Highly crosslinked and insoluble basic anion exchange resin used as anticholesteremic. It may also may reduce triglyceride levels.
A water-soluble vitamin of the B complex occurring in various animal and plant tissues. It is required by the body for the formation of coenzymes NAD and NADP. It has PELLAGRA-curative, vasodilating, and antilipemic properties.
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)
Hydrazines substituted by one or more methyl groups in any position.
Polyamines are organic compounds with more than one amino group, involved in various biological processes such as cell growth, differentiation, and apoptosis, and found to be increased in certain diseases including cancer.
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.
Hydrazines substituted with two methyl groups in any position.
A group of familial disorders characterized by elevated circulating cholesterol contained in either LOW-DENSITY LIPOPROTEINS alone or also in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins).
Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.

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)

Colestipol is a medication that is used to treat high cholesterol levels in the blood. It is a type of drug known as a bile acid sequestrant, which works by binding to bile acids in the digestive system and preventing them from being reabsorbed into the body. This leads to an increase in the breakdown of cholesterol in the liver and a decrease in the amount of cholesterol in the blood.

Colestipol is available as a powder that is mixed with water or other fluids before it is taken, and it is typically taken one or two times per day. Common side effects of colestipol include constipation, bloating, gas, and stomach pain. It may also interact with other medications, so it is important to inform your healthcare provider of all the medications you are taking before starting colestipol.

It's important to note that while colestipol can help lower cholesterol levels, it is not a cure for high cholesterol and should be used in conjunction with lifestyle modifications such as regular exercise and a healthy diet. As with any medication, it's essential to use colestipol under the guidance of a healthcare professional.

Niacin, also known as vitamin B3 or nicotinic acid, is a water-soluble vitamin that is essential for human health. It is a crucial component of the coenzymes NAD (nicotinamide adenine dinucleotide) and NADP (nicotinamide adenine dinucleotide phosphate), which play key roles in energy production, DNA repair, and cellular signaling.

Niacin can be obtained from various dietary sources, including meat, poultry, fish, legumes, whole grains, and fortified foods. It is also available as a dietary supplement and prescription medication. Niacin deficiency can lead to a condition called pellagra, which is characterized by symptoms such as diarrhea, dermatitis, dementia, and, if left untreated, death.

In addition to its role in energy metabolism and DNA repair, niacin has been shown to have potential benefits for cardiovascular health, including lowering LDL (low-density lipoprotein) cholesterol and triglyceride levels while raising HDL (high-density lipoprotein) cholesterol levels. However, high-dose niacin therapy can also have adverse effects, such as flushing, itching, and liver toxicity, so it should be used under the guidance of a healthcare professional.

In a medical context, "resins, plant" refer to the sticky, often aromatic substances produced by certain plants. These resins are typically composed of a mixture of volatile oils, terpenes, and rosin acids. They may be present in various parts of the plant, including leaves, stems, and roots, and are often found in specialized structures such as glands or ducts.

Plant resins have been used for centuries in traditional medicine and other applications. Some resins have antimicrobial, anti-inflammatory, or analgesic properties and have been used to treat a variety of ailments, including skin conditions, respiratory infections, and pain.

Examples of plant resins with medicinal uses include:

* Frankincense (Boswellia spp.) resin has been used in traditional medicine to treat inflammation, arthritis, and asthma.
* Myrrh (Commiphora spp.) resin has been used as an antiseptic, astringent, and anti-inflammatory agent.
* Pine resin has been used topically for its antimicrobial and anti-inflammatory properties.

It's important to note that while some plant resins have demonstrated medicinal benefits, they should be used with caution and under the guidance of a healthcare professional. Some resins can have adverse effects or interact with medications, and it's essential to ensure their safe and effective use.

Methylhydrazines are a class of organic compounds that contain a hydrazine functional group with one or more methyl substituents. Hydrazine is a simple inorganic compound with the formula N2H4, and it consists of a nitrogen atom bonded to four hydrogen atoms through nitrogen-hydrogen covalent bonds. When one or more of these hydrogens are replaced by a methyl group (CH3), we get methylhydrazines.

