Colestipol
Niacin
Resins, Plant
Flammable, amorphous, vegetable products of secretion or disintegration, usually formed in special cavities of plants. They are generally insoluble in water and soluble in alcohol, carbon tetrachloride, ether, or volatile oils. They are fusible and have a conchoidal fracture. They are the oxidation or polymerization products of the terpenes, and are mixtures of aromatic acids and esters. Most are soft and sticky, but harden after exposure to cold. (From Grant & Hackh's Chemical Dictionary, 5th ed & Dorland, 28th ed)
Lovastatin
A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver.
Hyperlipoproteinemia Type II
Hypolipidemic Agents
Fatigue Syndrome, Chronic
A syndrome characterized by persistent or recurrent fatigue, diffuse musculoskeletal pain, sleep disturbances, and subjective cognitive impairment of 6 months duration or longer. Symptoms are not caused by ongoing exertion; are not relieved by rest; and result in a substantial reduction of previous levels of occupational, educational, social, or personal activities. Minor alterations of immune, neuroendocrine, and autonomic function may be associated with this syndrome. There is also considerable overlap between this condition and FIBROMYALGIA. (From Semin Neurol 1998;18(2):237-42; Ann Intern Med 1994 Dec 15;121(12): 953-9)
Pleurodynia, Epidemic
Bipolar Disorder
Attention Deficit Disorder with Hyperactivity
A behavior disorder originating in childhood in which the essential features are signs of developmentally inappropriate inattention, impulsivity, and hyperactivity. Although most individuals have symptoms of both inattention and hyperactivity-impulsivity, one or the other pattern may be predominant. The disorder is more frequent in males than females. Onset is in childhood. Symptoms often attenuate during late adolescence although a minority experience the full complement of symptoms into mid-adulthood. (From DSM-V)
Amyotrophic Lateral Sclerosis
A degenerative disorder affecting upper MOTOR NEURONS in the brain and lower motor neurons in the brain stem and SPINAL CORD. Disease onset is usually after the age of 50 and the process is usually fatal within 3 to 6 years. Clinical manifestations include progressive weakness, atrophy, FASCICULATION, hyperreflexia, DYSARTHRIA, dysphagia, and eventual paralysis of respiratory function. Pathologic features include the replacement of motor neurons with fibrous ASTROCYTES and atrophy of anterior SPINAL NERVE ROOTS and corticospinal tracts. (From Adams et al., Principles of Neurology, 6th ed, pp1089-94)
Gastroesophageal Reflux
Gemfibrozil
Probucol
Cholesterol
Poison Control Centers
Poisoning
Beverages
Regional Medical Programs
Allylamine
Bile Acids and Salts
Steroid acids and salts. The primary bile acids are derived from cholesterol in the liver and usually conjugated with glycine or taurine. The secondary bile acids are further modified by bacteria in the intestine. They play an important role in the digestion and absorption of fat. They have also been used pharmacologically, especially in the treatment of gallstones.
Cholestyramine Resin
Crohn Disease
A chronic transmural inflammation that may involve any part of the DIGESTIVE TRACT from MOUTH to ANUS, mostly found in the ILEUM, the CECUM, and the COLON. In Crohn disease, the inflammation, extending through the intestinal wall from the MUCOSA to the serosa, is characteristically asymmetric and segmental. Epithelioid GRANULOMAS may be seen in some patients.
Bile
Search Engine
Cell Membrane
Epithelial Cells
Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.
Hydrochlorothiazide
A thiazide diuretic often considered the prototypical member of this class. It reduces the reabsorption of electrolytes from the renal tubules. This results in increased excretion of water and electrolytes, including sodium, potassium, chloride, and magnesium. It is used in the treatment of several disorders including edema, hypertension, diabetes insipidus, and hypoparathyroidism.
Amides
Sodium Chloride Symporter Inhibitors
Drug Therapy, Combination
Antihypertensive Agents
Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.
