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Plasma cholesterol and lathosterol levels in term infants in the early neonatal period.

Plasma cholesterol concentrations increase after birth. Whether this is due to increased cholesterol synthesis has not been reported. Additionally, it is not known if formulas, which lack cholesterol, result in higher rates of cholesterol synthesis than feeding breast milk. To address this, plasma lathosterol (quantitated by gas chromatography), a potential indicator of cholesterol synthesis, was measured in term infants at birth (cord) and 4 d of age fed either formula or breast milk (n = 6 each), normal adults (n = 6) at the expected nadir and peak of the diurnal rhythm (1700 h and 0830 h), and cholestyramine-treated hypercholesterolemic adults (n = 6). Plasma cholesterol and apo B increased, and apo AI (measured by immunoprecipitation) did not change over the first 4 d of life. The increase in plasma cholesterol was greater in the formula-fed infants compared with breast-fed infants. The plasma lathosterol concentrations (mumol/L) and the lathosterol:cholesterol ratios (10(2) x mmol lathosterol/mol cholesterol) decreased from birth to 4 d of age by 12 and 36%, respectively, in the breast-fed infants and by 20 and 46%, respectively, in formula-fed infants. The infant plasma lathosterol concentrations, however, were not different from normal adult levels [1700 h: 5.50 +/- 1.52 (SD); 0830 h: 6.18 +/- 1.80], but were lower than those of cholestyramine-treated adults (20.48 +/- 13.41). Sterol ratios of infants were higher than those of normal adults (1700 h: 112.5 +/- 26.0; 0830 h: 129.4 +/- 42.2), but not different from those of cholestyramine-treated adults (322.9 +/- 168.4).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Treatment of itching associated with intrahepatic cholestasis of pregnancy.

OBJECTIVE: To review the drug therapy for the treatment of itching associated with intrahepatic cholestasis of pregnancy (ICP). DATA SOURCES: A comprehensive literature search was conducted in MEDLINE (1966-July 2002) using the following MeSH terms: pregnancy, itching, intrahepatic cholestasis, cholestyramine, ursodeoxycholic acid, and phenobarbital. Current Contents (1966-July 2002), International Pharmaceutical Abstracts (1970-June 2002), and Cochrane Database were also searched using those terms. Web of Science search was used to search references found in articles. DATA SYNTHESIS: Eight clinical trials and several observational studies were identified evaluating the safety and efficacy of ursodeoxycholic acid (UDCA) in the treatment of ICP. Although these studies were small and inconsistent, improvement in maternal and fetal morbidity was demonstrated. Observational studies suggest that cholestyramine may be associated with improved maternal morbidity without a documented improvement in fetal outcome. Two observational studies evaluated the efficacy of phenobarbital for ICP treatment. Phenobarbital use was not associated with improved maternal or fetal morbidity/mortality. CONCLUSIONS: Data from large, well-designed, randomized, controlled trials of treatment of ICP are lacking. Data that are available support the use of UDCA as a first-line agent and cholestyramine as a second-line agent for treatment of ICP. There is little evidence to recommend phenobarbital in the treatment of itching associated with that condition.

Adult↗

Recent trends in the prescribing of cholesterol lowering drugs in Australia. A report from the Drug Utilization Subcommittee of the Pharmaceutical Benefits Advisory Committee.

OBJECTIVE: To determine the recent pattern of use of hypolipidaemic drugs in the Australian community. DESIGN: Drug utilisation study employing prescription data collected during the operation of the Australian Pharmaceutical Benefits Scheme (PBS). SETTING: Non-hospital drug use in Australia. PATIENTS: All patients, pensioners and non-pensioners, who received prescriptions for hypolipidaemic agents under the PBS between January 1987 and December 1989. MAIN OUTCOME MEASURES: The total number of prescriptions, average quantity dispensed with each prescription, defined daily doses (DDD) and Australian population figures for pensioners and non-pensioners were used to express the consumption of hypolipidaemic agents as DDD/1000 individuals/day. RESULTS: Between the March quarter 1987 and the December quarter 1989 prescribing of hypolipidaemics for the Australian community increased from 68,120 to 304,760 prescriptions per quarter, which translates to a rise in use from 1.2 to 5.2 DDD/1000 inhabitants/day. This included a rise in the use of clofibrate from 0.6 to 2.6 DDD/1000 inhabitants/day, and of cholestyramine from 0.6 to 1.9 DDD/1000 inhabitants/day. Prescribing of hypolipidaemics for pensioners increased from 29,569 to 123,440 prescriptions per quarter. This translated into a rise in use from 3.7 to 14.8 DDD/1000 pensioners/day. Notable rises were seen for clofibrate, 1.9 to 8.1 DDD/1000 pensioners/day, and cholestyramine, 1.6 to 4.7 DDD/1000 pensioners/day. In comparison published data from the Nordic countries and the United States showed a lower overall use of hypolipidaemics and declining consumption of clofibrate. CONCLUSIONS: The trend in Australia was unusual in that the use of clofibrate increased to a greater extent than that of the resins, cholestyramine and colestipol which are generally preferred for treatment of hypercholesterolaemia. Possible reasons for this include: the better tolerability of clofibrate; its readier availability during the study period; the recommendation by the Pharmaceutical Benefits Advisory Committee that clofibrate was the preferred drug when triglyceride levels were also elevated and the limited availability of newer hypolipidaemic agents.