The most common methylhydrazine is monomethylhydrazine (MMH), which has the molecular formula CH6N2. It is an colorless, oily liquid with an ammonia-like odor and is highly toxic and reactive. MMH is used as a rocket propellant due to its high specific impulse and density.

Another example of methylhydrazine is unsymmetrical dimethylhydrazine (UDMH), which has the molecular formula C2H8N2. UDMH is also a colorless, oily liquid with an ammonia-like odor and is used as a rocket propellant.

It's important to note that methylhydrazines are highly toxic and reactive compounds, and they require careful handling and storage. They can cause harm to the skin, eyes, respiratory system, and nervous system, and prolonged exposure can lead to serious health effects or death.

Polyamines are organic compounds with more than one amino group (-NH2) and at least one carbon atom bonded to two or more amino groups. They are found in various tissues and fluids of living organisms and play important roles in many biological processes, such as cell growth, differentiation, and apoptosis (programmed cell death). Polyamines are also involved in the regulation of ion channels and transporters, DNA replication and gene expression. The most common polyamines found in mammalian cells are putrescine, spermidine, and spermine. They are derived from the decarboxylation of amino acids such as ornithine and methionine. Abnormal levels of polyamines have been associated with various pathological conditions, including cancer and neurodegenerative diseases.

Lovastatin is a medication that belongs to a class of drugs called statins, which are used to lower cholesterol levels in the blood. It works by inhibiting HMG-CoA reductase, an enzyme that plays a crucial role in the production of cholesterol in the body. By reducing the amount of cholesterol produced in the liver, lovastatin helps to decrease the levels of low-density lipoprotein (LDL) or "bad" cholesterol and triglycerides in the blood, while increasing the levels of high-density lipoprotein (HDL) or "good" cholesterol.

Lovastatin is available in both immediate-release and extended-release forms, and it is typically taken orally once or twice a day, depending on the dosage prescribed by a healthcare provider. Common side effects of lovastatin include headache, nausea, diarrhea, and muscle pain, although more serious side effects such as liver damage and muscle weakness are possible, particularly at higher doses.

It is important to note that lovastatin should not be taken by individuals with active liver disease or by those who are pregnant or breastfeeding. Additionally, it may interact with certain other medications, so it is essential to inform a healthcare provider of all medications being taken before starting lovastatin therapy.

Dimethylhydrazines are organic compounds that consist of two methyl groups (-CH3) bonded to a hydrazine molecule (N2H4). The most common dimethylhydrazine is 1,2-dimethylhydrazine, which is a colorless liquid with an unpleasant odor. It is used as a rocket fuel and in the synthesis of other chemicals.

Dimethylhydrazines are highly reactive and can be hazardous to handle. They can cause skin and eye irritation, and prolonged exposure can lead to more serious health effects such as damage to the respiratory system, liver, and kidneys. Ingestion or inhalation of large amounts of dimethylhydrazines can be fatal.

It is important to handle dimethylhydrazines with care and follow proper safety precautions when working with them. This may include wearing protective clothing, gloves, and eye protection, as well as using appropriate ventilation and storage methods.

Hyperlipoproteinemia Type II, also known as Fredrickson Type II or Familial Combined Hyperlipidemia, is a genetic disorder characterized by elevated levels of low-density lipoprotein (LDL) cholesterol and/or triglycerides in the blood. This condition can lead to an increased risk of developing cardiovascular diseases such as atherosclerosis and coronary artery disease.

The disorder is caused by mutations in several genes involved in lipid metabolism, including APOB, LDLR, PCSK9, and APOE. These genetic defects result in impaired clearance of LDL particles from the bloodstream, leading to their accumulation and increased risk of cardiovascular disease.

Individuals with Hyperlipoproteinemia Type II typically have elevated levels of both LDL cholesterol and triglycerides, although some may only have one or the other elevated. The disorder can present at any age, but it is often diagnosed in adulthood during routine cholesterol screening.

