl in absolute ethanol for glacial acetic acid allowed for complete recovery (98-104%) of three different conjugated bile salts in the presence of the resin.

Animals↗

PubMed1983

Combined effects of cholestyramine and probucol on regression of atherosclerosis in rhesus monkey aortas.

Adult male rhesus monkeys were fed a high fat, high cholesterol diet for 13 months. During the subsequent 12 months this diet was continued, but the animals were also treated with cholestyramine and/or probucol. The combined drug treatment caused lowering of blood cholesterol without a change in HDL-cholesterol. Regression of plaques was more marked than in animals treated with either drug alone. Animals remained in good health during the treatment period.

Animals↗

PubMed1982

Bile acids and lipids in isolated rat hepatocytes: content, synthesis, and release, as affected by cholestyramine treatment of the donor rats.

Contents of bile acids and lipids, as well as rates of triglyceride synthesis, were determined in isolated hepatocytes from control or cholestyramine-fed rats (denoted below as "control" or "treated" hepatocytes, respectively). During a 3-hr incubation period, total bile acid production was markedly higher in "treated" cells than in "control" cells. With both kinds of cells a marked fall in production rate occurred after the first hour of incubation. Newly produced bile acids appeared in the conjugated form with both kinds of hepatocytes. "Control" cells produced only taurine-conjugated, while "treated" cells made both taurine-conjugated and glycine-conjugated bile acids. However, with exogenous taurine (0.5 mM), the latter cells also produced taurine-conjugated bile acids only. With both kinds of cells, cholic and beta-muricholic acids, but not dihydroxylated bile acids, appeared as newly formed species during the incubation. Addition of dialyzed rat serum to the incubation did not result in a stimulation of bile acid production, with either kind of hepatocytes. "Treated" cells had a slightly higher content of free cholesterol than control cells; contents of other lipids were not different. Fractional release of bile acids and lipids into the medium did not differ between the two kinds of cells. Triglyceride synthesis from added [14C]palmitate (0.5 mM) was 1.8-fold higher in "treated" than in "control" hepatocytes.

Animals↗

PubMed1982

The adsorption of bilirubin from aqueous solution onto solid cholestyramine and polyvinylpyrrolidone.

Shifts in the visible spectrum of aqueous bilirubin (BR) resulting from the addition of soluble polyvinylpyrrolidone (PVP) suggest specific interactions. Hence, isotherms were determined for the adsorption of BR from aqueous solution onto solid, cross-linked PVP and onto cholestyramine (CA) (used as a reference adsorbent) at 0, 10, 20 and 25 degrees C. Although adsorption onto PVP reaches equilibrium values more rapidly than for CA, the latter adsorbent has a larger capacity. Furthermore the isotherms for PVP are independent of temperature while those for CA show an increase in BR adsorbed with an increase in temperature.

Adsorption↗

PubMed1995

HIV-enteropathy and bile acid malabsorption: response to cholestyramine.

Chronic diarrhea and weight loss are common in patients with AIDS. We report on an AIDS patient with chronic diarrhea, steatorrhea, and marked weight loss. A 75SeHCAT test demonstrated that the diarrhea was mainly due to bile acid malabsorption. Therapy with cholestyramine dramatically reduced bowel movements and led to significant reversal of weight loss.

AIDS-Related Opportunistic Infections↗

PubMed1978

Prevalence of gallstones in hyperlipidemia and incidence during treatment with clofibrate and/or cholestyramine.

The present study provides no evidence that the prevalence of gallstones is increased in patients with hyperlipidemia. During the first year of treatment with clofibrate, the incidence of new gallstones appears to increase 8-fold. Cholestyramine, in doses of 16 g per day, does not seem to increase the incidence of stones, either when given alone or with clofibrate. Further studies on the cumulative risk of clofibrate and the long-term effect of clofibrate on biliary lipid composition are necessary to adequately define the risk/benefit ratio of this medication--with or without bile acid sequestrants. It is highly desirable to ascertain whether the concurrent administration of agents such as chenodeoxycholic or ursodeoxycholic acids could beneficially affect bile lipid composition and hence protect against gallstone formation during the initial period of clofibrate treatment.

