FENOFIBRATE

Dietary measures initiated before therapy should be continued. Response to therapy should be monitored by determination of serum lipid values. If after several months of fenofibrate administration serum lipid levels have not been reduced satisfactorily, complementary or different therapeutic measures should be considered.

Posology Adults Recommended daily dose:

One film-coated tablet (containing 160 mg fenofibrate) daily. Patients taking fenofibrate 200 mg capsules (one capsule daily) can be changed to [product name] (one film-coated tablet daily) without further dose adjustment. Elderly patients (≥ 65 years) No dose adjustment is necessary.

73 m2 (see “Patients with renal impairment”). 73 m2 is present. 73 m2, the dose of fenofibrate should not exceed 100 mg standard or 67 mg micronized once daily. 73 m2, fenofibrate should be discontinued.

Hepatic impairment:

Fenofibrate 160 mg is not recommended for use in patients with hepatic impairment due to the lack of data. Paediatric population The safety and efficacy of fenofibrate in children and adolescents younger than 18 years has not been established.

No data are available. Therefore, the use of fenofibrate is not recommended in paediatric patients under 18 years. g. a glass of water).

The most commonly reported ADRs during fenofibrate therapy are digestive or gastrointestinal disorders. The following undesirable effects have been observed during placebo- controlled clinical trials (n=2,344) and post-marketing a with the below indicated frequencies: The frequencies used in the following table are: common (≥ 1/100, < 1/10), uncommon (≥ 1/1,000, < 1/100), rare (≥1/10,000, < 1/1,000), not known (frequency cannot be estimated from the available data).

g. g. g. 031). 074). 5 μmol/L, and was reversible on discontinuation of fenofibrate treatment. The increased risk of venous thrombotic events may be related to the increased homocysteine level. The clinical significance of this is not clear.

Reporting of suspected adverse reactions Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. uk/yellow

Secondary causes of hyperlipidemia Secondary cause of hypercholesteria, such as uncontrolled type 2 diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinemia, obstructive liver disease or alcoholism should be adequately treated before fenofibrate therapy is considered.

Secondary cause of hypercholesteria 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).

Liver As with other lipid lowering agents, increases have been reported in transaminase levels in some patients during treatment with fenofibrate. 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. g. jaundice, pruritus), and diagnosis is confirmed by laboratory testing, fenofibrate therapy should be discontinued.

8). 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, resulting in the obstruction of the common bile duct.

Muscle Muscle toxicity, including 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, as well as patients above 70 years of age, personal or familial history of hereditary muscular disorders, renal impairment, hypothyroidism and high alcohol intake, may be at an increased risk of developing rhabdomyolysis.

For those 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 creatinine phosphokinase CPK (levels exceeding 5 times the upper limit of 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 combination of fenofibrate with a HMG-CoA reductase inhibitor or another fibrate should be reserved to patients with severe combined hyperlipidaemia and high cardiovascular risk without any history of muscular disease and with a close monitoring of potential muscle toxicity.

3). Fenofibrate should be used with caution in patients with mild to moderate renal insufficiency. 2). Reversible elevations in serum creatinine have been reported in patients receiving fenofibrate monotherapy or co-administered with statins.

Elevations in serum creatinine were generally stable over time with no evidence for continued increases in serum creatinine with long term therapy and tended to return to baseline following discontinuation of treatment. 4 % with statin monotherapy.

3 % of patients receiving co- administration therapy had clinically relevant increases in creatinine to values > 200 μmol/L. Treatment should be interrupted when the 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.

Fenofibrate 160 mg film-coated tablets contains lactose and sodium. Patients with rare hereditary problems of galactose intolerance, total lactase deficiency or glucose-galactose malabsorption should not take this medicine. This medicine contains less than 1 mmol sodium (23 mg) per film-coated tablet, that is to say essentially ‘sodium-free’.

1. − hepatic insufficiency (including biliary cirrhosis and unexplained persistent liver function abnormality). − known gall bladder disease. − severe renal insufficiency (estimated glomerular filtration rate < 30 mL/min per 1,73 m2).

− chronic or acute pancreatitis with the exception of acute pancreatitis due to severe hypertriglyceridemia. − known photoallergy or phototoxic reaction during treatment with fibrates or ketoprofen