Treatment for Hyperlipoproteinemia Type II typically involves lifestyle modifications such as a heart-healthy diet, regular exercise, and weight loss. Medications such as statins, ezetimibe, and PCSK9 inhibitors may also be prescribed to lower LDL cholesterol levels and reduce the risk of cardiovascular disease.

Hypolipidemic agents are a class of medications that are used to lower the levels of lipids (fats) in the blood, particularly cholesterol and triglycerides. These drugs work by reducing the production or increasing the breakdown of fats in the body, which can help prevent or treat conditions such as hyperlipidemia (high levels of fats in the blood), atherosclerosis (hardening and narrowing of the arteries), and cardiovascular disease.

There are several different types of hypolipidemic agents, including:

1. Statins: These drugs block the action of an enzyme called HMG-CoA reductase, which is necessary for the production of cholesterol in the liver. By reducing the amount of cholesterol produced, statins can help lower LDL (bad) cholesterol levels and increase HDL (good) cholesterol levels.
2. Bile acid sequestrants: These drugs bind to bile acids in the intestines and prevent them from being reabsorbed into the bloodstream. This causes the liver to produce more bile acids, which requires it to use up more cholesterol, thereby lowering LDL cholesterol levels.
3. Nicotinic acid: Also known as niacin, this drug can help lower LDL and VLDL (very low-density lipoprotein) cholesterol levels and increase HDL cholesterol levels. It works by reducing the production of fatty acids in the liver.
4. Fibrates: These drugs are used to treat high triglyceride levels. They work by increasing the breakdown of fats in the body and reducing the production of VLDL cholesterol in the liver.
5. PCSK9 inhibitors: These drugs block the action of a protein called PCSK9, which helps regulate the amount of LDL cholesterol in the blood. By blocking PCSK9, these drugs can help lower LDL cholesterol levels.

It's important to note that hypolipidemic agents should only be used under the guidance and supervision of a healthcare provider, as they can have side effects and may interact with other medications.