Aged↗

Effect of combination therapy with lipid-reducing drugs in patients with coronary heart disease and "normal" cholesterol levels. A randomized, placebo-controlled trial. Harvard Atherosclerosis Reversibility Project (HARP) Study Group.

BACKGROUND: Combination drug therapy has been shown to decrease cholesterol levels in hyperlipidemic patients. However, its efficacy has not been well studied in patients previously considered to be normolipidemic, many of whom are now candidates for this therapy. OBJECTIVE: To determine the efficacy and tolerability of multidrug therapy designed to improve low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol levels in patients with coronary heart disease and average lipid levels. DESIGN: Randomized, placebo-controlled, 2.5-year trial comparing patients receiving usual care with patients receiving stepped-care drug therapy. INTERVENTION: Stepped-care therapy (pravastatin, nicotinic acid, cholestyramine, and gemfibrozil) to decrease total cholesterol levels to less than 4.1 mmol/L (160 mg/dL) and the ratio of LDL cholesterol to HDL cholesterol to less than 2.0. SETTING: 2 academic, urban, tertiary care hospitals. PATIENTS: 91 patients (80 men and 11 women) with coronary heart disease, a mean age of 60 years, total cholesterol levels less than 6.4 mmol/L (250 mg/dL) at baseline, and ratios of total cholesterol to HDL cholesterol greater than 4.0 at baseline. MEASUREMENTS: Fasting serum lipoprotein profile, fasting apolipoprotein levels, and frequency of adverse effects. Patients were assessed every 6 weeks during drug titration and every 3 months thereafter. RESULTS: Mean lipid levels at baseline were as follows: total cholesterol, 5.5 mmol/L (214 mg/dL); LDL cholesterol, 3.6 mmol/L (140 mg/dL); HDL cholesterol, 1.1 mmol/L (42 mg/dL); and triglycerides, 1.8 mmol/L (159 mg/dL). With pravastatin, changes in levels from baseline were -22% for total cholesterol, -32% for LDL cholesterol +8% for HDL cholesterol, and -15% for triglycerides (P < 0.001 for all comparisons). With the addition of 1.5 g of nicotinic acid, additional changes were -6% for total cholesterol (P < 0.002). -11% for LDL cholesterol, +8% for HDL cholesterol, and -10% for triglycerides (P < 0.001 for all comparisons). With 2.25 to 3 g of nicotinic acid, these changes were -7% for total cholesterol (P = 0.007), -14% for LDL cholesterol (P < 0.001), +6% for HDL cholesterol (P = 0.02), and -13% for triglycerides (P = 0.03). With cholestyramine, total cholesterol and LDL cholesterol levels were unchanged compared with the previous step; the change in HDL cholesterol level was -8% (P = 0.03); and the change in triglyceride level was +46% (P < 0.001). With gemfibrozil, total cholesterol level was unchanged; the additional change in LDL cholesterol level was +12% (P = 0.09); the change in HDL cholesterol level was +12% (P = 0.03); and the change in triglyceride level was -37% (P < 0.001). Apolipoprotein B levels decreased by 25% overall (P < 0.001); lipoprotein(a) levels did not change significantly. Adverse effects were primarily attributable to nicotinic acid or cholestyramine. In 18 of the 35 patients (50%) whose baseline LDL cholesterol levels were greater than 3.35 mmol/L (130 mg/dL), pravastatin decreased LDL cholesterol levels to 2.6 mmol/L (100 mg/dL) or less by 6 weeks; 70% of patients needed combination therapy to reach this National Cholesterol Education Program goal during the 2.5 years of the study. Adding nicotinic acid to pravastatin produced LDL cholesterol levels of 2.6 mmol/L or less in 15 more of these 35 patients, so that 94% (n = 33) of the patients receiving these two drugs reached this goal. CONCLUSIONS: To reach current goals for LDL cholesterol levels, most normolipidemic patients with coronary heart disease in this study needed combination therapy. Pravastatin with nicotinic acid and pravastatin with gemfibrozil are well-tolerated combinations that can maintain target LDL cholesterol levels, decrease triglyceride levels, and increase HDL cholesterol levels. Adding resin to these combinations produced no further benefit.

