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145-mg: Secondary cause of hypercholesterolemia eg, as uncontrolled type 2 diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinemia, obstructive liver disease, pharmacological treatment, alcoholism, should be adequately treated before fenofibrate is initiated.
For hyperlipidaemic patients taking estrogens or contraceptives containing oestrogens it should be ascertained whether the hyperlipidaemia is of primary or secondary nature (possible elevation of lipid values caused by oral oestrogen).
Liver Function: As with other lipid lowering agents, increases have been reported in transaminase levels in some patients. In the majority of cases these elevations were transient, minor and asymptomatic. It is recommended that transaminase levels are monitored every 3 months during the first 12 months of treatment and thereafter, periodically. Attention should be paid to patients who develop increase in transaminase levels and therapy should be discontinue if [aspartate aminotransferase (ASAT) serum glutamic oxaloacetic transaminase (SGOT)] and alanine aminotransferase (ALAT) [serum glutamic pyruvic transaminase (SGPT)] levels increase to >3 times the upper limit of normal range. When symptoms indicative of hepatitis occur (eg, jaundice, pruritus), laboratory tests are to be conducted for verification and discontinuation of fenofibrate therapy may be considered.
Pancreas: Pancreatitis has been reported in patients taking fenofibrate. This occurrence may represent a failure of efficacy in patients with severe hypertriglyceridemia, a direct drug effect or a secondary phenomenon mediated through biliary tract stone or sludge formation with obstruction of the common bile duct.
Muscle: Muscle toxicity, including very rare cases of rhabdomyolysis, has been reported with administration of fibrates and other lipid-lowering agents. Patients with hypoalbuminemia and renal insufficiency in their personal history have a higher incidence of myotoxicity. Muscle toxicity should be suspected in patients presenting diffuse myalgia, myositis, muscular cramps and weakness and/or marked increases creatinine phosphokinase (CPK) (levels exceeding 5 times the upper normal range). In such cases treatment with fenofibrate should be stopped.
Patients with pre-disposing factors for myopathy and/or rhabdomyolysis including >70 years, personal or familial history of hereditary muscular disorders, renal impairment, hypoalbuminaemia, hypothyroidism ang high alcohol intake, may be at increased risk of developing rhabdomyolysis. For these patients, the putative benefits and risk of fenofibrate therapy should be carefully weighed up.
The risk of muscle toxicity may be increased if Colestrim Supra is administered with another fibrate or an HMG-CoA reductase inhibitor (statins), especially in cases of preexisting muscular disease. Consequently, the co-prescription of fenofibrate with a statin should be reserved to patients with severe combined dyslipidemia and high cardiovascular risk without any history of muscular disease. This combination therapy should be used with caution and patients should be monitored closely for signs of muscle toxicity.
Renal Function: Treatment should be interrupted in case of an increase in creatinine levels >50% and upper limit of normal (ULN). It is recommended that creatinine is measured during the first 3 months after initiation of treatment and thereafter, periodically. Colestrim Supra contains lactose therefore, patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency of glucose-galactose malabsorption should not take Colestrim Supra.
Colestrim Supra contains sucrose therefore, patients with rare hereditary problems of fructose intolerance, glucose-galactose malabsorption of sucrase-isomaltase insufficiency should not take Colestrim Supra.
Colestrim Supra tablet should not be taken in patients allergic to soya lecithin or related due to the risk of hypersensitivity reactions.
160-mg: Initial Therapy: Laboratory studies should be done to ascertain that the lipid levels are consistently abnormal before instituting fenofibrate therapy. Every attempt should be made to control serum lipids with appropriate diet, exercise, weight loss in obese patients and control of any medical problems eg, diabetes mellitus and hypothyroidism that are contributing to the lipid abnormalities. Medications known to exacerbate hypertriglyceridemia (blockers, thiazides, estrogens) should be discontinued or changed if possible, prior to consideration of triglyceride lowering the drug therapy.