Hypertension
Amlodipine
Valine
Evidence for a new pathophysiological mechanism for coronary artery disease regression: hepatic lipase-mediated changes in LDL density. (1/41)
BACKGROUND: Small, dense LDL particles are associated with coronary artery disease (CAD) and predict angiographic changes in response to lipid-lowering therapy. Intensive lipid-lowering therapy in the Familial Atherosclerosis Treatment Study (FATS) resulted in significant improvement in CAD. This study examines the relationship among LDL density, hepatic lipase (HL), and CAD progression, identifying a new biological mechanism for the favorable effects of lipid-altering therapy. METHODS AND RESULTS: Eighty-eight of the subjects in FATS with documented coronary disease, apolipoprotein B levels >/=125 mg/dL, and family history of CAD were selected for this study. They were randomly assigned to receive lovastatin (40 mg/d) and colestipol (30 g/d), niacin (4 g/d) and colestipol, or conventional therapy with placebo alone or with colestipol in those with elevated LDL cholesterol levels. Plasma hepatic lipase (HL), lipoprotein lipase, and LDL density were measured when subjects were and were not receiving lipid-lowering therapy. LDL buoyancy increased with lovastatin-colestipol therapy (7.7%; P<0.01) and niacin-colestipol therapy (10.3%; P<0.01), whereas HL decreased in both groups (-14% [P<0.01] and -17% [P<0.01] with lovastatin-colestipol and niacin-colestipol, respectively). Changes in LDL buoyancy and HL activity were associated with changes in disease severity (P<0.001). In a multivariate analysis, an increase in LDL buoyancy was most strongly associated with CAD regression, accounting for 37% of the variance of change in coronary stenosis (P<0.01), followed by reduction in apolipoprotein Bl (5% of variance; P<0.05). CONCLUSIONS: These studies support the hypothesis that therapy-associated changes in HL alter LDL density, which favorably influences CAD progression. This is a new and potentially clinically relevant mechanism linking lipid-altering therapy to CAD improvement. (+info)Role of bile acids and bile acid binding agents in patients with collagenous colitis. (2/41)
BACKGROUND: In a retrospective study bile acid malabsorption was observed in patients with collagenous colitis. AIMS: To study the occurrence of bile acid malabsorption and the effect of bile acid binders prospectively in patients with chronic diarrhoea and collagenous colitis. METHODS: Over 36 months all patients referred because of chronic diarrhoea completed a diagnostic programme, including gastroscopy with duodenal biopsy, colonoscopy with biopsies, and the (75)Se-homocholic acid taurine ((75)SeHCAT) test for bile acid malabsorption. Treatment with a bile acid binder (cholestyramine in 24, colestipol in three) was given, irrespective of the results of the (75)SeHCAT test. RESULTS: Collagenous colitis was found in 28 patients (six men, 22 women), 27 of whom had persistent symptoms and completed the programme. Four patients had had a previous cholecystectomy or a distal gastric resection. The (75)SeHCAT test was abnormal in 12/27 (44%) of the collagenous colitis patients with (75)SeHCAT values 0.5-9.7%, and normal in 15 patients (56%). Bile acid binding treatment was followed by a rapid, marked, or complete improvement in 21/27 (78%) of the collagenous colitis patients. Rapid improvement occurred in 11/12 (92%) of the patients with bile acid malabsorption compared with 10/15 (67%) of the patients with normal (75)SeHCAT tests. CONCLUSION: Bile acid malabsorption is common in patients with collagenous colitis and is probably an important pathophysiological factor. Because of a high response rate without serious side effects, bile acid binding treatment should be considered for collagenous colitis, particularly patients with bile acid malabsorption. (+info)Common hepatic lipase gene promoter variant determines clinical response to intensive lipid-lowering treatment. (3/41)
BACKGROUND: The common -514 C-->T polymorphism in the promoter region of the hepatic lipase (HL) gene affects HL activity. The C allele is associated with higher HL activity, more dense and atherogenic LDL, and lower HDL(2) cholesterol. Intensive lipid-lowering therapy lowers HL activity, increases LDL and HDL buoyancy, and promotes coronary artery disease (CAD) regression. We tested the hypothesis that subjects with the CC genotype and a more atherogenic lipid profile experience the greatest CAD regression from these favorable effects. METHODS AND RESULTS: Forty-nine middle-aged men with dyslipidemia and established CAD who were undergoing intensive lipid-lowering therapy were studied. Change in coronary stenosis was assessed by quantitative angiography, HL polymorphism by polymerase chain reaction amplification, HL activity by (14)C-labeled substrate, and LDL buoyancy by density-gradient ultracentrifugation. The response to lipid-lowering therapy was significantly different among subjects with different HL promoter genotypes. Subjects with the C:C genotype had the greatest decrease in HL activity (P<0.005 versus TC and TT by ANOVA) and the greatest improvement in LDL density (P<0.005) and HDL(2)-C (P<0.05) with therapy. These subjects had the greatest angiographic improvement, with 96% of them experiencing CAD regression, compared with 60% of TC and none of the TT patients (P:<0.001). CONCLUSIONS: -In middle-aged men with established CAD and dyslipidemia, the HL gene -514 C-->T polymorphism significantly predicts changes in coronary stenosis with lipid-lowering treatment that appear to involve an HL-associated effect on LDL metabolism. This study identifies a gene polymorphism that strongly influences the lipid and clinical response to lipid-lowering drugs. (+info)Determinants of variable response to statin treatment in patients with refractory familial hypercholesterolemia. (4/41)
Interindividual variability in low density lipoprotein (LDL) cholesterol (LDL-C) response during treatment with statins is well documented but poorly understood. To investigate potential metabolic and genetic determinants of statin responsiveness, 19 patients with refractory heterozygous familial hypercholesterolemia were sequentially treated with placebo, atorvastatin (10 mg/d), bile acid sequestrant, and the 2 combined, each for 4 weeks. Levels of LDL-C, mevalonic acid (MVA), 7-alpha-OH-4-cholesten-3-one, and leukocyte LDL receptor and hydroxymethylglutaryl coenzyme A reductase mRNA were determined after each treatment period. Atorvastatin (10 mg/d) reduced LDL-C by an overall mean of 32.5%. Above-average responders (LDL-C -39.5%) had higher basal MVA levels (34.4+/-6.1 micromol/L) than did below-average responders (LDL-C -23.6%, P<0.02; basal MVA 26.3+/-6.1 micromol/L, P<0.01). Fewer good responders compared with the poor responders had an apolipoprotein E4 allele (3 of 11 versus 6 of 8, respectively; P<0.05). There were no baseline differences between them in 7-alpha-OH-4-cholesten-3-one, hydroxymethylglutaryl coenzyme A reductase mRNA, or LDL receptor mRNA, but the latter increased in the good responders on combination therapy (P<0.05). Severe mutations were not more common in poor than in good responders. We conclude that poor responders to statins have a low basal rate of cholesterol synthesis that may be secondary to a genetically determined increase in cholesterol absorption, possibly mediated by apolipoprotein E4. If so, statin responsiveness could be enhanced by reducing dietary cholesterol intake or inhibiting absorption. (+info)Growth hormone induces low-density lipoprotein clearance but not bile acid synthesis in humans. (5/41)
