Fibre 200
Fenofibrate is a fibric acid derivative, a prodrug comprising fenofibric acid linked to an isopropyl ester. Fenofibrate is rapidly hydrolyzed after oral ingestion to its pharmacologically active form, fenofibric acid. The effects of fenofibric acid seen in clinical practice have been explained in vivo in transgenic mice and in vitro in human hepatocyte cultures by the activation of peroxisome proliferator activated receptor α (PPARα)
It lowers lipid levels by activating peroxisome proliferator-activated receptor alpha (PPARα). PPARα activates lipoprotein lipase and reduces apoprotein CIII (an inhibitor of lipoprotein lipase activity), which increases lipolysis and elimination of triglyceride-rich particles from plasma. The resulting fall in triglycerides produces an alteration in the size and composition of LDL from small, dense particles (which are thought to be atherogenic due to their susceptibility to oxidation), to large buoyant particles. These larger particles have a greater affinity for cholesterol receptors and are catabolized rapidly
PPARα also increases apoproteins AI and AII, reduces VLDL- and LDL-containing apoprotein B, and increases HDL-containing apoprotein AI and AII. Fenofibrate also reduces serum uric acid levels in hyperuricemic and normal individuals by increasing the urinary excretion of uric acid.
Fenofibrate is a fibric acid derivative, a prodrug comprising fenofibric acid linked to an isopropyl ester. Fenofibrate is rapidly hydrolyzed after oral ingestion to its pharmacologically active form, fenofibric acid. The effects of fenofibric acid seen in clinical practice have been explained in vivo in transgenic mice and in vitro in human hepatocyte cultures by the activation of peroxisome proliferator activated receptor α (PPARα)
It lowers lipid levels by activating peroxisome proliferator-activated receptor alpha (PPARα). PPARα activates lipoprotein lipase and reduces apoprotein CIII (an inhibitor of lipoprotein lipase activity), which increases lipolysis and elimination of triglyceride-rich particles from plasma. The resulting fall in triglycerides produces an alteration in the size and composition of LDL from small, dense particles (which are thought to be atherogenic due to their susceptibility to oxidation), to large buoyant particles. These larger particles have a greater affinity for cholesterol receptors and are catabolized rapidly
PPARα also increases apoproteins AI and AII, reduces VLDL- and LDL-containing apoprotein B, and increases HDL-containing apoprotein AI and AII. Fenofibrate also reduces serum uric acid levels in hyperuricemic and normal individuals by increasing the urinary excretion of uric acid.
Fenofibrate is a fibric acid derivative, a prodrug comprising fenofibric acid linked to an isopropyl ester. Fenofibrate is rapidly hydrolyzed after oral ingestion to its pharmacologically active form, fenofibric acid. The effects of fenofibric acid seen in clinical practice have been explained in vivo in transgenic mice and in vitro in human hepatocyte cultures by the activation of peroxisome proliferator activated receptor α (PPARα)
It lowers lipid levels by activating peroxisome proliferator-activated receptor alpha (PPARα). PPARα activates lipoprotein lipase and reduces apoprotein CIII (an inhibitor of lipoprotein lipase activity), which increases lipolysis and elimination of triglyceride-rich particles from plasma. The resulting fall in triglycerides produces an alteration in the size and composition of LDL from small, dense particles (which are thought to be atherogenic due to their susceptibility to oxidation), to large buoyant particles. These larger particles have a greater affinity for cholesterol receptors and are catabolized rapidly
PPARα also increases apoproteins AI and AII, reduces VLDL- and LDL-containing apoprotein B, and increases HDL-containing apoprotein AI and AII. Fenofibrate also reduces serum uric acid levels in hyperuricemic and normal individuals by increasing the urinary excretion of uric acid.
Dosage & Administration
For adult patients with hypertriglyceridemia, the initial dose is 67 to 200 mg per day.
For the treatment of adult patients with hypercholesterolemia or mixed hyperlipidemia, the initial dose of Fenofibrate is 200 mg per day.
Dose should be individualized according to patient response. Fenofibrate should be given with meal there by, optimizing the bioavailability of the medication. Or, as directed by the registered physician.
Interactions
Oral Anticoagulants: Caution should be exercised when anticoagulants are given in conjunction with fenofibrate. The dosage of the anticoagulants should be reduced to maintain the prothrombin time at the desired level to prevent bleeding complications.
Resins: Since bile acid sequestrants may bind other drugs given concurrently, patients should take fenofibrate at least 1 hour before or 4-6 hours after a bile acid binding resin to avoid impending its absorption.
Cyclosporine: Because cyclosporine can produce nephrotoxicity with decreases in creatinine clearance and rises in serum creatinine, and because renal excretion is the primary elimination route of fibrate drugs including fenofibrate, there is a risk that an interaction will lead to deterioration.
Contraindications
Fenofibrate is contraindicated in patients with-
Hypersensitivity to fenofibrate or any component of this medication.
Known photoallergy or phototoxic reaction during treatment with fibrates or ketoprofen.
Severe liver dysfunction, gallbladder disease, biliary cirrhosis, severe renal disorders.
Chronic or acute pancreatitis with the exception of acute pancreatitis due to severe hypertriglyceridemia.
Pregnancy and lactation
Side-Effects
Digestive: hepatitis, cholelithiasis, cholecystitis, hepatomegaly
Musculoskeletal: myalgia, myasthenia, rhabdomyolysis
Skin and appendages: photosensitivity, eczema
Cardiovascular: peripheral edema, angina, palpitations, tachycardia, and migraine
Pregnancy
Pregnancy Category C. Fenofibrate should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
Nursing mothers: Fenofibrate should not be used in nursing mothers. Because of the potential for tumorigenicity seen in animal studies, a decision should be made whether to discontinue nursing or to discontinue the drug.
Precautions
Increased risk of cholelithiasis, pancreatitis, skeletal muscle effects. Patient at risk of
rhabdomyolysis. Renal impairment. Pregnancy.
Therapeutic Class
Fibrates
Storage Conditions
Store at cool & dry place. Protect from light and moisture.