"Colestipol Hydrochloride". Drugs.com. "colestipol (Colestid)". MedicineNet. Mutschler E, Schäfer-Korting M (2001). ... ISBN 3-8047-1763-2. "Colestipol structure". Clinical Pharmacology. "Colestipol structure". Beth Israel Deaconess Medical Center ... 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 ...
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 US, Lodalis in Canada) Wilcox C, Turner J ...
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Bile acid binding resins, such as colestipol, cholestyramine, and colesevelam, function by binding bile acids, increasing their ...
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... colestipol MeSH D25.720.259 - cyanoacrylates MeSH D25.720.259.341 - enbucrilate MeSH D25.720.259.341.110 - bucrylate MeSH ...
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... colestipol MeSH D02.092.782.258 - diamines MeSH D02.092.782.258.174 - cadaverine MeSH D02.092.782.258.368 - ethylenediamines ...
C10AB08 Ciprofibrate C10AB09 Etofibrate C10AB10 Clofibride C10AB11 Choline fenofibrate C10AC01 Colestyramine C10AC02 Colestipol ...
"Colestipol Hydrochloride". Drugs.com. "colestipol (Colestid)". MedicineNet. Mutschler E, Schäfer-Korting M (2001). ... ISBN 3-8047-1763-2. "Colestipol structure". Clinical Pharmacology. "Colestipol structure". Beth Israel Deaconess Medical Center ... 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 ...
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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. ...
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Cholestyramine Colestipol Lovastatin Probucol,/td,\r\n,/tr,\r\n,tr,\r\n,td width=343,,strong,Gastric medications,/strong,,/ ... Cholestyramine Colestipol Lovastatin Probucol,/td,\r\n,/tr,\r\n,tr,\r\n,td width=343,,strong,Gastric medications,/strong,,/ ...
If you are taking any of these drugs: Azathioprine, cholestyramine, colesevelam, colestipol, norfloxacin with metronidazole, or ...
Colestipol ( Safe. Compatible. Minimal risk for breastfeeding and infant.). *Colestyramine ( Safe. Compatible. Minimal risk for ...
Colestipol (Colestid) Corticosteroids: Corticosteroids, including prednisone or methylprednisolone (Medrol), may increase ...
Colestipol: (Moderate) Colestipol can bind with and possibly decrease the oral absorption of orally administered vitamin A, ... Administer other drugs at least 1 hour before or at least 4 to 6 hours after the administration of colestipol. Conjugated ...
Some of the medications, such as Caduet, Lescol (Fluvastatin), Colestid (Colestipol) and Praulent (Alirocumab) may require no- ...
Colestipol (Colestid®). *Mildly lowers LDL ("bad") cholesterol. *Constipation. *Nausea. *Bloating. Nitrates. Isosorbide ...
  • Colestipol (trade names Colestid, Cholestabyl) is a bile acid sequestrant used to lower blood cholesterol, specifically low-density lipoprotein (LDL). (wikipedia.org)
  • If you have an allergy to colestipol or any other part of Colestid (colestipol granules). (drugs.com)
  • You must check to make sure that it is safe for you to take Colestid (colestipol granules) with all of your drugs and health problems. (drugs.com)
  • Tell all of your health care providers that you take Colestid (colestipol granules). (drugs.com)
  • Take other drugs at least 1 hour before or 4 hours after you take Colestid (colestipol granules). (drugs.com)
  • Low vitamin K levels have happened in people taking Colestid (colestipol granules) for a long time. (drugs.com)
  • Hemorrhoids may get worse with Colestid (colestipol granules). (drugs.com)
  • You will need to talk about the benefits and risks of using Colestid (colestipol granules) while you are pregnant. (drugs.com)
  • Use Colestid (colestipol granules) as ordered by your doctor. (drugs.com)
  • You may also mix Colestid (colestipol granules) with cereals, soups, and fruits like applesauce or crushed pineapple. (drugs.com)
  • Buy Colestid (Colestipol) from a Canadian Pharmacy. (canpharm.com)
  • Colestid (Colestipol) is a prescription medication used to treat high cholesterol. (canadianpharmacyking.com)
  • Bile acid sequestrants (cholestyramine or colestipol) raise triglyceride levels and are not appropriate therapy for hypertriglyceridemia. (moviecultists.com)
  • Subject has consumed medicines or foodstuff that may affect pharmacological or pharmacokinetic properties of chenodeoxycholic acid (for example: Antacids (aluminum containing), Bile acid sequestrants such as (cholestyramine or colestipol), Clofibrate, Coumarin-derivative anticoagulants, Estrogens & oral contraceptive) two weeks before dosing, during the study and two weeks after dosing. (who.int)