Algorithms↗

[Evolution and treatment response in microscopic colitis].

AIM: To study the clinical characteristics, treatment response and evolution in patients with microscopic colitis. MATERIAL AND METHODS: We performed a retrospective analysis of 24 patients (15 with collagenous colitis and 9 with lymphocytic colitis). Clinical and diagnostic features, treatment response and evolution according to the presence of maintenance therapy were evaluated. RESULTS: The mean age of the patients was 59.7 years and most were male. Nine patients took non-steroidal anti-inflammatory drugs (NSAID). No significant association was found with other drugs. Four patients presented associated rheumatological disease. Most patients presented insidious-onset diarrhea without pathological products, which was frequently associated with other symptoms (abdominal pain, bloating, weight loss, asthenia, tenesmus, and incontinence). Seven patients showed a slight increase in globular sedimentation rate. Fat in stools and radiological investigations (transit and opaque enema) were normal in patients who underwent these tests. Endoscopy revealed non-specific alterations in 42% of the patients while results were normal in the remaining patients. One patient showed clinical improvement on withdrawal of NSAIDs and 4 patients improved spontaneously. Clinical response was achieved in 7 of 13 patients treated with antimotility drugs, in 8 of 9 patients treated with salicylates, in 3 treated with oral corticoids, in 1 treated with cholestyramine and in 1 treated with topical budesonide. Nineteen patients required no maintenance therapy, 4 were administered salicylates and 1 was administered cholestyramine. After a mean follow-up of 42 months, evolution was chronic and intermittent in 14 patients and chronic and continuous in 1; 9 patients presented a single episode. No significant differences were found between patients administered maintenance therapy and those who were not or between collagenous colitis and lymphocytic colitis in the parameters analyzed. CONCLUSIONS: Microscopic colitis constitutes a group of diseases characterized by chronic diarrhea, few systemic effects and minimal radiological and/or endoscopic alterations. Evolution is characterized by recurrent episodes, with good response to treatment with cholestyramine, salicylates or corticoids when required.

Adult↗

Atorvastatin plus pravastatin for the treatment of heterozygous familial hypercholesterolaemia--a pilot study.

The most common side-effect of statins, mainly during dose titration, is liver toxicity, In these cases, sufficient control of low density lipoprotein cholesterol (LDL-C) in patients with heterozygous familial hypercholesterolaemia (HFH) becomes problematical. In patients with intolerance to resins as well, especially in the presence of coronary artery disease (CAD), it is practically impossible to reach the LDL-C treatment goal. This study included seven HFH patients with CAD, who presented with alanine amino transferase levels greater than three times the upper normal limit during dose titration of atorvastatin or simvastatin of from 20 mg/day to 40 mg/day. They could not tolerate concomitant cholestyramine administration, and presented with LDL-C levels significantly higher than the treatment goal (100 mg/dl; 2.6 mmol/l). In these patients, a combination of two statins with different pharmacokinetics (20 mg/day of atorvastatin plus 40mg/day of pravastatin) was administered for a mean period of one year. Efficacy was compared with that of monotherapy with each drug alone and with that of 40 mg of atorvastatin in 13 patients, who could also not tolerate resin co-administration, and that of 40 mg/day of atorvastatin plus 12 g of cholestyramine in 30 patients, with similar pretreatment LDL-C levels. No increase in serum transaminases and no symptom or sign of myopathy was recorded during the administration of the combination of the two statins for a mean period of 12 months. The atorvastatin plus pravastatin regimen was more effective than both monotherapies and equally effective with the 40 mg of atorvastatin and the 40 mg of atorvastatin plus 12 g of cholestyramine regimens in reducing LDL-C (59% vs. 57% and 61%, respectively) and triglyceride levels (31% vs. 32% and 28%, respectively), while it also had a better effect on high density lipoprotein cholesterol (13% vs. 7% and 8%). The data suggest that the atorvastatin-pravastatin combination has a highly beneficial effect on all lipid parameters, without causing hepatotoxicity, in HFH patients with CAD who are sensitive to higher doses of statins in monotherapy. These results require confirmation in larger studies.