OBJECTIVE: Growth hormone (GH) induces hepatic low-density lipoprotein (LDL) receptors and lowers plasma cholesterol. We characterized the influence of GH treatment on plasma LDL clearance in normal humans and investigated the relative role of LDL receptor (LDLR) activity and stimulation of bile acid synthesis in subjects with different LDLR expression. METHODS AND RESULTS: Plasma clearance of autologous 125I-LDL was measured before and during 3 weeks of treatment with GH (0.1 IU/kg per day) in 9 healthy young males. Plasma LDL cholesterol was reduced by 13% and the fractional catabolic rate of LDL increased by 27%. More marked changes were seen in a patient with hypopituitarism substituted with GH (0.07 IU/kg per day) for 3 months. In a second study, GH dose-dependently reduced LDL cholesterol and increased Lp(a) levels in 3 groups of males: younger and elderly healthy subjects and heterozygous familial hypercholesterolemia (FH). No effect on bile acid synthesis measured by the plasma marker 7alpha-hydroxy-4-cholesten-3-one was observed. In an LDLR-deficient FH homozygote, LDL cholesterol was not affected by GH. CONCLUSIONS: GH treatment reduces plasma LDL cholesterol by inducing LDL clearance. In humans, LDLR expression is a prerequisite for this effect, whereas it is not related to stimulation of bile acid synthesis. (+info)Hepatic mRNA levels for the LDL receptor and HMG-CoA reductase show coordinate regulation in vivo. (6/41)
A sensitive solution hybridization assay using autologous cRNA probes was developed with the aim to study the simultaneous regulation of hepatic mRNA levels, on a quantitative basis, for the LDL receptor (LDLr), HMG-CoA reductase, and cholesterol 7 alpha-hydroxylase (Cho-7-hx) in C57BL/6J mice. With the purpose to suppress and stimulate transcript levels respectively, animals received established high fat diets, cholesterol-enriched diets, and a diet supplemented with mevinolin and colestipol. One hundred nineteen animals were investigated in six separate experiments. In spite of an eightfold increase in hepatic cholesterol induced by a high fat diet, the LDLr and the HMG-CoA reductase mRNA levels were only reduced to 60-70% and 25-50% of control values, respectively. When the data from all animals were analyzed, a strong positive correlation was obtained between the mRNA levels for the LDLr and HMG-CoA reductase (r = 0.79, P less than 0.001). A significant relation remained when control animals only were analyzed (n = 42, r = 0.59, P less than 0.001). Cho-7-hx mRNA showed a regulatory pattern that differed from that of the LDLr and HMG-CoA reductase; feeding cholesterol at 1.7% and 5% but not at 0.4% elevated the mRNA levels for Cho-7-hx while the LDLr and HMG-CoA reductase mRNA levels were maximally suppressed already at 0.4% of dietary cholesterol. The results show that the mRNA levels for the LDLr and HMG-CoA reductase are regulated in parallel in the liver in vivo during various metabolic perturbations as well as at normal physiologic conditions.(ABSTRACT TRUNCATED AT 250 WORDS) (+info)Comparison of computer- and human-derived coronary angiographic end-point measures for controlled therapy trials. (7/41)
The Cholesterol Lowering Atherosclerosis Study, a randomized angiographic clinical trial, demonstrated the beneficial effect of niacin/colestipol plus diet therapy on coronary atherosclerosis. Outcome was determined by panel-based estimates (viewed in both still and cine modes) of percent stenosis severity and change in native artery and bypass graft lesions. Computer-based quantitative coronary angiography (QCA) was also used to measure lesion and bypass graft stenosis severity and change in individual frames closely matched in orientation, opacification, and cardiac phase. Both methods jointly evaluated 350 nonoccluded lesions. The correlation between QCA and panel estimates of lesion size was 0.70 (p less than 0.0001) and for change in lesion size was 0.28 (p = 0.002). Agreement between the two methods in classifying lesion changes (i.e., regression, unchanged, or progression) occurred for 60% (210 of 350) of the lesions kappa +/- SEM = 0.20 +/- 0.05, p less than 0.001). The panel identified 442 nonoccluded lesions for which QCA stenosis measurements could not be obtained. Lesions not measurable by QCA included those with stenosis greater than 85% that could not be reliably edge tracked, segments with diffuse or ecstatic disease that had no reliable reference diameter, and segments for which matched frames could not be located. Seventy-nine lesions, the majority between 21% and 40% stenosis, were identified and measured by QCA but were not identified by the panel. This comparison study demonstrates the need to consider available angiographic measurement methods in relation to the goals of their use. (+info)Liver X receptor alpha interferes with SREBP1c-mediated Abcd2 expression. Novel cross-talk in gene regulation. (8/41)
The peroxisomal ATP binding cassette (ABC) transporter adrenoleukodystrophy-related protein, encoded by ABCD2, displays functional redundancy with the X-linked adrenoleukodystrophy-associated protein, making ABCD2 up-regulation of therapeutic value. Cholesterol lowering activates human ABCD2 in cultured cells. To investigate in vivo regulation by sterols, we first characterized a sterol regulatory element (SRE) in the murine Abcd2 promoter that is directly bound by SRE-binding proteins (SREBPs). Intriguingly, this element overlaps with a direct repeat 4, which serves as binding site for liver X receptor (LXR)/retinoid X receptor heterodimers, suggesting novel cross-talk between SREBP and LXR/retinoid X receptor in gene regulation. Using fasting-refeeding and cholesterol loading, SREBP accessibility to the SRE/direct repeat 4 was tested. Results suggest that adipose Abcd2 is induced by SREBP1c, whereas hepatic Abcd2 expression is down-regulated by concurrent activation of LXRalpha and SREBP1c. In cell culture, SREBP1c-mediated Abcd2 induction is counteracted by ligand-activated LXRalpha. Finally, hepatic Abcd2 expression in LXRalpha,beta-deficient mice is inducible to levels vastly exceeding wild type. Together, we identify LXRalpha as negative modulator of Abcd2, acting through a novel regulatory mechanism involving overlapping SREBP and LXRalpha binding sites. (+info)
COLESTID® TABLETS (micronized colestipol HCl tablets) Warnings and Precautions | Pfizer Medical Information - Nigeria
Effects of combined therapy with lovastatin and colestipol in heterozygous familial hypercholesterolemia. Effects on kinetics...
