Indicated for:

Treatment of Hypercholesterolemia:

• Adjunctive therapy to diet for the reduction of LDL-C, total-C, Triglycerides and apo B in adult patients with primary hypercholesterolemia or mixed dyslipidemia (Fredrickson Types IIa and IIb). Lipid altering agents should be used in addition to a diet restricted in saturated fat and cholesterol when response to diet and non-pharmacological interventions alone has been inadequate.

Treatment of Hypertriglyceridemia:

• Adjunctive therapy to diet for treatment of adult patients with hypertriglyceridemia (Fredrickson Types IV and V hyperlipidemia). Improving glycemic control in diabetic patients showing fasting chylomicronemia will usually reduce fasting triglycerides and eliminate chylomicronemia thereby obviating the need for pharmacologic intervention.

Drug therapy is not indicated for patients with Type I hyperlipoproteinemia, who have elevations of chylomicrons and plasma triglycerides, but who have normal levels of very low density lipoprotein (VLDL).

Therapy should be withdrawn in patients who do not have an adequate response after 2 months of treatment with the maximum recommended dose of 200 mg per day.

Markedly elevated levels of serum triglycerides (e.g., > 2000 mg/dL) may increase the risk of developing pancreatitis. The effect of fenofibrate therapy on reducing this risk has not been adequately studied.

LOFIBRA is contraindicated in patients with hepatic or severe renal dysfunction, including primary biliary cirrhosis and patients with unexplained persistent liver function abnormality.

LOFIBRA is contraindicated in patients with preexisting gallbladder disease.

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 above 3 times the normal limit.

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.

The use of fibrates alone, including fenofibrate capsules may occasionally be associated with myositis, myopathy or rhabdomyolysis. Patients receiving fenofibrate and complaining of muscle pain, tenderness or weakness should have prompt medical evaluation for myopathy, including serum creatine kinase level determination. If myopathy/myositis is suspected or diagnosed, fenofibrate therapy should be stopped.

Anaphylaxis and angioedema have been reported postmarketing with fenofibrate. In some cases, reactions were life-threatening and required emergency treatment.

Severe cutaneous adverse drug reactions (SCAR), including Stevens-Johnson Syndrome, Toxic Epidermal Necrolysis, and Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS), have been reported postmarketing, occurring days to weeks after initiation of fenofibrate.

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.

Pulmonary embolus (PE) and deep vein thrombosis (DVT) were observed at higher rates in the fenofibrate than the placebo-treated group.

Elevations in serum creatinine have been reported in patients on fenofibrate.

Caution should be exercised when coumarin anticoagulants are given in conjunction with fenofibrate.The dosage of the anticoagulants should be reduced to maintain the prothrombin time/inr at the desired level to prevent bleeding complications. Frequent prothrombin time/inr determinations are advisable until it has been definitely determined that the prothrombin time/inr has stabilized.

The combined use of fenofibrate and HMG-CoA reductase inhibitors should be avoided unless the benefit of further alterations in lipid levels is likely to outweigh the increased risk of this drug combination.

Since bile acid sequestrants may bind other drugs given concurrently, patients should take fenofibrate at least one hour before or 4 to 6 hours after a bile acid binding resin to avoid impeding its absorption.

Pancreatitis has been reported in patients taking fenofibrate, gemfibrozil and clofibrate.

–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.

Safety in pregnant women has not been established. Animal studies: maternal toxicity.

It is not known whether fenofibrate is excreted into milk. Because many drugs are excreted in human milk and because of the potential for serious adverse reactions in nursing infants from fenofibrate, a decision should be made whether to discontinue nursing or administration of fenofibrate taking into account the importance of the drug to the lactating woman.

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• Use in patients under the age of 18. GoToSource 

• Dosage greater than 200 mg per day. GoToSource

• Management of diabetic macular edema. GoToSource

• Diabetic peripheral neuropathy. GoToSource 

• Inhibit cell proliferation in TP53 wild type and deficient lung cancer cells. GoToSource 

• Erosive hand osteoarthritis. GoToSource

• Bone xanthoma. GoToSource

• Gout. GoToSource

• Improve hyperglycemia and insulin resistance, improve wound healing and reduce apoptosis and oxidative stress in severely burned patients. GoToSource

• Nonalcoholic fatty liver disease. GoToSource

Acute pancreatitis (inflammation of pancreas). GoToSource

Rhabdomyolysis (destruction of skeletal muscle). GoToSource

Increased risk of gallstone disease. GoToSource

Lichenoid drug eruption. GoToSource

Generalized exanthematous pustulosis (severe skin reaction). GoToSource  

Hepatitis (inflammation of the liver) and cholestatic hepatitis (decrease in bile flow). GoToSource

Polymyositis (inflammation of muscles). GoToSource

Myopathy (disease of muscle tissue). GoToSource

Thrombocytopenia (deficiency of platelets in the blood). GoToSource

Anemia and neutropenia (low levels of neutrophils, a type of white blood cell). GoToSource

Venous thrombosis (blood clot that forms within a vein) and pulmonary embolism (blockage in one of the pulmonary arteries in lungs). GoToSource

Constipation. GoToSource

Asthenia (abnormal weakness or lack of energy), hyperthermia (high body temperature) and pancytopenia (too few blood cells, red blood cells, white blood cells and platelets). GoToSource 

Photosensitivity (extreme sensitivity to ultraviolet rays). GoToSource

Decline in visual memory. GoToSource

Higher risk of cardiovascular events or death in patients with diabetes. GoToSource

Nephrotoxicity (kidney damage). GoToSource

Lawsuits filed for liver damage, memory loss, muscle damage, cardiomyopathy and diabetes.