Cholelithiasis↗

PubMed1995

Clinical trial of a combination of rice bran fiber and cholestyramine for promotion of fecal excretion of retained polychlorinated dibenzofuran and polychlorinated biphenyl in Yu-Cheng patients.

A clinical trial using the combination of rice bran fiber (RBF) and cholestyramine (CHO) was carried out on Yu-Cheng patients in 1993-1994. By the analysis of blood and stool samples collected from the patients before and after (or during in the case of stool), it was verified that the administration of RBF and CHO is effective for excretion of polychlorinated biphenyl (PCB) (p < 0.05) and polychlorinated dibenzofuran (PCDF), especially 2, 3, 4, 7, 8-pentachlorodibenzofuran (p < 0.05). However, the degree of effectiveness varied upon individual patients from 60 to 160% for 2, 3, 4, 7, 8-pentachlorodibenzofuran, from 30 to 110% for 1, 2, 3, 4, 7, 8-hexachlorodibenzofuran and from 50 to 190% for PCB, respectively.

Benzofurans↗

PubMed1994

[Biochemical and functional study of the liver during treatment of familial hyperlipoproteinemia with Mevacor (lovastatin) and Vasosan S (cholestyramine)].

The aim of our study was the biochemical and functional examination of the liver during the therapy of familiar hyperlipoproteinemia by means of MevacorR (lovostatine) in comparison with the treatment by Vasosan S (cholestyramine). We examined 20 patients treated with a daily dose of MevacorR being 20-40 mg and, 18 patients treated with a daily dose of Vasosan S being 16-32 g for the period of 12 weeks. During the therapy the total cholesterol, LDL-cholesterol, HDL-cholesterol, triacylglycerols, hepatic enzymes (AST, ALT, ALP) activity, functional test of the liver, biological half-time of antipyrine (t 1/2 antipyrine) were investigated at the onset and at the end of the study. We discovered that at the end of the treatments by MevacorR and Vasosan S the hypolipidemic effect increased (cholesterol p < 0.001, LDL cholesterol p < 0.001), and there was difference in the effect on HDL-cholesterol and in that on triacylglycerols. During the treatment we discovered that due to both medicaments the liver enzymes activity increased to a different extent. At the beginning of the study the antipyrine biological half-time statistically increased in both investigated groups, namely in comparison with the control group. At the end of the treatments in both groups the antipyrine half-time was prolonged, however not significantly. Prior to long-term therapy by hypolipidemics the authors recommend biochemical and functional examination of the liver. (Tab. 4, Fig. 8, Ref. 7.)

Cholestyramine Resin↗

PubMed1993

[Effects of treatment with rice bran fiber and cholestyramine on clinical and laboratory findings in Yusho patients].

To investigate the therapeutic effects of rice bran fiber (30 g/day) and cholestyramine (12 g/day) for Yusho, clinical signs and symptoms, and laboratory examinations were studied before, during and after 14 day-treatment in four patients with Yusho. The increases of bowel movements and abdominal distention were observed in two of these patients, although no effect was seen in physical findings. In peripheral blood cells, red blood cell counts decreased significantly, from 430 +/- 47 x 10(4)/mm3 (mean +/- SD) to 378 +/- 48 x 10(4)/mm3 (p < 0.01) after therapy. Hemoglobin as well as hematocrit levels were also reduced significantly afer the therapy. However, no significant effect of the treatment was observed in white blood cell counts or platelet counts. In biochemical parameters, a significant depression was observed in total cholesterol levels after the therapy (from 262 +/- 31 mg/dl to 179 +/- 33 mg/dl; p < 0.005). A significant elevations was observed in serum levels of alanine aminotransferase and sodium, while significant depressions were found in serum levels of cholinesterase, total protein, albumin, gamma-globulin, and potassium.

Benzofurans↗

PubMed1977

Influence of isoproterenol and cholestyramine on acute gastric mucosal ulcerogenesis.