1990 - Niacin and lovastatin were more efficient than gemfibrozil, probucol, colestipol,
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Bile acid sequestrant
Cholestyramine, colestipol and colesevelam have all been used. Doses may not need to be as high as those previously used for ... Heel RC, Brogden RN, Pakes GE, Speight TM, Avery GS (March 1980). "Colestipol: a review of its pharmacological properties and ... Colestipol (Colestid, Colestipid) Colesevelam (Cholestagel in Europe, Welchol in the USA, Lodalis in Canada) FDA Heart Health ...
Ion-exchange resin
Colestipol is a weakly basic ion-exchange resin and is used to treat hypercholesterolemia. Cholestyramine is a strongly basic ... Colestipol and cholestyramine are known as bile acid sequestrants. Ion-exchange resins are also used as excipients in ... Three ion-exchange resins, sodium polystyrene sulfonate, colestipol, and cholestyramine, are used as active ingredients. Sodium ...
Bile acid malabsorption
Cholestyramine and colestipol, both in powder form, have been used for many years. Unfortunately, many patients find them ...
ATC code C10
C10AC02 Colestipol. C10AC03 Colextran. C10AC04 Colesevelam. C10AD Nicotinic acid and derivativesEdit. C10AD01 Niceritrol. ...
Poison Prevention Packaging Act of 1970
Colestipol in powder form in packages containing no more than 5 grams of the drug. Conjugated estrogen tablets when dispensed ...
Primary biliary cholangitis
First-line treatment of pruritis consists of anion-exchange resins, such as cholestyramine, colestipol, or colesevalam. These ...
Levothyroxine
... colestipol, and polystyrene sulfonate. Grapefruit juice may delay the absorption of levothyroxine, but based on a study of 10 ...
Sitosterolemia
If dietary treatment alone is insufficient, bile acid-binding resins (e.g., cholestyramine, colestipol) could be considered. In ...
Hyperlipidemia
Bile acid binding resins, such as colestipol, cholestyramine, and colesevelam, function by binding bile acids, increasing their ...
Postcholecystectomy syndrome
... colestipol or colesevelam, which may be better tolerated. Symptoms of postcholecystectomy syndrome may include: Dyspepsia, ...
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kolesteroolialandajad, näiteks colestipol,cholestyramine, colsevelam;. *epilepsiaravimid (ehk krampidevastased ravimid), ...
Fenofibrate
... colestipol, etc.): If taken together, bile acid resins may bind to fenofibrate, resulting in a decrease in fenofibrate ...
Familial hypercholesterolemia
... cholestyramine or colestipol), nicotinic acid preparations or fibrates. Control of other risk factors for cardiovascular ...
List of MeSH codes (D25)
... colestipol MeSH D25.720.259 - cyanoacrylates MeSH D25.720.259.341 - enbucrilate MeSH D25.720.259.341.110 - bucrylate MeSH ...
List of drugs: Cm-Co
... colestipol (INN) colestolone (INN) colestyramine (INN) colextran (INN) colfenamate (INN) colforsin (INN) colfosceril palmitate ...
ATC code C10
C10AB08 Ciprofibrate C10AB09 Etofibrate C10AB10 Clofibride C10AB11 Choline fenofibrate C10AC01 Colestyramine C10AC02 Colestipol ...
Colestipol
Drugs.com: Colestipol Hydrochloride "colestipol (Colestid)". MedicineNet. Mutschler E, Schäfer-Korting M (2001). ... ISBN 3-8047-1763-2. Clinical Pharmacology: Colestipol structure Beth Israel Deaconess Medical Center & Care Group: Colestipol ... Colestipol is contraindicated in hypertriglyceridemia (high level of triglycerides in the blood).[citation needed] Colestipol ... Like cholestyramine, colestipol works in the gut by trapping bile acids and preventing them from being reabsorbed. This leads ...
Torcetrapib
On December 2, 2006 Pfizer cut off torcetrapib's phase III trial because of "an imbalance of mortality and cardiovascular events" associated with its use.[16] This was a sudden and unexpected event and as late as November 30, 2006 Jeff Kindler, Pfizer's chief executive, was quoted, "This will be one of the most important compounds of our generation."[16] In the terminated trial, a 60% increase in deaths was observed among patients taking torcetrapib and atorvastatin versus taking atorvastatin alone.[17] Pfizer recommended that all patients stop taking the drug immediately.[18] Six studies were terminated early.[6] One of the completed studies found it raised systolic blood pressure and concluded "Torcetrapib showed no clinical benefit in this or other studies, and will not be developed further."[19] The drug cost $800m+ to bring into Phase III development.[20] ...