Analysis of Variance↗

Evaluation of the use of serum lathosterol concentration to assess whole-body cholesterol synthesis in rabbits.

Serum lathosterol concentration in rabbits was assessed as a possible indicator of whole-body cholesterol synthesis. In random-bred New Zealand White (NZW) rabbits fed a control diet or a diet containing either cholesterol, simvastatin, or cholestyramine, neither serum lathosterol concentration nor the serum lathosterol:total cholesterol ratio systematically corresponded with the anticipated rate of cholesterol synthesis. In control rabbits and those fed simvastatin or cholestyramine, whole-body cholesterol synthesis, which was calculated from the sterol balance, was correlated with serum lathosterol concentration when expressed relative to cholesterol in very low, intermediate, and low density lipoproteins (VLDL + IDL + LDL) (r = 0.61; n = 23; P = 0.002). The low correlation coefficient indicates that the predictive value of the lathosterol: (VLDL + IDL + LDL) cholesterol ratio is limited when applied to individual rabbits. Cholesterol and simvastatin feeding reduced the group mean serum lathosterol:(VLDL + IDL + LDL) cholesterol ratio, whereas cholestyramine in the diet raised the group mean ratio in the NZW rabbits. We conclude that the serum lathosterol:(VLDL + IDL + LDL) cholesterol ratio may be an indicator of group mean rates of whole-body cholesterol synthesis in rabbits but may not yield reliable information on individual rabbits. The lathosterol:(VLDL + IDL + LDL) cholesterol ratio predicted that in hyperresponsive inbred rabbits, showing an excessive hypercholesterolemia after cholesterol feeding, baseline whole-body cholesterol synthesis is lower than in hyporesponsive rabbits. Addition of cholesterol to the diet caused a reduction of predicted cholesterol synthesis in hypo- but not in hyper-responsive rabbits.

Animals↗

Immunochemical determination of human cholesterol 7 alpha-hydroxylase.

To produce antibodies for determination of the protein mass of human cholesterol 7 alpha-hydroxylase, a fusion protein was prepared from an in-frame fusion gene containing the cDNA for human cholesterol 7 alpha-hydroxylase near the 3' terminus of the lacZ gene of Escherichia coli. The fusion protein was purified by (NH4)2SO4 fractionation and gel-filtration chromatography on a Sephacryl column. Rabbits were immunized with this fusion protein and antisera were obtained. IgG was prepared by submitting antisera to chromatography on protein-A--Sepharose. Antibodies directed against bacterial proteins including beta-galactosidase were removed by affinity chromatography on a column to which bacterial proteins of E. coli containing beta-galactosidase had been immobilized. Evidence that the antibodies are indeed reactive against human liver cholesterol 7 alpha-hydroxylase was obtained by immunoblot analysis with human cholesterol 7 alpha-hydroxylase expressed in COS cells from the coding region of the human cholesterol 7 alpha-hydroxylase cDNA. The antiserum inhibited the activity of cholesterol 7 alpha-hydroxylase in human liver microsomes by approximately 70%. On immunoblotting of solubilized human liver microsomes, a positive band was obtained at a position corresponding to the protein mass for human cholesterol 7 alpha-hydroxylase. When calibration was performed using the fusion protein, a linear relationship was observed between the density and the amount of protein. Proportionality was also observed between the density and the amount of protein for microsomes of COS cells transfected with the coding region of the human cholesterol 7 alpha-hydroxylase cDNA. Liver microsomes from patients treated with cholestyramine (n = 3) were shown to contain levels of cholesterol 7 alpha-hydroxylase protein approximately twofold higher than those of liver microsomes from untreated patients (n = 6; P < 0.02), whereas cholesterol 7 alpha-hydroxylase activity was approximately six-fold higher in liver microsomes from the cholestyramine-treated patients than in the corresponding preparations from the untreated patients (P < 0.02). The higher activities observed in cholestyramine-treated patients, therefore, cannot be explained only by an increased amount of protein, suggesting a posttranslational mechanism to increase the activity of human cholesterol 7 alpha-hydroxylase in addition to the transcriptional control.

