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The high-density lipoprotein (HDL) cholesterol level is a strong predictor of cardiovascular events in epidemiologic studies. Until recently, it has been less extensively studied as a therapeutic target. To assess the angiographic and clinical effects of a pharmacologic strategy to increase HDL cholesterol levels. Randomized, double-blind, placebo-controlled trial conducted from 1993 to 1996. Outpatient specialty clinic of a large U.S. military medical center. 143 military retirees younger than 76 years of age with low HDL cholesterol levels and angiographically evident coronary disease. Gemfibrozil, niacin, and cholestyramine or corresponding placebos, with aggressive dietary and lifestyle intervention at baseline. Change from baseline to 30 months and a composite measure of clinical events that included hospitalization for angina, myocardial infarction, transient ischemic attack and stroke, death, and cardiovascular procedures. At baseline, mean (+/-SD) lipid values were as follows: total cholesterol, 5.1 +/- 0.8 mmol/L (196 +/- 31 mg/dL); low-density lipoprotein (LDL) cholesterol, 3.3 +/- 0.7 mmol/L (128 +/- 27 mg/dL); and HDL cholesterol, 0.9 +/- 0.2 mmol/L (34 +/- 6 mg/dL). Compared with placebo, the pharmacologically treated group experienced a 20% (95% CI, 14.8% to 24.3%) decrease in total cholesterol level, a 36% (CI, 28.4% to 43.5%) increase in HDL cholesterol level, a 26% (CI, 19.1% to 33.7%) decrease in LDL cholesterol level, and a 50% (CI, 40.5% to 59.2%) reduction in triglyceride levels. Focal coronary stenosis increased by 1.4% in the placebo group but decreased by 0.8% in the drug group (difference, -2.2 percentage points [CI, -4.2 to -0.1 percentage points]). A composite cardiovascular event end point was reached in 26% of patients in the placebo group and 13% of those in the drug group (difference, 13.7 percentage points [CI, 0.9 to 26.5 percentage points]). Side effects, particularly flushing and gastrointestinal intolerance, were more common in the drug group but rarely led to withdrawal from the study. The study was small and used a composite clinical outcome. Whether improvements in angiographic findings were due to reductions in LDL cholesterol or increases in HDL cholesterol was not established. Flushing may have led to inadvertent unblinding in patients who were randomly assigned to active study drugs. A combination regimen aimed at increasing HDL cholesterol levels improves cholesterol profiles, helps prevent angiographic progression of coronary stenosis, and may prevent cardiovascular events in some people who exercise regularly and eat low-fat diets.

Aim/Background Cholestyramine may improve fecal incontinence, but its use has not been assessed. We report our experience with the use of cholestyramine in the treatment of fecal incontinence. Materials and methods Twenty-one patients (19 female, mean age 65 years) with fecal incontinence (≥1 episode/week) received cholestyramine along with biofeedback therapy (group A). Stool frequency, stool consistency (Bristol scale), number of incontinent episodes, satisfaction with bowel function (VAS), and anorectal physiology were assessed at 3 months and at 1 year after treatment. Data were compared with a matched group of 21 incontinent subjects (19 female, mean age 64 years) who received biofeedback alone (group B). Results At 3 months and at 1 year, group A patients showed decreased stool frequency ( p  < 0.01), stool consistency ( p  = 0.001), and number of incontinent episodes ( p  < 0.04). In contrast, stool frequency ( p  = 0.8) and stool consistency (0.23) were not different from baseline in group B subjects. In both groups, there was improvement in the satisfaction with bowel function ( p  < 0.05), anal sphincter pressures ( p  < 0.05) and ability to retain saline infusion ( p  < 0.05). Mean dose of cholestyramine used was 3.6 g; 13 subjects (62%) required dose titration, and 7 (33%) subjects reported minor side effects. Conclusion Cholestyramine is safe and useful adjunct for the treatment of diarrhea and fecal incontinence. Most patients require small doses, and dose titration is important. The improvement in stool characteristics favors a drug effect, over and above the benefits of biofeedback therapy.