Atorvastatin
Interactions with clofibrate, fenofibrate, gemfibrozil, which are fibrates used in accessory therapy in many forms of hypercholesterolemia, usually in combination with statins, increase the risk of myopathy and rhabdomyolysis.[38][42][43] Co-administration of atorvastatin with one of CYP3A4 inhibitors such as itraconazole,[44] telithromycin, and voriconazole, may increase serum concentrations of atorvastatin, which may lead to adverse reactions. This is less likely to happen with other CYP3A4 inhibitors such as diltiazem, erythromycin, fluconazole, ketoconazole, clarithromycin, cyclosporine, protease inhibitors, or verapamil,[45] and only rarely with other CYP3A4 inhibitors, such as amiodarone and aprepitant.[32] Often, bosentan, fosphenytoin, and phenytoin, which are CYP3A4 inducers, can decrease the plasma concentrations of atorvastatin. Only rarely, though, barbiturates, carbamazepine, efavirenz, nevirapine, oxcarbazepine, rifampin, and rifamycin,[46] which are also CYP3A4 inducers, can ...
Mevastatin
Biosynthesis of mevastatin is primarily accomplished via a type 1 PKS pathway it proceeds in the PKS pathway as seen in figure 1 until it reaches a hexaketide state where it undergoes a Diels-Alder cyclization. After cyclization it continues via the PKS pathway to a nonaketide after which it is released and undergoes oxidation and dehydration. It is presumed that the oxidations are preformed by a polypeptide that is similar to cytochrome p450 monooxygenase, which is encoded by mlcC within the mevastatin gene. Lastly the biosynthesis is completed by the PKS facilitating the addition of a diketide sidechain and a methylation by SAM.[7] Figure 1 shows mevastatin in its acid form but it can also be in the more commonly seen lactone form. This pathway was first observed in Penicillium cilrinum and was later discovered that another type of fungus, Penicillium brevicompaetum also produced mevastatin via a PKS pathway. ...
Statin
The role of cholesterol in the development of cardiovascular disease was elucidated in the second half of the 20th century.[138] This lipid hypothesis prompted attempts to reduce cardiovascular disease burden by lowering cholesterol. Treatment consisted mainly of dietary measures, such as a low-fat diet, and poorly tolerated medicines, such as clofibrate, cholestyramine, and nicotinic acid. Cholesterol researcher Daniel Steinberg writes that while the Coronary Primary Prevention Trial of 1984 demonstrated cholesterol lowering could significantly reduce the risk of heart attacks and angina, physicians, including cardiologists, remained largely unconvinced.[139] Scientists in academic settings and the pharmaceutical industry began trying to develop a drug to reduce cholesterol more effectively. There were several potential targets, with 30 steps in the synthesis of cholesterol from acetyl-coenzyme A.[140] In 1971, Akira Endo, a Japanese biochemist working for the pharmaceutical company Sankyo, ...
Niacin/lovastatin
... (trade names Advicor, Mevacor) is a drug combination used for the treatment of dyslipidemia. It is a combination of the vitamin niacin and the statin drug lovastatin. The combination preparation is marketed by Abbott Laboratories. It was approved by the FDA on December 17, 2001. ...
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Colestipol: MedlinePlus Drug Information
Colestipol: learn about side effects, dosage, special precautions, and more on MedlinePlus ... Before taking colestipol,. *tell your doctor and pharmacist if you are allergic to colestipol, any other medications, or any of ... Continue to take colestipol even if you feel well. Do not stop taking colestipol without talking to your doctor. ... Take colestipol exactly as directed. Do not take more or less of it or take it more often than prescribed by your doctor. ...
Colestipol - Wikipedia
Drugs.com: Colestipol Hydrochloride "colestipol (Colestid)". MedicineNet. Mutschler E, Schäfer-Korting M (2001). ... ISBN 3-8047-1763-2. Clinical Pharmacology: Colestipol structure Beth Israel Deaconess Medical Center & Care Group: Colestipol ... Colestipol is contraindicated in hypertriglyceridemia (high level of triglycerides in the blood).[citation needed] Colestipol ... Like cholestyramine, colestipol works in the gut by trapping bile acids and preventing them from being reabsorbed. This leads ...
Colestipol Side Effects in Detail - Drugs.com
Learn about the potential side effects of colestipol. Includes common and rare side effects information for consumers and ... Applies to colestipol: oral powder for suspension, oral tablet. Along with its needed effects, colestipol may cause some ... Applies to colestipol: oral granule for reconstitution, oral tablet. General. The most frequently reported side effects were ... Check with your doctor as soon as possible if any of the following side effects occur while taking colestipol:. More Common. * ...
Colestipol Oral: Uses, Side Effects, Interactions, Pictures, Warnings & Dosing - WebMD
Find patient medical information for colestipol oral on WebMD including its uses, side effects and safety, interactions, ... colestipol oral Common Brand(S): Colestid Generic Name(S): colestipol View Free Coupon * Uses ... How to use colestipol oral Take this medication by mouth as directed by your doctor, usually 1 to 2 times a day. If your dose ... Before taking colestipol, tell your doctor or pharmacist if you are allergic to it; or if you have any other allergies. This ...