One thesis concerning the pathogenesis of "stress ulcer" states that the combination of (1) bile acid-induced H+ "back diffusion" and (2) gastric mucosal ischemia is acutely Hg) to induce ischemia, this thesis was further tested by selectively mitigating either the ischemic or the back diffusion components of the model. Vascularized wedges of proximal canine gastric wall mounted on Lucite chambers were studied. With the mucosa directly visualized, control group A (6 dogs) was subjected sequentially to (1) topical acid test solution alone (ATS), (2) ATS + S, and (3) ATS + S + topical 5 mM Na taurocholate (TC). Study group B (6 dogs): (1) ATS, (2) ATS + S + the beta adrenergic agonist, isoproterenol, 1.5 microng per kg-min infused into the splenic artery, and (3) ATS + S + TC + isoproterenol. Study group C (6 dogs): (1) ATS, (2) ATS + S + the bile acid binding resin, cholestyramine (C), 4 g per liter, and (3) ATS + S + TC + C. During each period the net flux of H+, the electrical potential difference, and the aminopyrine clearance (AC) were determined. Mucosal damage (intramucosal hemorrhage, erosions, and ulcers, graded 0 to 5) was assessed blindly by an independent observer using photographs. The results indicate (1) that, despite H+ back diffusion comparable to ATS + S + TC, intraarterial isoproterenol significantly protects against lesion formation by increasing AC, and (2) that, despite a reduction in AC comparable to ATS + S + TC, topical C significantly protects against lesion formation by preventing excessive back diffusion of H+.

Administration, Topical↗

PubMed1977

Pruritus in sickle cell disease: response to cholestyramine.

Even in the absence of gallstones, the hepatobiliary system should be suspected as a possible cause of pruritus in a patient with sickle cell disease. A case is presented in which a sickle cell patient had severe pruritus relieved by cholestyramine therapy.

Adult↗

PubMed1997

Antibiotic and cholestyramine treatment of chronic diarrhea in HIV-infected children.

BACKGROUND: Chronic diarrhea is a common feature in children infected with human immunodeficiency virus (HIV), and is associated with an increased risk of death in these patients. To describe the effects of an empiric treatment on diarrhea and body weight on HIV-infected pediatric patients. PATIENTS: Eleven vertically HIV-infected children with chronic diarrhea were treated with oral gentamicin, metronidazole and cholestyramine for 3 to 5 days. RESULTS: In children not infected by Cryptosporidium the treatment resulted in a 50% reduction of stool frequency and a 9% increase in body weight. No statistically significant effect was found in children harbouring this parasite. Diarrhea relapsed within 1-2 months in 3/3 children with Cryptosporidium and in 1/8 children without Cryptosporidium (p < 0.05). No untoward side effects from the treatment were observed. CONCLUSIONS: These results suggest that an empiric treatment of this type should be attempted early in HIV-infected children with chronic diarrhea, particularly in those not infected by Cryptosporidium.

Anti-Bacterial Agents↗

PubMed1995

Metabolism of apolipoprotein B in primary moderate hypercholesterolaemia: effects of acipimox and cholestyramine therapy.

The effects of combined therapy with acipimox (1250 mg/day) and cholestyramine (20 g/day) were examined in a group of 7 subjects with primary moderate hypercholesterolaemia (total cholesterol >=7 mmol/L). Radiolabeled VLDL subfraction turnovers were performed at baseline, during acipimox therapy and during combined therapy. Acipimox and combined therapies lowered plasma low density lipoprotein (LDL)-cholesterol by 20% (P<0.001) and 27% (P<0.001) respectively. The marked fall in LDL-cholesterol associated with acipimox therapy, was due to a reduced production rate of LDL (apolipoprotein) apoB. This is shown to be a result of reduced direct LDL apoB production, reduced IDL to LDL transfer consistent with inhibition of hepatic triglyceride lipase, and with a reduction in the overall throughput of VLDL1 apoB. With combined therapy both reduced production and increased catabolism of apoB containing LDL precursors and of LDL itself have to be invoked to explain the fall in plasma LDL-cholesterol.

Adult↗

PubMed1965