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Measurements of plasma prednisolone concentrations in two patients who received orally 37.5 and 75 mg of the drug respectively showed no differences when 8 g of cholestyramine was given with the corticosteroid. Thus, no influence of cholestyramine on the bioavailability of orally administered prednisolone could be demonstrated.
Two patients with diarrhea and pseudomembranous colitis associated with lincomycin hydrochloride monohydrate and clindamycin phosphate therapy were treated with cholestyramine resin, with prompt remission of symptoms.
The binding of bile salts to cholestyramine was studied under varying conditions of pH and added electrolyte. The taurine-conjugated bile salts were strongly absorbed by the anion-exchange resin at low pH and in the presence of chloride anions. Glycocholic acid binding was very weak at low pH but increased strongly with increasing pH. The presence of chloride ions strongly decreased the amount of glycocholate bound by the anion-exchange resin.
The intrinsic factor-mediated binding of cyanocobalamin to cholestyramine was studied in vitro under varying conditions of pH, added electrolyte, and bile salt. The intrinsic factor-cyanocobalamin complex was adsorbed strongly by the resin at pH 3 in the presence of neutral salt and low concentrations of glycocholic acid. An increase in glycocholic acid concentration as well as neutral pH decreased the observed binding, although significant amounts of cyanocobalamin-intrinsic factor complex remained bound after incubation at pH 6.8. Cyanocobalamin alone was not adsorbed by the resin.
The effects of three compounds known to have hypocholesterolemic activity in several species were investigated on the rat prostate and the hormone-dependent R-3327 rat prostatic adenocarcinoma. Cholestyramine, colestipol, and ADR-132 are bile acid-sequestering anion exchange resins which were fed to separate groups of adult male Copenhagen X Fischer (F1) hybrid rats in doses of 0.25%, 1.00%, and 2.00% of diet. The results indicate that serum cholesterol levels in tumor-bearing rats and controls fed these compounds for 29 days were not reduced. The body and organ weights as well as the histological features of the prostate gland, seminal vesicles, and the R-3327 tumor were unaffected by these agents.
It was recently reported that both cholesterol 7 alpha-hydroxylase CYP7 and sterol 27-hydroxylase CYP27 are subject to negative feedback control by bile acids in isolated rat hepatocytes and rat liver (Twisk et al., (1995) Biochem. J. 305, 505-511; Vlahcevic et al. XIII International Bile Acid Meeting, September 30-October 2, 1994, Abstract 17). In the present work a series of experiments was performed to study whether there is a coordinate regulation of CYP7 and CYP27 also in rabbit liver. Treatments of rabbits with cholic acid or cholestyramine resulted in marked suppression and induction, respectively, of CYP7 mRNA. In contrast, there were no significant effects on the CYP27 mRNA expression, amount of CYP27 protein or mitochondrial 27-hydroxylase activity. Thus, there is an apparent difference between rat and rabbit with respect to regulation of CYP27 by bile acids. It is concluded that, in rabbit, there is little or no coordinate regulation of CYP7 and CYP27 at a transcriptional level, and that CYP27 is not subject to a negative feedback control by bile acids neither at a transcriptional nor at a posttranscriptional level.
The hypocholesterolemic cation resins, cholestyramine and colestipol, have variable effects on the absorption parameters of a number of lipophillic, anion drugs. Because of the unpredictable nature of this interaction, we have assessed in human volunteers the effect of these resins on the rate and total absorption of phenytoin. Our results indicate that these resins do not affect the absorption parameters of phenytoin and that special care does not have to be exercised when these agents are co-administered.
Hepatic and serum phytosterol concentrations were compared in the rat under basal conditions and during activated cholesterol and bile acid production due to squalene and cholestyramine feeding. Both treatments consistently decreased hepatic and serum levels of sitosterol and campesterol and, unlike esterified cholesterol, esterified plant sterols were not increased in liver during squalene feeding. Serum levels of phytosterols were decreased quite proportionately to those in the liver. The hepatic levels of sitosterol and campesterol closely correlated with each other, but not with cholesterol levels. The percentage esterification of both phytosterols was lower than that of cholesterol. The results indicate that activation of hepatic sterol production leads to depletion of hepatic plant sterols. It is suggested that poor esterification of plant sterols may contribute to this decrease.
