Fenostad 67

Rx

Indication:

Fenostad 67 is indicated as an adjunct to diet and other non-pharmacological treatment (e.g. exercise, weight reduction) for the following:

• Treatment of severe hypertriglyceridaemia with or without low HDL cholesterol.
• Mixed hyperlipidaemia when a statin is contraindicated or not tolerated.
• Mixed hyperlipidaemia in patients at high cardiovascular risk in addition to a statin when triglycerides and HDL cholesterol are not adequately controlled.

Dosage:

Adults

The recommended dose is 200 mg daily administered as 1 capsule of Fenostad 67 TID.

The dose can be titrated up to 267 mg daily administered as 1 capsule of Fenostad 67 QID, if required. This maximum dose is not recommended in addition to a statin.

Elderly patients (≥ 65 years old): No dose adjustment is necessary, except for decreased renal function with eGFR < 60 mL/min/1.73 m².

Renal impairment: eGFR < 30 mL/min per 1.73 m²: should not use. eGFR is between 30 and 59 mL/min per 1.73 m²: £ 100 mg standard or 67 mg micronized once daily. If the eGFR decreases persistently to < 30 mL/min per 1.73 m², fenofibrate should be discontinued.

Hepatic impairment: Not recommended for use.

Paediatric population: One capsule (67 mg) micronised fenofibrate/day/20 kg body weight.

Usage:

Fenostad 67 should be swallowed whole during a meal.

• Hypersensitivity to any of the active substance or excipients.
• Hepatic insufficiency.
• Known gallbladder disease.
• Severe renal insufficiency.
• 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.

Common: Abdominal pain, nausea, vomiting, diarrhoea, flatulence, transaminases increased, blood homocysteine level increased.

Secondary causes of hyperlipidemia: Uncontrolled type 2 diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinemia, obstructive liver disease, pharmacological treatment, alcoholism, should be adequately treated before fenofibrate therapy is considered. 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).

Liver function: 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.

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 putative benefits and risks of fenofibrate therapy should be carefully weighed up in patients with pre-disposing factors for myopathy and/or rhabdomyolysis, including age above 70 years, personal or familial history of hereditary muscular disorders, renal impairment, hypothyroidism and high alcohol intake.
• Fenofibrate should be stopped in patients presenting diffuse myalgia, myositis, muscular cramps and weakness and/or marked increases in creatine phosphokinase (CPK) (levels exceeding 5 times the normal range).
• 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 preexisting muscular disease. Consequently, the co-prescription of fenofibrate with a 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.

Renal function

• Fenostad 67 are contraindicated in severe renal impairment.
• 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 in patients receiving fenofibrate monotherapy or co-administered with statins.
• 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.

In children: Only an hereditary disease (familial hyperlipidaemia) justifies early treatment, and the precise nature of the hyperlipidaemia must be determined by genetic and laboratory investigations. It is recommended to begin treatment with controlled dietary restrictions for a period of at least 3 months. Proceeding to medicinal treatment should only be considered after specialist advice and only in severe forms with clinical signs of atherosclerosis and/or xanthomata and/or in cases where patients suffer from atherosclerotic cardiovascular disease before the age of 40.

Excipients: This drug contains sucrose (sugar spheres). Patients with rare hereditary problems of fructose intolerance, glucose-galactose malabsorption or sucrase-isomaltase insufficiency should not take this medicine.

Fenostad 67 should only be used during pregnancy after a careful benefit/risk assessment. Fenofibrate should not be used during breast-feeding. Patients should be aware of how they react to drug before driving or operating machinery.