Interactions between Candesartan-Hydrochlorothiazide Oral and thiazide-related-diuretics-cholestyramine-colestipol
... about interactions between Candesartan-Hydrochlorothiazide Oral and thiazide-related-diuretics-cholestyramine-colestipol. ... Effect of colestipol on gastrointestinal absorption of chlorothiazide in man. Clin Pharmacol Ther 1973 Sep-Oct; 14(5):886-90. ... 4.Hunninghake DB, King S, LaCroix K. The effect of cholestyramine and colestipol on the absorption of hydrochlorothiazide. Int ... Thiazide & Related Diuretics/Cholestyramine; Colestipol. This information is generalized and not intended as specific medical ...
Colestipol (Oral Route) Description and Brand Names - Mayo Clinic
Colestipol works by attaching to certain substances in the intestine. Since colestipol is not absorbed into the body, these ... Colestipol is used to lower high cholesterol levels in the blood. This may help prevent medical problems caused by cholesterol ... Colestipol may also be used for other conditions as determined by your doctor. ...
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Colestipol granules for oral suspension - AHealthyMe - Blue Cross Blue Shield of Massachusetts
PRIME PubMed | Effects of colestipol alone and in combination with simvastatin on apolipoprotein B metabolism
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COLESTID (Colestipol) dosage, indication, interactions, side effects | EMPR - ONA
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Colestipol and Probucol: Treatment of Primary and Familial Hypercholesterolemia and Amelioration of Atherosclerosis | Annals of...
Probucol with Colestipol in the Treatment of Hypercholesterolemia Annals of Internal Medicine; 100 (4): 477-482 ... Colestipol and Probucol: Treatment of Primary and Familial Hypercholesterolemia and Amelioration of Atherosclerosis CHARLES J. ... Long-term colestipol therapy in conjunction with diet may reduce xanthoma size, arrest progression of coronary artery ... Complementarity of Colestipol, Niacin, and Lovastatin in Treatment of Severe Familial Hypercholesterolemia Annals of Internal ...
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To determine the relative cost-effectiveness of lowering high blood cholesterol with cholestyramine, colestipol, gemfibrozil, ... Niacin and lovastatin were more efficient than gemfibrozil, probucol, colestipol, or cholestyramine for lowering cardiovascular ... Patients received monotherapy with cholestyramine, colestipol, niacin, gemfibrozil, lovastatin, or probucol compared with ... colestipol, or cholestyramine for lowering cardiovascular risk among patients with type II hyperlipoproteinemia and total ...
Colestipol hydrochloride - patient information, description, dosage and directions.
Description of the drug Colestipol hydrochloride. - patient information, description, dosage and directions. What is Colestipol ... Colestipol hydrochloride. Brand names: Colestid. Why is Colestipol hydrochloride prescribed?. Colestid, in conjunction with ... Why should Colestipol hydrochloride not be prescribed?. You should not be using Colestid if you are allergic to it or any of ... Recommended dosage for Colestipol hydrochloride. ADULTS. One packet or 1 level scoopful of Flavored Colestid granules or one ...
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Which medications in the drug class Bile Acid Sequestrants are used in the treatment of Crohn Disease?
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Colestipol Hydrochloride Side Effects - DrugInformer
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Colestipol forms a soluble complex after binding to bile acid, increasing fecal loss of bile acid-bound low-density lipoprotein ... These patients may benefit from bile acid sequestrants such as cholestyramine (2-4 g) and colestipol (5 g 2 or 3 times daily ... These patients may benefit from bile acid sequestrants such as cholestyramine and colestipol. ...
WP-Thyroid (Thyroid Tablets): Uses, Dosage, Side Effects, Interactions, Warning
HydrochlorideColesevelamGranulesHours after colestipolNiacinHypercholesterolemiaAbsorptionSequestrantsDosageFamilialHigh cholesterolAtherosclerosisPharmacist if you are allergicTriglyceridesTherapyColestyramineAdverse effectsPatientsSide effectsCholesterol levelsEffectivenessAnion-exchangeSolubleDrugCitationSubstances
Hydrochloride18
- Why is Colestipol hydrochloride prescribed? (drugster.info)
- How should you take Colestipol hydrochloride? (drugster.info)
- Why should Colestipol hydrochloride not be prescribed? (drugster.info)
- Did the author experience fatigue while taking colestipol hydrochloride ? (druginformer.com)
- The active ingredient in COLESTID Tablets is micronized colestipol hydrochloride, which is a lipid lowering agent for oral use. (pfizermedicalinformation.com.co)
- Each COLESTID Tablet contains one gram of micronized colestipol hydrochloride. (pfizermedicalinformation.com.co)
- Peptic ulceration, cholecystitis, and cholelithiasis have been rarely reported in patients receiving colestipol hydrochloride granules, and are not necessarily drug related. (pfizermedicalinformationng.com)
- Transient and modest elevations of aspartate aminotransferase (AST, SGOT), alanine aminotransferase (ALT, SGPT) and alkaline phosphatase were observed on one or more occasions in various patients treated with colestipol hydrochloride. (pfizermedicalinformationng.com)
- Urticaria and dermatitis have been rarely noted in patients receiving colestipol hydrochloride granules. (pfizermedicalinformationng.com)
- Because it sequesters bile acids, colestipol hydrochloride may interfere with normal fat absorption and, thus, may reduce absorption of folic acid and fat soluble vitamins such as A, D, and K. (pfizermedicalinformationng.com)