Adult↗

Multiple-dose lorazepam kinetics: shuttling of lorazepam glucuronide between the circulation and the gut during day- and night-time dosing intervals in response to feeding.

Lorazepam kinetics were examined in seven healthy males age 18 to 30 years after single- and multiple-dose lorazepam administration and in the presence and absence of neomycin and cholestyramine to block the enterohepatic circulation of the drug. Methods used a simultaneous i.v./p.o. dosing regimen with provision to measure lorazepam clearance during day- and night-time dosing intervals. The day-time steady-state clearance of free lorazepam measured 7.55 +/- 1.95 ml/min/kg (mean +/- S.D.) and was identical to that observed after single-dose administration (7.68 +/- 3.19 ml/min/kg). Neomycin and cholestyramine increased lorazepam clearances 5 to 45% (P < or = .05) as would be expected for interruption of an enterohepatic circulation and in keeping with previous observations under nonsteady-state conditions. Lorazepam clearances were the same during the day as during the night, except in the presence of neomycin and cholestyramine, where night-time clearances were significantly greater (10.16 +/- 3.52 vs. 8.77 +/- 2.43 ml/min/kg, P < or = .05). Urinary recoveries of lorazepam glucuronide, on the other hand, were greater during the day than during the night (114 +/- 11 vs. 77 +/- 15%, P < or = .05) and in all cases were greater than 100% of the administered dose for that interval. Thus, there is a diurnal variation in lorazepam elimination consistent with a fasting-induced increase in hepatic glucuronidation during the night. This, combined with the relative inactivity of the gut during this period, serves to trap the glucuronide and delay its transfer back to the systemic circulation and urine.

Administration, Oral↗

The patient at risk: who should we be treating?

Both the European Atherosclerosis Society and the US National Cholesterol Education Program have issued revised guidelines for the prevention of coronary heart disease (CHD), based on a multitude of recent epidemiological and angiographic studies. Both authorities agree that a target plasma low-density lipoprotein cholesterol (LDL-C) level is the single most important parameter, this target level being different for primary and secondary prevention. The introduction of statins for the treatment of hypercholesterolaemia provides an important tool to enable target LDL-C levels to be reached in most cases of primary prevention. For secondary prevention, however, the target LDL-C levels--2.6 mmol/l (100 mg/dl)--may be achieved in only a fraction of cases. Others may require the concomitant administration of other cholesterol-lowering drugs, such as bile-acid sequestrants (resins) and/or derivatives of fibric acid (fibrates). The use of statin-fibrate combinations has been discouraged since the report by the US Food and Drug Administration of 12 sporadic cases of myositis or rhabdomyolysis. During the past 7 years, however, 21 clinical trials have examined the efficacy and safety of statin-fibrate combinations in a total of 486 patients with a variety of dyslipidaemias. Overall, the combinations were proven to be effective and safe, and the incidence of abnormalities in liver function tests and levels of creatine kinase (CK) was low. A double-blind study has been carried out at the Hadassah University Hospital to examine the efficacy and safety of fluvastatin when combined with either cholestyramine (group 1) or bezafibrate (group 2) for the treatment of 38 patients with heterozygous familial hypercholesterolaemia (FH). Patients in group 2 showed a reduction in plasma LDL-C levels of 35% and in LDL-C to high-density lipoprotein cholesterol (HDL-C) ratio of 45% compared with 32% and 38% respectively in group 1. Both cholestyramine and bezafibrate produced an additional benefit of a 13% reduction in LDL-C levels in comparison with fluvastatin as monotherapy. An open-label ongoing study on a larger cohort of FH patients reveals that a decrease in plasma LDL-C levels of up to 38.5% may be achieved with a combination of fluvastatin 80 mg/day and bezafibrate 400 mg/day. In both studies, biochemical safety analyses revealed no notable abnormalities in liver function tests or levels of CK. It was concluded that fluvastatin-bezafibrate is a very effective synergistic therapy for heterozygous FH and is superior to a fluvastatin-cholestyramine combination.