  • 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-colesevelam, cholestyramine and colestipol-and nicotinic acid are other types of medicine that may be used to reduce cholesterol levels. (hopkinsmedicine.org)
  • Two other types of medicines that lower cholesterol levels are bile acid sequestrants, such as colesevelam, cholestyramine, and colestipol, and nicotinic acid (niacin). (uhhospitals.org)
  • Like cholestyramine, colestipol works in the gut by trapping bile acids and preventing them from being reabsorbed. (wikipedia.org)
  • 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)
  • 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)
  • A subgroup analysis of the on-trial antioxidant vitamin intake database acquired in the Cholesterol Lowering Atherosclerosis Study, a randomized, placebo-controlled, serial angiographic clinical trial evaluating the risk and benefit of colestipol-niacin on coronary artery disease progression. (nih.gov)
  • Beneficial effects of colestipol-niacin on coronary atherosclerosis. (ecureme.com)
  • He continues intravenous Ig for infectious prophylaxis and colestipol for diarrhea. (cancernetwork.com)
  • colestipol decreases levels of chenodiol by inhibition of GI absorption. (medscape.com)
  • Sucralfate, cholestyramine, and colestipol can decrease the absorption of furosemide. (bidrx.com)
  • Like cholestyramine, colestipol works in the gut by trapping bile acids and preventing them from being reabsorbed. (wikipedia.org)
  • Cholestyramine (or colestipol ) may reduce the itching. (nih.gov)
  • bile acid sequestrants (such as cholestyramine [Questran®] and colestipol [Colestid®]) to lower blood cholesterol levels. (nih.gov)
  • Bile-acid binding agents such as cholestyramine, colestipol , and colesevelam have been investigated for IBS-D. (nih.gov)
  • Cholestyramine and colestipol are effective in sequestering bile salts in the enteric lumen. (medscape.com)
  • Patients may benefit from bile acid sequestrants such as cholestyramine and colestipol. (medscape.com)
  • Vitamin E absorption may be altered when taking the pharmaceuticals Cholestyramine, Colestipol, or Orlistat. (drweil.com)
  • Cholestyramine and colestipol can decrease the absorption of metolazone . (webmd.com)
  • If you are taking either of these drugs, separate metolazone from cholestyramine by at least 4 hours and from colestipol by at least 2 hours. (webmd.com)
  • If you are also taking cholestyramine or colestipol, take enalapril/hydrochlorothiazide at least 4 hours before or at least 4 to 6 hours after either of those drugs. (healthlinkbc.ca)
  • OLYAEI, DEMATTOS BENNETT Atorvastatin Cholestyramine Colestipol Fluvastatin Gemfibrozil Lovastatin Pravastatin Simvastatin Starting dose forex powerpoint mgday 4 g bid 5 gbid 20 mg daily 600 poewrpoint 5 mg daily 10-40 mg daily 5-20 mg daily Maximum dose 80 mgday 24 gday 30 gday 80 mgday 600 bid 20 mgday 80 mgday 20 mgday Table 5. (binaryoptionsxpert.com)
  • The active ingredient in colestipol hydrochloride tablets is micronized colestipol hydrochloride, which is a lipid lowering agent for oral use. (nih.gov)
  • Each colestipol hydrochloride tablet contains one gram of micronized colestipol hydrochloride. (nih.gov)
  • Colestipol hydrochloride tablets are light yellow in color and are tasteless and odorless. (nih.gov)
  • Colestipol hydrochloride tablets contain no calories. (nih.gov)
  • Colestipol hydrochloride binds bile acids in the intestine forming a complex that is excreted in the feces. (nih.gov)
  • Since colestipol hydrochloride is an anion exchange resin, the chloride anions of the resin can be replaced by other anions, usually those with a greater affinity for the resin than the chloride ion. (nih.gov)
  • Colestipol hydrochloride is hydrophilic, but it is virtually water insoluble (99.75%) and it is not hydrolyzed by digestive enzymes. (nih.gov)
  • The high molecular weight polymer in colestipol hydrochloride apparently is not absorbed. (nih.gov)
  • In humans, less than 0.17% of a single 14 C-labeled colestipol hydrochloride dose is excreted in the urine when given following 60 days of dosing of 20 grams of colestipol hydrochloride per day. (nih.gov)
  • The increased fecal loss of bile acids due to colestipol hydrochloride administration leads to an increased oxidation of cholesterol to bile acids. (nih.gov)
  • Although colestipol hydrochloride produces an increase in the hepatic synthesis of cholesterol in man, serum cholesterol levels fall. (nih.gov)
  • Serum triglyceride levels may increase or remain unchanged in colestipol hydrochloride treated patients. (nih.gov)
  • The decline in serum cholesterol levels with colestipol hydrochloride treatment is usually evident by one month. (nih.gov)
