Description : 
Fenofibrate is a lipid regulating agent. Fenofibric acid, the active metabolite of fenofibrate, produces reductions in total cholesterol, LDL cholesterol, apolipoprotein B, total triglycerides and triglyceride-rich lipoprotein (VLDL) in treated patients. In addition, treatment with fenofibrate results in increases in high density lipoprotein (HDL) and apoproteins apoAI and apoAII.

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 (alpha) [PPAR (alpha)]. Through this mechanism, fenofibrate increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apoprotein C-III (an inhibitor of lipoprotein lipase activity).

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. Activation of PPAR (alpha) also induces an increase in the synthesis of apoproteins A-I, A-II and HDL-cholesterol.

Treatment of Hypercholesterolaemia  : 
Fenofibrate is indicated as adjunctive therapy to diet for the reduction of LDL-C, Total-C, Triglycerides and Apo B and to increase HDL-C in adult patients with primary hypercholesterolaemia or mixed dyslipidaemia (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 (see National Cholesterol Education Program [NCEP] Treatment Guidelines, below).

TABLE. NCEP GUIDELINES FOR LIPID MANAGEMENT
Risk category LDL goal (mg/dl) LDL level at which to consider drug therapy (mg/dl) CHD or CHD risk equivalents* (10-yr risk>20%) <100 ≥ 130 (100-129: drug optional) 2+ risk factors ** (10-yr risk ≤ 20%) <130 10-yr risk 10%-20%: ≥ 130 10-yr risk <10%: ≥ 160 0-1 risk factor ** <160 ≥ 190 (160-189; LDL-lowering drug optional)

Coronary heart disease or peripheral vascular disease (including symptomatic carotid artery disease).

Other risk factors for coronary heart disease (CHD) include: age (males ≥ 45 years, females ≥ 55 years or premature menopause without estrogen replacement therapy); family history of premature CHD; current cigarette smoking; hypertension, confirmed HDL-C ≥ 40 mg/dL ( ≤ 0.91 mmol/L); and diabetes mellitus. Subtract 1 risk factor if HDL-C is ≥ 60 mg/dL ( ≥ 1.6 mmol/L).

Treatment of Hypertriglyceridaemia
Fenofibrate is also indicated as adjunctive therapy to diet for treatment of adult patients with hypertriglyceridaemia (Fredrickson Types IV and V hyperlipidemia).

Dosage And Administration :
Patients should be placed on an appropriate lipid-lowering diet before receiving fenofibrate, and should continue this diet during treatment with fenofibrate. Fenofibrate should be given with meals, thereby optimizing the bioavailability of the medication.

The recommended dosage in primary hypercholesterolemia or mixed hyperlipidemia is one Capsule once daily

Contraindications
* Hypersensitivity to fenofibrate
* Hepatic or severe renal dysfunction, including primary biliary cirrhosis, and patients
   With unexplained persistent liver function abnormality.
* Preexisting gallbladder disease

Warnings and Precautions
Drug Interactions
Oral Anticoagulants: 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.

HMG-CoA reductase inhibitors: 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.
The combined use of fibric acid derivatives and HMG-CoA reductase inhibitors has been associated with rhabdomyolysis, markedly elevated creatine kinase (CK) levels and myoglobinuria, leading in a high proportion of cases to acute renal failure.

Resins: Since bile acid sequestrants may bind other drugs given concurrently, patients should take fenofibrate Capsules, micronized, at least 1 hour before or 4-6 hours after a bile acid binding resin to avoid impeding 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. The benefits and risks of using fenofibrate with immunosuppressants and other potentially nephrotoxic agents should be carefully considered, and the lowest effective dose employed.

Liver Function :
Fenofibrate at doses equivalent to 107 mg to 160 mg per day has been associated with increases in serum transaminases [AST (SGOT) or ALT (SGPT)]. In a pooled analysis of 10 placebo-controlled trials, increases to > 3 times the upper limit of normal occurred in 5.3% of patients taking fenofibrate versus 1.1% of patients treated with placebo..

The incidence of increases in transaminase related to fenofibrate therapy appear to be dose-related.

Regular periodic monitoring of liver function, including serum ALT (SGPT) should be performed for the duration of therapy with Fenacor and therapy discontinued if enzyme levels persist above three times the normal limit.

Cholelithiasis
Fenofibrate, like clofibrate and gemfibrozil, may increase cholesterol excretion into the bile, leading to cholelithiasis. If cholelithiasis is suspected, gallbladder studies are indicated. Fenacor therapy should be discontinued if gallstones are found.

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 creatine 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.

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

Renal impairment
Fenofibric acid is known to be substantially excreted by the kidney, and the risk of adverse reactions to this drug may be greater in patients with impaired renal function. The dosage of fenofibrate should be minimized in patients of severe renal impairment, while no modification of dosage is required in patients having moderate renal impairment. Hence Fenacor 160 mg is not recommended for use in patients of severe renal impairment.

Pregnancy
Category C
Fenofibrate has been shown to be embryocidal and teratogenic in rats when given in doses 7 to10 times the maximum recommended human dose and embryocidal in rabbits when given at 9 times the maximum recommended human dose (on the basis of mg/m 2 surface area).
There are no adequate and well-controlled studies in pregnant women. Fenofibrate should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Lactation
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.
Pediatric Use
Safety and efficacy in pediatric patients have not been established.

Geriatric use
Fenofibric acid is known to be substantially excreted by the kidney, and the risk of adverse reactions to this drug may be greater in patients with impaired renal function. Because elderly patients are more likely to have decreased renal function, care should be taken.

Side effects
The drug is generally well tolerated. Reported side effects include hepatitis, cholelithiasis, cholecystitis, hepatomegaly, myalgia, myasthenia, rhabdomyolysis, photosensitivity and eczema.

Overdosage
There is no specific treatment for overdose with fenofibrate. General supportive care of the patient is indicated, including monitoring of vital signs and observation of clinical status, should an overdose occur. If indicated, elimination of unabsorbed drug should be achieved by emesis or gastric lavage; usual precautions should be observed to maintain the airway. Because fenofibrate is highly bound to plasma proteins, hemodialysis should not be considered.

Presentation :
Fenacor-160 Blister of 10 Capsules
Fenacor-200 Blister of 7 Capsules

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