Aged↗

Regression of atherosclerotic plaques in rhesus monkeys. Angiographic, morphologic, and angiochemical changes.

On a diet with high levels of cholesterol and sucrose, a beta-lipoproteinemia developed in rhesus monkeys that is similar to type II human hyperlipidemia. Lesion regression appeared in response to drastic lowering of serum cholesterol (SC) levels. This experiment analyzed angiochemical responses on the addition of a bile-acid sequestrant to continued atherogenic feeding, which resulted in ranges of moderate cholesterolemia that mimick those that occur in man. After two years of atherogenic diet, fatty fibrous plaques were demonstrated in ten monkeys; then cholestyramine resin, 1.5 g/100 g of the atherosclerotic diet, was added to the food of eight monkeys, whereas two served as controls during a 12-month regression period. Six adult control monkeys that did not receive the atherosclerotic diet were also killed. Seven experimental animals overall showed plaque regression when SC level fell from 400 +/- 130 to 237 +/- 74 mg/dL; one animal showed angiographic combinations of progression and regression. Angiochemical evaluation demonstrated discordant data with instances of decreased plaque cholesterol content and increased levels of collagen. On the average, plaque regression and final composition were related to absolute levels of SC reduction induced by cholestyramine. Regression required that the threshold levels of cholesterol be below 200 mg/dL. Plaques regressed mainly by lipid absorption; in this experiment and, in particular, arterial segments, collagen content sometimes increased.

Animals↗

Lipoprotein(a) levels and risk of coronary heart disease in men. The lipid Research Clinics Coronary Primary Prevention Trial.

OBJECTIVE: To examine the relationship between elevated levels of lipoprotein(a) [Lp(a)] and coronary heart disease (CHD) risk in a prospective study. DESIGN: Nested case-control study. The cohort consisted of participants in the Lipid Research Clinics Coronary Primary Prevention Trial. SETTING: Lipid research clinics. PARTICIPANTS: The Lipid Research Clinics Coronary Primary Prevention Trial participants (n = 3806) were men, aged 35 to 59 years, with plasma cholesterol levels of 6.85 mmol/L (265 mg/dL) or greater, low-density lipoprotein cholesterol levels of 4.91 mmol/L (190 mg/dL) or greater, and triglyceride levels less than 3.39 mmol/L. Subjects were randomly assigned to either cholestyramine or placebo treatment. The Lp(a) levels were measured in plasma samples obtained prior to randomization in 233 cases (participants who developed CHD in the course of the study) and 390 matched CHD-free controls. A total of 96.95% of the subjects were white, 2.25% were black, and 0.80% were of other race. MAIN OUTCOME MEASURE: Coronary heart disease (either fatal or nonfatal) events during a follow-up of 7 to 10 years. RESULTS: The Lp(a) levels were significantly higher (21%) in cases than in controls (23.7 mg/dL [0.59 mmol/L] and 19.5 mg/dL [0.49 mmol/L], respectively; P < .02). This difference was still statistically significant (P < .01) after controlling for age, body mass index, cigarette smoking, blood pressure, low-density lipoprotein cholesterol level, and high-density lipoprotein cholesterol level. When subjects were divided by treatment, both cholestyramine-treated and placebo-treated CHD subjects had Lp(a) levels 20% to 22% greater than their matched controls. However, possibly because of smaller sample sizes, these differences were no longer statistically significant. CONCLUSIONS: Our data are consistent with the concept that an elevated Lp(a) level is an independent risk factor for CHD in hypercholesterolemic white men.

Adult↗

The cause and treatment of postvagotomy diarrhoea.

Six patients with watery postvagotomy diarrhoea and 4 patients with intractable diabetic diarrhoea were treated with cholestyramine. The diarrhoea responded completely to therapy, during which the stool content of water, sodium, postassium and magnesium fell. Two of the patients, while receiving cholestyramine, had a rise in faecal fat, but this was not accompanied by diarrhoea, the stools being well formed. Evidence is presented which suggests that the mechanism of diarrhoea is similar in both disorders and is due to division or neuropathy of the hepatic fibres of the vagus nerve. This results is distension of the gallbladder, contraction of which expels increased quantities of bile salts, which swamp the reabsorptive capacity of the small intestine and induce diarrhoea by direct action on the colon. If this theory is valid, cholecystectomy, by preventing large quantities of concentrated bile salts from suddenly entering the gut, may result in improvement of postvagotomy and diabetic diarrhoea.