  • When colestipol hydrochloride is discontinued, serum cholesterol levels usually return to baseline levels within one month. (nih.gov)
  • Although the significance of this finding has not been established in clinical studies, the elevation of the lipoprotein LpAI particle within the HDL fraction is consistent with an antiatherogenic effect of colestipol hydrochloride, even though little change is observed in HDL cholesterol (HDL-C). (nih.gov)
  • Modification of the carcinogenic process in colorectal cancer by endogenous and exogenous factors: effect of colestipol hydrochloride on tumors induced by dimethylhydrazine. (nih.gov)
  • The effect of the bile acid sequestrant, colestipol hydrochloride, on the incidence of dimethylhydrazine-induced tumors of the large intestine was determined in male Swiss mice. (nih.gov)
  • 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)
  • tell your doctor and pharmacist if you are allergic to colestipol, any other medications, or any of the ingredients in colestipol preparations. (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)
  • See the "Colestipol Precautions" section. (rxwiki.com)
  • Colestipol comes as tablets and granules to take by mouth. (medlineplus.gov)
  • A 65-year-old man with type IIa dyslipidemia who received flavored colestipol granules 2 scoops/day for 3 months developed asymptomatic hepatotoxicity. (nih.gov)
  • Colestipol granules in the colon: macroscopic and microscopic findings. (nih.gov)
  • Low dose colestipol in adolescents with familial hypercholesterolaemia. (nih.gov)
  • 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 will decrease the level or effect of cholic acid by drug binding in GI tract. (medscape.com)
  • colestipol will decrease the level or effect of vitamin D by Other (see comment). (medscape.com)
  • 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). (nih.gov)
  • Since colestipol has the capacity to bind a number of chemical agents, the different biological effects probably reflect the multifactorial nature of colorectal cancer with the end result dependent on the balance between opposing factors. (nih.gov)
  • One week after discontinuing colestipol, serum transaminases fell dramatically, with some returning to normal limits. (nih.gov)
  • When carcinogen-treated animals received dietary colestipol (0.52%, w/w) from 4 weeks prior to the first injection of dimethylhydrazine until the time of death, there was an increase in the number of tumors per tumor-bearing animal to 2.23. (nih.gov)
  • In an attempt to understand the nature of this enhancement, animals were administered dietary colestipol at different times in relation to the administration of the carcinogen. (nih.gov)
  • Colestipol is a prescription medication used in combination with dietary changes to treat high cholesterol . (rxwiki.com)
  • Colestipol is a nonabsorbable resin. (nih.gov)
  • Natural Medicines Comprehensive Database (La Base Exhaustiva de Datos de Medicamentos Naturales) clasifica la eficacia, basada en evidencia científica, de acuerdo a la siguiente escala: Eficaz, Probablemente Eficaz, Posiblemente Eficaz, Posiblemente Ineficaz, Probablemente Ineficaz, Ineficaz, e Insuficiente Evidencia para Hacer una Determinación. (medlineplus.gov)
  • pre-initiation colestipol exposure, 2.23. (nih.gov)
  • colestipol decreases levels of lomitapide by drug binding in GI tract. (medscape.com)
  • if you are taking gemfibrozil (Lopid), take it 2 hours before or 2 hours after colestipol. (medlineplus.gov)
  • Treatment with colestipol results in a significant increase in lipoprotein LpAI. (nih.gov)
  • This is not a complete list of colestipol side effects. (rxwiki.com)
  • Tomar fosfato de sodio o potasio por vía oral o por vía intravenosa es eficaz para prevenir o tratar los niveles bajos de fosfato en la sangre. (medlineplus.gov)
  • Es probable que tomar sales de fosfato por vía oral sea eficaz para tratar los niveles altos de calcio en la sangre. (medlineplus.gov)
  • Tomar fosfato de potasio por vía oral puede ayudar a prevenir la formación de cálculos renales de calcio en personas con niveles altos de calcio en la orina. (medlineplus.gov)
  • Colestipol may cause side effects. (medlineplus.gov)
  • Common side effects of colestipol include constipation, gas, and nausea. (rxwiki.com)
  • Serious side effects have been reported with colestipol. (rxwiki.com)
  • The selective administration of colestipol in relation to carcinogen administration may prove useful in elucidating the various factors involved in the etiology of this disease. (nih.gov)
  • Four weeks after colestipol was discontinued, all liver function tests were normal. (nih.gov)