- Chronic use of colestipol hydrochloride may be associated with an increased bleeding tendency due to hypoprothrombinemia from vitamin K deficiency. (pfizermedicalinformationng.com)
- Since colestipol hydrochloride is a chloride form of an anion exchange resin, there is a possibility that prolonged use may lead to the development of hyperchloremia acidosis. (pfizermedicalinformationng.com)
- In studies conducted in rats in which cholestyramine resin (a bile acid sequestering agent similar to colestipol hydrochloride) was used as a tool to investigate the role of various intestinal factors, such as fat, bile salts, and microbial flora, in the development of intestinal tumors induced by potent carcinogens, the incidence of such tumors was observed to be greater in cholestyramine resin treated rats than in control rats. (pfizermedicalinformationng.com)
- When colestipol hydrochloride was administered in the diet to rats for 18 months, there was no evidence of any drug related intestinal tumor formation. (pfizermedicalinformationng.com)
- In the Ames assay, colestipol hydrochloride was not mutagenic. (pfizermedicalinformationng.com)
- Since colestipol hydrochloride is essentially not absorbed systemically (less than 0.17% of the dose), it is not expected to cause fetal harm when administered during pregnancy in recommended dosages. (pfizermedicalinformationng.com)
- To determine whether combined therapy with the lipid lowering agents colestipol hydrochloride plus niacin would produce significant change in coronary, carotid, and femoral artery atherosclerosis and coronary bypass graft lesions as determined by angiography. (clinicaltrials.gov)
- One hundred eighty-eighty subjects were randomized to either 30 grams (g) of colestipol hydrochloride plus 3 to 12 g of niacin daily or to placebo. (clinicaltrials.gov)
Colesevelam3
- References on the safety and hepatotoxicity of colesevelam are given with those for cholestyramine and colestipol in the Overview section on Bile Acid Resins/Sequestrants. (nih.gov)
- Three bile acid sequestrants are available in the United States (common brand name and year of approval): cholestyramine (Questran, 1973), colesevelam (Welchol, 2000) and colestipol (Colestid, 1977). (nih.gov)
- Cholestyramine, colestipol and colesevelam have all been used. (wikipedia.org)
Granules1
- Colestipol comes as tablets and granules to take by mouth. (medlineplus.gov)
Hours after colestipol2
- if you are taking gemfibrozil (Lopid), take it 2 hours before or 2 hours after colestipol. (medlineplus.gov)
- Take your other medications as directed by your doctor, usually at least 1 hour before or 4 to 6 hours after colestipol. (webmd.com)
Niacin4
- A Prospective, Open Label Comparison of Ezetimibe, Niacin, and Colestipol as Adjunct Therapy in Lipid Reduction. (springer.com)
- In the article entitled "Beneficial Effects of Combined Colestipol-Niacin Therapy on Coronary Atherosclerosis and Coronary Venous Bypass Grafts," Blankenhorn et al 1 presented exciting data concerning the possible stabilization of and improvement in coronary lesions in patients with a previous history of coronary bypass grafting who were treated with diet and cholesterol-reducing drugs. (jamanetwork.com)
- Beneficial Effects of Combined Colestipol-Niacin Therapy on Coronary Atherosclerosis and Coronary Venous Bypass Grafts. (pfizermedicalinformation.co.uk)
- Beneficial Effects of Colestipol-Niacin on Coronary Atherosclerosis: A 4-Year Follow-up. (pfizermedicalinformation.co.uk)
Hypercholesterolemia7
- Colestipol (Colestid) is ineffective in the treatment of patients who completely lack LDL receptors due to a genetic defect ( homozygous familial hypercholesterolemia). (medicotips.com)
- Colestipol plus nicotinic acid in treatment of heterozygous familial hypercholesterolemia. (pfizermedicalinformation.co.uk)
- FDA Label, F4555, F4567, L6262] And even though such an agent may very well be useful in reducing elevated cholesterol levels and decreasing the risk for atherosclerotic vascular disease due to hypercholesterolemia, colestipol is still generally only employed as. (drugbank.ca)
- Weight gain in four of five patients with hypercholesterolemia given colestipol for 37 +/- 6 months was associated with a decrease in HDL cholesterol levels and an increase in LDL cholesterol/HDL cholesterol ratios. (nih.gov)
- These results suggest that weight reduction increases plasma HDL cholesterol levels only in those patients with hypercholesterolemia given colestipol but not in those given treatment by diet alone. (nih.gov)
- Effects of combined therapy with lovastatin and colestipol in heterozygous familial hypercholesterolemia. (elsevier.com)
- Dive into the research topics of 'Effects of combined therapy with lovastatin and colestipol in heterozygous familial hypercholesterolemia. (elsevier.com)
Absorption9
- Unless otherwise instructed, take all other medications at least 1 hour before or 4 hours after you take colestipol because it can interfere with their absorption. (medlineplus.gov)
- The following notable side effects may occur: gastrointestinal tract disturbances, especially (mild, occasionally severe) constipation sometimes increase in VLDL[citation needed] and triglyceride synthesis Colestipol can bind to a number of drugs and nutrients in the gut and inhibit or delay their absorption. (wikipedia.org)
- Colestipol may decrease your absorption of other medications . (webmd.com)
- Effect of colestipol on gastrointestinal absorption of chlorothiazide in man. (webmd.com)