Patients with severe hypercholesterolemia may need greater cholesterol reductions than can beachieved with statin therapy alone. The primary objective of this trial was to compare the efficacy of a combination of rosuvastatin plus cholestyramine with that of rosuvastatin alone for reducing low-density lipoprotein cholesterol (LDL-C) levels after 6 weeks of treatment In this open-label, multicenter, randomized, parallel-group, comparator trial, adult patients withsevere hypercholesterolemia (LDL-C level, 190–400 mg/dL) received rosuvastatin 40 mg/d for 6 weeks after a 6-week dietary lead-in period and were then randomized to 6 weeks of treatment with rosuvastatin 80 mg/d alone or rosuvastatin 80 mg/d plus cholestyramine 16 g/d (8 g BID with meals). Of 153 eligible patients, 147 (83 men, 64 women; mean [SD] age, 54.5 [13.7] years; mean [SD] bodyweight, 81.3 [14.4] kg) received randomized treatment, and 144 had postbaseline measurements and were included in the analysis. The mean (SD) reduction in LDL-C was 522% (13.0%) after treatment with rosuvastatin 40 mg, and the least squares mean (SE) reductions in LDL-C were 56.4% (1.8%) and 60.5% (1.8%) after treatment with rosuvastatin 80 mg alone (n = 69) and rosuvastatin 80 mg plus cholestyramine (n = 75), respectively. No significant differences between treatments were found for these or other lipid measurements. Incremental LDL-C reductions >30% were obtained in 29% (22/75) of patients receiving combination therapy and 4% (3/69) of patients receiving rosuvastatin alone. The combination therapy was less well tolerated, primarily due to gastrointestinal symptoms; otherwise, the treatments were generally well tolerated. In this group of patients with severe hypercholesterolemia, the combination of rosuvastatin80 mg with cholestyramine 16 g/d did not provide a significantly greater efficacy benefit than rosuvastatin alone.

Bile acid sequestrants (BASs), including cholestyramine, colestipol, and colesevelam, are widely used in endocrine and gastrointestinal disorders. However, their long-term safety remains under-characterized. This study leveraged real-world pharmacovigilance data to evaluate underreported and subclass-specific adverse events (AEs) associated with BASs. We analyzed 5,286 AE reports related to BASs from the FDA Adverse Event Reporting System (2004-2024) using four disproportionality methods: Reporting Odds Ratio (ROR), Proportional Reporting Ratio (PRR), Bayesian Confidence Propagation Neural Network (BCPNN), and Multi-item Gamma Poisson Shrinker (MGPS). AE signals were assessed at both the System Organ Class (SOC) and Preferred Term (PT) levels. Time-to-onset (TTO) analysis was also performed. All three BASs showed prominent gastrointestinal AEs. Cholestyramine was notably associated with oropharyngeal irritation (e.g., throat irritation, ROR = 21.89; oropharyngeal discomfort, ROR = 36.53), while colestipol presented mechanical risks such as dysphagia (ROR = 21.51) and choking (ROR = 67.44). Colesevelam exhibited musculoskeletal toxicity, including myalgia (ROR = 4.74) and muscle spasms (ROR = 3.43). Consensus signals across all methods further revealed novel AEs such as dysgeusia, dental abnormalities, gastroesophageal reflux disease, and fecaloma. TTO analysis showed that most AEs occurred within the first month of therapy, with 15-16% persisting beyond 6 months. This large-scale FAERS study updates the safety profiles of BASs, highlighting distinct risk patterns and delayed complications. The findings support personalized monitoring strategies that consider both drug-specific characteristics and temporal AE patterns.

[...] colesevelam has not been extensively studied in combination with thiazolidinediones. Because hypoglycemia is considered a major, if not the main, cause of increased morbidity and mortality in patients with longstanding type 2 diabetes and comorbidities, colesevelam, with its low risk of hypoglycemia, is an ideal choice for antidiabetes therapy.

The post-Coronary Artery Bypass Graft (Post-CABG) trial has shown that aggressive compared to moderate lowering of low-density lipoprotein cholesterol (LDL-C) delayed the progression of obstructive disease in aortocoronary saphenous vein grafts and in the left main coronary artery. Patients had been allocated to high- and low-dose lovastatin therapy for a 4-5 year period. The present study evaluated the effect of LDL-C lowering and the role of cardiovascular risk factors on the progression of arteriosclerosis in the distal abdominal aorta and common iliac arteries. From one of the participating centers of the post-CABG trial, 145 patients who had adequate imaging of the aortoiliac arteries at baseline and follow-up were included. Angiographic outcomes, presumed to reflect progression of arteriosclerosis and obtained from lumen diameter (LD) measurements using quantitative cineangiography, were as follows: significant decrease of the minimum lumen diameter (LD) and increase of the maximum LD, percent lumen stenosis, and percent lumen dilatation. These outcomes were not significantly less frequent in patients randomly allocated to aggressive compared to moderate LDL-C lowering. Of 9 cardiovascular risk factors, only 2 were significantly related to progression of aortoiliac arteriosclerosis. Current smoking predicted both percent lumen stenosis increase and, to a lesser degree, percent lumen dilatation increase (p=0.010 and p=0.055, respectively). Abnormally high body mass index (BMI ≥25 kg/m2) correlated with percent lumen dilatation increase (p=0.006). Aggressive compared to moderate LDL-C lowering did not prevent or delay the progression of aortoiliac arteriosclerosis. Smoking predicted both lumen narrowing and dilatation presumably caused by arteriosclerosis. Abnormally high BMI, reflecting overweight or obesity, was strongly associated with vessel dilatation.

Cholestyramine carries a risk of hyperchloraemic metabolic acidosis. Being cognisant of this drug-induced adverse event may reduce diagnostic delays. Emergency physicians should be alert about this condition, in particular among patients with pre-existing chronic kidney disease, or who are taking spironolactone.