Rabbits were fed diets enriched with cholestanol or cholesterol (3.5 g/wk) for 4-12 weeks. During cholestanol feeding, the concentration of cholestanol in blood serum, liver, heart and aorta increased 15-30 times. In serum and liver, the concentration of cholesterol also increased. Cholestanol-fed rabbits developed inflammatory changes in the liver, with proliferation of small bile ducts. Liver tests were only slightly abnormal. Morphological atherosclerosis of the aorta was only occasionally seen in rabbits receiving cholestanol for eight weeks or less. During cholesterol feeding, the amounts of cholesterol in different tissues increased dramatically, most in the aorta. Morphological atherosclerosis in the aorta was found in all rabbits fed cholesterol-enriched diets for more than four weeks. Brain cholestanol was doubled in rabbits fed cholestanol for eight weeks, whereas brain sterols did not change significantly during cholesterol feeding. After an additional regression period with cholestyramine for eight weeks, the increased content of cholestanol in the brain was unchanged in cholestanol-fed rabbits. These observations are discussed in relation to the cholestanolosis of the brain that develops in the rare inherited human disease cerebrotendinous xanthomatosis.
Cholesteryl ester hydrolase (CEH), triacylglycerol lipase (TGL) and retinyl palmitate hydrolase (RPH) were measured in 104,000 x g supernatants from rat liver under optimal conditions for measurement of cytosolic CEH. Similar levels of hydrolytic activity were seen with oil droplet dispersions of cholesteryl oleate, trioleoylglycerol and retinyl palmitate. No cytosolic TGL activity was seen with substrate presented in the triton-albumin emulsion used for measurement of lipoprotein lipase-like TGL associated with hepatic plasma membrane. Cytosolic CEH, TGL and RPH were differentially partially purified by both ammonium sulfate precipitation and anion exchange fast protein liquid chromatography (FPLC). Of the tree activities, only CEH was stimulated by cholestyramine feeding and by activators of protein kinases A and C. All three activities were inhibited by alkaline phosphatase treatment, although to different degrees. It is concluded that these activities are catalyzed by at least three differentially regulated enzymes with a high degree of specificity for their respective substrates.
Severe perianal skin inflammation in six patients, following continent reservoir operation and ileoanal anastomosis, resistant to ordinary therapy, was treated with cholestyramine ointment twice a day. Cure was achieved within ten days.
The aim of this study was to examine whether tauroursodeoxycholate (TUDC) and cholestyramine resin (CR) enhance biliary carcinogenesis in the hamster model. A cholecystoduodenostomy with dissection of the extrahepatic bile duct on the distal end of the common duct was performed on Syrian hamsters. The hamsters were then divided randomly into 3 groups: control group, TUDC-treated group, and CR-treated group. All animals received N-nitrosobis(2-oxopropyl)amine (BOP) to initiate pancreaticobiliary cancer. The experiment was terminated at week 16 and the number of neoplastic lesions was counted microscopically. In the TUDC group, the intrahepatic biliary carcinogenesis was more accelerated than that observed in the control group, but no promoting effect was seen in the pancreas, gallbladder, or extrahepatic bile duct. In the CR group, both the intrahepatic biliary and the gallbladder carcinogenesis were inhibited compared with that observed in the control group and the TUDC group. TUDC enhanced the intrahepatic bile duct carcinogenesis, whereas CR inhibited both the intrahepatic bile duct and the gallbladder carcinoma. Bile acids were suggested to promote biliary carcinoma in the hamster model.
INTRODUCTION: To investigate the efficacy of treatment with diclofenac-cholestyramine on postoperative pain and functional outcome after total hip arthroplasty, a randomised double-blind study was conducted. MATERIALS AND METHODS: A total of 245 patients received postoperative treatment with 75 mg or 150 mg diclofenac p.o. daily for 14 days. RESULTS: Patients who received 75 mg diclofenac per day needed paracetamol as an additional analgesic significantly more often (p=0.0162) than patients who were treated with 150 mg diclofenac daily (75 mg twice a day). The incidence of adverse gastrointestinal events was significantly lower in the group receiving 75 mg diclofenac daily than in the group receiving the higher dose (23.1% vs 37.1%; p=0.025). Six months after the operation, no differences were observed between the two groups with regard to pain or functionality measured in terms of overall mobility of the hip. No patient of either group developed clinically relevant heterotopic ossifications. CONCLUSION: Treatment with a dose of 75 mg diclofenac once daily-if necessary with the additional use of paracetamol-is a favourable option for the postoperative care of THA.