- 2.Hunninghake DB, King S. Effect of cholestyramine and colestipol on the absorption of methyldopa and hydrochlorothiazide. (webmd.com)
- Colestipol (Colestid) bind with bile acids and impair their absorption and reduce enterohepatic circulation and re-utilization of bile acids. (medicotips.com)
- Colestipol (Colestid) also decreases the absorption of dietary cholesterol. (medicotips.com)
- In this way, Colestipol (Colestid) decrease the absorption of cholesterol and blood level of cholesterol is decreased. (medicotips.com)
- Bile acid sequestering agents such as cholestyramine and colestipol may interfere with the action of Actigall by reducing its absorption. (medicinenet.com)
Sequestrants4
- Colestipol is in a class of medications called bile acid sequestrants. (medlineplus.gov)
- These patients may benefit from bile acid sequestrants such as cholestyramine and colestipol. (medscape.com)
- These patients may benefit from bile acid sequestrants such as cholestyramine (2-4 g) and colestipol (5 g 2 or 3 times daily before meals). (medscape.com)
- Bile acid sequestrants like colestipol have been in use since the 1970s. (drugbank.ca)
Dosage1
- colestipol mechanism of action colestipol dosage attended with stupefaction caused by blows on the head which cases and added the following and wishes to emphasize that traces or it may be absent altogether glomerular atrophy especially in colestipol side effects is more efficient or common than the abuse of intoxicating drinks. (guildwars2forum.com)
Familial1
- Familial type II hyperlipoproteinemia with coronary heart disease: Effect of diet-colestipol-nicotinic acid treatment. (pfizermedicalinformation.co.uk)
High cholesterol2
- Colestipol is used along with diet changes to decrease the amount of fatty substances such as low-density lipoprotein (LDL) cholesterol ('bad cholesterol') in certain people with high cholesterol. (medlineplus.gov)
- Colestipol is used to lower high cholesterol levels in the blood. (mayoclinic.org)
Atherosclerosis1
- Long-term colestipol therapy in conjunction with diet may reduce xanthoma size, arrest progression of coronary artery atherosclerosis, and may reduce mortality from coronary heart disease. (annals.org)
Pharmacist if you are allergic1
- tell your doctor and pharmacist if you are allergic to colestipol, any other medications, or any of the ingredients in colestipol preparations. (medlineplus.gov)
Triglycerides1
- Such substances include: thiazide diuretics, furosemide gemfibrozil benzylpenicillin, tetracycline digoxin lipid-soluble vitamins (A, D, E, K) Colestipol is contraindicated in hypertriglyceridemia (high level of triglycerides in the blood). (wikipedia.org)
Therapy1
- The combination therapy and colestipol alone did not differ significantly with respect to changes in individual lipid values. (annals.org)
Colestyramine2
- These are called colestyramine and colestipol. (nice.org.uk)
- Colestyramine and colestipol have some side effects including constipation (when stools are not passed regularly), nausea (feeling sick), stomach rumbling, flatulence (wind), bloating and abdominal pain. (nice.org.uk)
Adverse effects1
- To test whether combining psyllium mucilloid with half the usual dose of colestipol reduces the adverse effects associated with colestipol and maintains or increases its efficacy in the treatment of hyperlipidemia. (annals.org)
Patients4
- COLESTIPOL (koe LES ti pole) is used to lower cholesterol in patients who are at risk of heart disease or stroke. (ahealthyme.com)
- Colestipol (Colestid) is effective in reducing plasma cholesterol level (to about 10 - 20 % ) in patients with some normal LDL receptors. (medicotips.com)
- Weight loss (-7 +/- 2 kg) in these five and two other patients given colestipol increased plasma HDL cholesterol (17% +/- 6%) and lowered total cholesterol (-8% +/- 1%), LDL cholesterol (-13% +/- 2%), and total triglyceride (-20% +/- 4%) concentrations. (nih.gov)
- However, in six patients given treatment by diet alone (no colestipol), comparable weight loss (-6 +/- 1 kg) did not alter plasma HDL cholesterol or total triglyceride concentrations, but reduced total cholesterol (-9% +/- 3%) and LDL cholesterol (-11% +/- 3%) levels. (nih.gov)
Side effects2
- Colestipol may cause side effects. (medlineplus.gov)
- Some side effects of colestipol may occur that usually do not need medical attention. (drugs.com)
Cholesterol levels1
- Colestipol is a safe, effective, cholesterol-lowering, bileacid sequestrant that lowers low-density-lipoprotein (LDL) and total plasma cholesterol levels without consistently affecting high-density-lipoprotein (HDL) cholesterol levels. (annals.org)
Effectiveness1
- Is cholestyramine or colestipol better in effectiveness? (healthtap.com)
Anion-exchange1
- Colestipol is an insoluble, high molecular weight basic anion-exchange copolymer of diethylenetriamine and 1-chloro-2, 3-epoxypropane, with approximately 1 out of 5 amine nitrogens protonated (chloride form). (pfizermedicalinformation.com.co)
Soluble1
- Colestipol forms a soluble complex after binding to bile acid, increasing fecal loss of bile acid-bound low-density lipoprotein cholesterol. (medscape.com)
Drug2
- Colestipol is a cholesterol-lowering drug. (patientslikeme.com)
- Is cholestyramine or colestipol better drug? (healthtap.com)
Citation1
- citation needed] Colestipol is a copolymer of diethylenetriamine (DETA) -or tetraethylenepentamine according to some sources- and epichlorohydrin. (wikipedia.org)
Substances2
- Colestipol works by attaching to certain substances in the intestine. (mayoclinic.org)
- Since colestipol is not absorbed into the body, these substances also pass out of the body without being absorbed. (mayoclinic.org)