Adult↗

Excretion of chlordecone by the gastrointestinal tract: evidence for a nonbiliary mechanism.

Workers exposed to chlordecone (Kepone), a toxic organochlorine pesticide, excreted larger amounts of chlordecone in bile than in stool, suggesting that it may undergo enterohepatic recirculation. We found in a single subject that equal amounts of chlordecone and of its reduced metabolite, chlordecone alcohol, were excreted in bile at a rate four times as great as in stool. When biliary contents were diverted from the intestine through a T tube, fecal excretion of chlordecone alcohol was abolished, presumably due to interruption of its passage via bile to intestine. This change was not accompanied by disappearance of chlordecone from the stool. The amount of chlordecone in stool when bile was diverted was increased six- to tenfold over that when diverted bile was continuously infused into the duodenum. Analogous experiments with [14C]-chlordecone-treated rats in which bile flow was exteriorized through a plastic cannula showed that the excretion of radioactivity in feces was in the same range when bile was reinfused in the duodenum or was totally diverted. Moreover, in rats with bile diverted, cholestyramine, an anion-exchange resin which binds chlordecone in vitro, doubled the excretion of radioactivity in stool. A similar effect was observed in intact animals. We conclude that chlordecone enters the intestinal lumen from a nonbiliary source, probably the gut, and that net excretion of chlordecone from this source can be augmented by cholestyramine.

Bile↗

Regulation of fecal bile acid excretion in male golden Syrian hamsters fed a cereal-based diet with and without added cholesterol.

The objective of these studies was to investigate the comparative physiology and regulation of bile acid metabolism in the male Golden Syrian hamster by measuring the rate of fecal bile acid excretion and bile acid pool size in animals fed a cereal-based diet either alone, or with added cholesterol or cholestyramine. In group-housed hamsters fed only the plain diet fecal bile acid excretion in animals at 6, 10, and 15 weeks of age averaged 11.0, 8.0, and 6.9 mumol/d per 100 g body weight (bw), respectively. Pool size, measured by subtracting from the total amount of bile acid washed out over 12 hours of biliary diversion the amount of bile acid excreted in the stools over the same period, equalled 17.8 mumol/100 g bw in 15-week-old hamsters fed the plain diet. Hence, under basal conditions, these animals turned over about 38% of their bile acid pool daily. In hamsters fed a diet with 3% cholestyramine for 18 days, fecal bile acid excretion averaged 20.6 mumol/d per 100 g bw, and the pool size contracted to 5.8 mumol/100 g bw. In matching animals fed a diet containing 0.12% cholesterol for 30 days, hepatic cholesterol levels increased from 1.9 +/- 0.1 to 12.6 +/- 0.7 mg/g, fecal bile acid excretion increased marginally from 5.8 to 8.0 mumol/day per 100 g bw, while pool size was unchanged (16.6 mumol/100 g bw). When the cholesterol content of the diet was raised to 1.0%, hepatic cholesterol levels reached 66.5 +/- 2.6 mg/g, but bile acid excretion remained at 8 mumol/d per 100 g bw. These data define some of the basal features of bile acid metabolism in the hamster, and substantiate the view that the marked cholesterolemic response of this species may relate partly to a limited ability to convert dietary cholesterol to bile acid.

Animals↗

Regulation of early cholesterol biosynthesis in rat liver: effects of sterols, bile acids, lovastatin, and BM 15.766 on 3-hydroxy-3-methylglutaryl coenzyme A synthase and acetoacetyl coenzyme A thiolase activities.

