Berafen Special Precautions

Fenofibrates should not be given to patients with severe hepatic impairment or significant liver disease, gallstones or gallbladder disorders or hypoalbuminaemic states such as nephrotic syndrome. It should be used with caution in renal impairment and is contraindicated if creatinine clearance is below 15 mL/minute unless the patient is on dialysis.
Secondary causes of hyperlipidaemia: Secondary causes of hyperlipidaemia, such as uncontrolled type 2 diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinemia, obstructive liver disease, pharmacological treatment and alcoholism should be adequately treated before Fenofibrate therapy is initiated. Secondary cause of hypercholesterolemia related to pharmacological treatment can be seen with diuretics, β-blocking agents, estrogens, progestogens, combined oral contraceptives, immunosuppressive agents and protease inhibitors. In these cases, it should be ascertained whether the hyperlipidaemia is of primary or secondary nature (possible elevation of lipid values caused by these therapeutic agents).
Renal function: Fenofibrate 200 mg capsules are contraindicated in severe renal impairment.
Fenofibrate 200 mg capsules should be used with caution in patients with mild to moderate renal insufficiency. Dose should be adjusted in patients whose estimated glomerular filtration rate is 30 to 59 mL/min/1.73 m².
Reversible elevations in serum creatinine have been reported in monotherapy or co-administered with statins. Elevations in serum creatinine were generally stable overtime with no evidence for continued increases in serum creatinine with long term therapy and tended to return to baseline following discontinuation of treatment.
During clinical trials, 10% of patients had a creatinine increase from baseline greater than 30 μmol/L with co-administered Fenofibrate and simvastatin versus 4.4% with statin monotherapy. 0.3% of patients receiving co-administration had clinically relevant increases in creatinine to values >200 μmol/L.
Treatment should be interrupted when creatinine level is 50% above the upper limit of normal. It is recommended that creatinine is measured during the first 3 months after initiation of treatment and periodically thereafter.
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 discontinued if AST (SGOT) and ALT (SGPT) levels increase to more than 3 times the upper limit of the normal range. When symptoms indicative of hepatitis occur (e.g., jaundice, pruritus) and diagnosis is confirmed by laboratory testing, Fenofibrate therapy should be discontinued.
Pancreas: Pancreatitis has been reported in patients taking Fenofibrate. This occurrence may represent a failure of efficacy in patients with severe hypertriglyceridaemia, a direct drug effect, or a secondary phenomenon mediated through biliary tract stone or sludge formation, resulting in the obstruction of the common bile duct.
Muscle: Muscle toxicity, including very rare cases of rhabdomyolysis, with or without renal failure has been reported with administration of fibrates and other lipid-lowering agents. The incidence of this disorder increases in cases of hypoalbuminaemia and previous renal insufficiency. Patients with pre-disposing factors for myopathy and/or rhabdomyolysis, including ages 70 years, personal or familial history of hereditary muscular disorders, renal impairment, hypothyroidism and high alcohol intake, may also be at an increased risk of developing rhabdomyolysis. For these patients, the putative benefits and risks of Fenofibrate therapy should be carefully weighed up.
Muscle toxicity should be suspected in patients presenting diffuse myalgia, myositis, muscular cramps, and weakness and/or marked increases in CPK (levels exceeding 5 times the normal range). In such cases, treatment with Fenofibrate should be stopped.
The risk of muscle toxicity may be increased if the drug is administered with another fibrate or an HMG-CoA reductase inhibitor, especially in cases of pre-existing muscular disease. Consequently, the co-prescription of Fenofibrate with an HMG-CoA reductase inhibitor or another fibrate should be reserved to patients with severe combined dyslipidaemia and high cardiovascular risk without any history of muscular disease and a close monitoring of potential muscle toxicity.
This medicine contains lactose. Patients with rare hereditary problems of galactose intolerance, total lactase deficiency or glucose-galactose malabsorption should not take this medicine.