Continued Therapy: Periodic determination of serum lipids should be obtained during the initial therapy in order to establish the lowest effective dose of fenofibrate. Therapy should be withdrawn in patients who do not have an adequate response after 2 months of treatment with the maximum recommended dose of 160 mg/day.
Pancreatitis: Pancreatitis has been reported in patients taking fenofibrate, gemfibrozil and clofibrate. The occurrence may represent a failure of efficacy in patients with severe hypertriglyceridemia, a direct drug effect, or a secondary phenomenon medicated through biliary tract stone or sludge formation with obstruction of the common bile duct.
Hypersensitivity Reactions: Acute hypersensitivity reactions include severe skin rashes requiring patient hospitalization and treatment with steroids have occurred very rarely during treatment with fenofibrate, including rare spontaneous reports of Stevens-Johnson syndrome and toxic epidermal necrolysis.
Hematological Changes: Mild to moderate hemoglobin, hematocrit and white blood cell decreases have been observed in patients following initiation of fenofibrate therapy. However, these levels stabilize during long-term administration. Extremely rare spontaneous reports of thrombocytopenia and agranulocytosis have been received during post-marketing surveillance. Periodic blood counts are recommended during the first 12 months of fenofibrate administration.
Liver Function: Fenofibrate at doses equivalent to 107-160 mg/day has been associated with increase in serum transaminases. When transaminase determinations were followed either after discontinuation treatment or during continued treatment, a return to normal limits was usually observed. The incidence of increase in transaminases related to fenofibrate therapy appears to be dose-related.
Hepatocellular, chronic active and cholestatic hepatitis associated with fenofibrate therapy have been reported after exposure to weeks to several years. In extremely rare cases, cirrhosis has been reported in association with chronic active hepatitis. Regular periodic monitoring of liver function including serum ALT (SGPT) should be performed for the duration of therapy with fenofibrate and therapy discontinued if enzyme levels persist >3 times the normal limit.
Skeletal Muscle: The use of fibrates alone, including fenofibrate may occasionally be associated with myopathy. Treatment with drugs of the fibrate class has been associated on rare occasions with rhabdomyolysis, usually in patients with impaired renal function. Myopathy should be considered in any patient with diffuse myalgias, muscle tenderness or weakness, and/or marked elevations of creatinine phosphokinase levels. Patients should be advised to report promptly unexplained muscle pain, tenderness or weakness, particularly if accompanied by malaise or fever. CPK levels should be assessed in patients reporting these symptoms and fenofibrate therapy should be discontinued if markedly elevated CPK levels occur or myopathy is diagnosed.
Cholelithiasis: Fenofibrate, like clofibrate and gemfibrozil, may increase cholesterol excretion into the bile, leading to cholelithiasis. If cholelithiasis is suspected, gallbladder studies are indicated; fenofibrate therapy should be discontinued if gallstones are found.
Special Populations: Renal Impairment: The use of Colestrim Supra should be avoided in patients who have severe renal impairment. Dose reduction is required in patients with mild to moderate renal impairment. Monitoring renal function in patients with renal impairment is recommended.
Hepatic Impairment: The use of Colestrim Supra has not been evaluated in subjects with hepatic impairment.
Effects on the Ability to Drive or Operate Machinery: Fenofibrate tablets 145 mg has no influence on the ability to drive and use machines.
Use in pregnancy: Pregnancy Category C: Safety in pregnant women has not been established. There are no adequate and well-controlled studies of fenofibrate in pregnant women. Fenofibrate should not be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
Use in lactation: Fenofibrate should not be used in nursing mothers. A decision should be made whether to discontinue Colestrim, taking into account the importance of Colestrim to the mother.
Use in children: Safety and effectiveness have not been established in pediatric patients.
Use in the elderly: Fenofibric acid is known to be substantially excreted by the kidney and the risk of adverse reactions to Colestrim Supra may be greater in patients with impaired renal function. Fenofibric acid exposure is not influenced by age. Since elderly patients have a higher incidence of renal impairment, dose selection for the elderly should be made on the basis of renal function. Elderly patients with normal renal function should require no dose modifications. Consider monitoring renal function in elderly patients taking Colestrim Supra.