Cytosolic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase catalyzes the formation of HMG-CoA, the substrate for the rate-controlling enzyme in the cholesterol biosynthetic pathway. To explore the regulation in liver, we developed a new, accurate, and reliable reversed-phase ion-pair chromatographic assay that uses nonradioactive substrates and n-propionyl coenzyme A as an internal recovery standard. The hepatic activities were measured in rats treated with cholesterol, sitosterol, cholic acid, deoxycholic acid, ursodeoxycholic acid, cholestyramine, bile fistula, lovastatin, and BM 15.766, an inhibitor of 7-dehydrocholesterol delta7-reductase, and were compared with microsomal HMG-CoA reductase and cytosolic acetoacetyl coenzyme A (AcAc-CoA) thiolase activities. HMG-CoA synthase activity was effectively suppressed in synchrony with HMG-CoA reductase activity by treatments with cholesterol (-41%, P < .05), cholic acid (-72%, P < .005), and deoxycholic acid (-62%, P < .05). However, ursodeoxycholic acid increased activity 84% (P < .05) and intravenous sitosterol did not change activity. AcAc-CoA thiolase activities also paralleled HMG-CoA reductase and HMG-CoA synthase activities, but differences were not statistically significant. In contrast to inhibition, up-regulation of hepatic HMG-CoA synthase activities by cholestyramine, bile fistula, and lovastatin was much less than HMG-CoA reductase activities. In addition, BM 15.766 did not stimulate synthase activity, whereas lovastatin increased activity 2.4-fold. Thus, hepatic HMG-CoA synthase activity was regulated coordinately with HMG-CoA reductase, and responded more forcefully to regulatory stimuli than acetoacetyl-CoA thiolase activity but usually less than HMG-CoA reductase.

Acetyl-CoA C-Acetyltransferase↗

Drug therapy of inflammatory bowel disease.

Although the etiology of inflammatory bowel disease is unknown and specific therapy is unavailable, enough information on existing empiric agents is available to allow rational therapy. These agents include sulfasalazine, steroids, immunosuppressive drugs, metronidazole and cholestyramine. Sulfasalazine is a two-part molecule that depends on bacterial cleavage in the colon to deliver locally acting 5-aminosalicylate, whose mechanism of action may relate to inhibition of prostaglandin synthesis. The other half of the molecule, sulfapyridine, is responsible for most of the side effects of the drug. While the efficacy of sulfasalazine in the treatment and prevention of attacks of ulcerative colitis is well established, its use in Crohn's disease appears to be limited to patients with active colitis and ileo-colitis. Sulfasalazine is of major benefit in preventing relapses in patients with ulcerative colitis in remission. New formulations of 5-aminosalicylate may allow delivery of the apparently active moiety to the small bowel and colon without concomitant sulfapyridine toxicity. Corticosteroids are highly effective in acute attacks of ulcerative colitis and Crohn's ileitis and ileo-colitis; the mechanism of antiinflammatory action remains speculative. However, maintenance therapy with steroids is ineffective in preventing relapses or recurrent attacks of either ulcerative colitis or Crohn's disease. Steroid enemas allow topical administration to patients with distal colitis and proctitis with few systemic side effects. In children with growth failure associated with active Crohn's disease, amelioration by steroid therapy may actually restore normal growth. Immunosuppressive agents such as azathioprine and 6-mercaptopurine are of little value in active Crohn's disease when administered alone; however, in combination with other agents they may help diminish steroid dose, close fistulae and prevent relapse. Their mode of action likely depends on long-term cytostatic effects on immune effector cells. Concern for leukopenia and the development of late malignancy has limited their use to patients not responding to other therapies. Metronidazole, an antimicrobial agent that is effective against anaerobes, has recently been shown useful in Crohn's disease involving the colon and perianal area. Its mechanism of action is uncertain, but may be related to its antibacterial actions on anaerobes. Cholestyramine can be successfully used to control bile salt-induced diarrhea in Crohn's patients with terminal ileal resections. Effective drug therapy of inflammatory bowel disease is only part of a total program of management including reassurance, frequent explanation, well-timed use of surgery, and an understanding physician.

Adjuvants, Immunologic↗

Comparative squalene synthase gene expression in mouse liver and testis.

RNA from various mouse organs was analyzed by Northern hybridization to determine the response of squalene synthase (SQS) mRNA to dietary cholesterol, or lovastatin and cholestyramine, administration. Two size-classes of highly abundant mouse SQS (mSQS) mRNAs of approximately 1.9 and 2.0 kb were found in testis. These transcripts were unresponsive to sterol regulation. A single size-class of liver mSQS mRNA of approximately 1.9 kb was sterol-regulated. Studies using primer extension and 5' rapid amplification of cDNA ends (RACE) indicated that the size differences in liver and testis mSQS transcripts were due to variations in the lengths of the 5' untranslated regions (UTRs). The longest testis 5' UTR extended approximately 106 nt 5' of the primary transcription initiation site in liver of mice fed lovastatin and cholestyramine. These results suggest that tissue-specific promoter elements control the transcriptional regulation of the promoters for the mSQS gene in liver and testis.

5' Untranslated Regions↗