Serum levels of 7 alpha-hydroxycholesterol (7 alpha (OH)C) were found to increase considerably in hypercholesterolemic patients treated with cholestyramine. After 3-5 days, the normal level, which is in the range of 0.04 mg/l, rose to 1 mg/l. When the treatment was stopped it decreased rapidly with a half-life analogous to that of LDLs. This phenomenon was also observed in non-hypercholesterolemic humans. More than 75% of 7 alpha (OH)C is carried in blood by the LDLs.
Twelve subjects with primary type IIA hyperlipoproteinaemia were treated with cholestyramine under metabolic ward conditions in order to study the timing of effects of different serum lipoprotein classes. After 1 day's treatment changes occurred in all 3 classes, i.e., very low (VLDL), low (LDL) and high (HDL) density lipoprotein classes. VLDL increased abruptly and remained constant during treatment. The ratio of cholesterol/triglycerides decreased suggesting the formation of larger particles. LDL cholesterol decreased continuously suggesting a different mechanism behind this effect than that on VLDL. LDL triglyceride remained constant indicating a relative increase of LDL1. HDL cholesterol decreased while HDL triglycerides increased. All changes made the lipoprotein pattern more "type IV-like". The findings were in agreement with an increased formation of VLDL and an increased flux of lipoprotein through the cascade VLDL-IDL-LDL1-LDL2.
The effect of 3 months' treatment with cholestyramine on lipoprotein lipids was investigated in 12 patients. VLDL, LDL and HDL were separated by preparative ultracentrifugation. There was a significant decrease of serum cholesterol and phospholipids and an increase of serum triglycerides. All the VLDL-lipids increased by nearly 30%. The LDL-lipids decreased with a tendency for normalisation of their atypical lipid composition. The small but significant alterations of HDL triglycerides and cholesterol are correlated with the corresponding alterations of the other lipoproteins; the HDL-phospholipids were unchanged. The LDL/HDL-lipid ratios were decreased but not normalised. The 30% decrease of LDL-cholesterol is negatively correlated with an increase in all the VLDL-lipids.
Timed pregnant (8 days) Sprague-Dawley rats were fed ground stock diet (CON) or ground stock diet with 4% cholestyramine (CTR) until day 20 of gestation. Animals in both groups gained weight equally well during the study period (CON (n = 7), 308 +/- 7 g; CTR (n = 6), 315 +/- 7 g, mean +/- SEM). At the end of the study period, plasma cholesterol in the CTR group was significantly greater than that in the control group (CON n = 7, 91 +/- 4 mg/dl; CTR (n = 6), 108 +/- 5 mg/dl, P less than 0.05). The fecal excretion of both neutral steroids and bile acids, studied for 3 days between days 15 and 18 of gestation, was significantly enhanced by CTR treatment. (Neutral steroids: CON, 3.9 +/- 0.3; CTR, 10.4 +/- 0.3, P less than 0.05. Bile acids: CON, 7.6 +/- 0.4; CTR, 25.8 +/- 1.7, P less than 0.05, mg/100 g body wt/day). Bile acid pool size, measured at day 20 of gestation, however, was not significantly different. Consistent with these results was the finding that hepatic cholesterol 7 alpha-hydroxylase activity (the rate-limiting enzyme of bile acid biosynthesis) measured at day 20 of gestation was significantly enhanced by CTR treatment (CON (n = 4), 14.7 +/- 1.7; CTR (n = 4), 34.8 +/- 3.3, pmoles/mg/min, P less than 0.05). The atypical finding of hypercholesterolemia, despite the CTR-induced enhanced turnover of cholesterol, may be due to changes in the homeostatic mechanisms of cholesterol and bile acid metabolism during pregnancy.
Groups of 10 female Wistar rats (aged 4 weeks) were fed for 29 days either a low-cholesterol commercial diet, a commercial diet containing 2% (w/w) cholesterol, 0.5% cholate and 5% olive oil or a diet containing 2% cholestyramine. The rats were then fed the low-cholesterol commercial diet for the next 91 days and the high-cholesterol diet for another 29 days. There was no significant difference between the groups in the increase of cholesterol in serum and liver during the last period of cholesterol feeding. A fourth group of 10 animals was fed the diet containing cholesterol and cholate during the entire experimental period of 149 days. By the end of the experiment serum cholesterol in these animals was lower and liver cholesterol was higher than in the 3 groups fed the high-cholesterol diet during days 120-149 of the experiment. This study does not present evidence for imprinting effects of early diet manipulation on the later cholesterolemic response to a high cholesterol diet.