LIPANTHYL SUPRA Tablet

Hypercholesterolaemia and hypertriglyceridaemia alone or combined (typesⅡa, Ⅱb, Ⅳdyslipidaemias, as well as typesⅢand Ⅴdyslipidaemias) in patient s unresponsive to dietary and other non-drug therapeutic measures (e.g. weight reduction or increased physical activity), particularly when there is evidence of associated risk factors such as hypertension and smoking.

The treatment of secondary hyperlipoproteinaemias is indicated if the hyperlipoproteinaemia persists despite effective treatment of the underlying disease (e.g. dyslipidaemia in diabetes mellitus).

Dietary measures initiated before therapy should be continued.

Dosage

Adults: 160mg daily.

Elderly patients: without renal impairment, the usual adult dose is recommended

Patients with renal impairment: see the package insert about the details.

Children: the use of the 160mg dosage from is contraindicated.

Patients with hepatic impairment: see the package insert about the details.

Method of administration:

Tablets should be swallowed whole during a meal.

In children,

During pregnancy or lactation

In patients with liver insufficiency (including biliary cirrhosis and unexplained persistent liver function abnormality),

Severe chronic kidney diseases

IN patients hypersensitive to fenofibrate and/or excipients

Known photo allergy or phototoxic reaction during treatment with fibrates or ketoprofen

Chronic or acute pancreatitis with the exception of acute pancreatitis due to severe hypertriglyceridemia

Known gallbladder disease

In patients allergic to peanut or arachis oil or soya lecithin or related products due to the risk of hypersensitivity reactions.

Gastrointestinal disorders

Common: digestive, gastric or intestinal disorders (abdominal pain, nausea, vomiting, diarrhoea, and flatulence)

Uncommon: pancreatitis

Hepato-biliary disorders

Common: moderately elevated levels of serum transaminases.

Uncommon: cholelithiasis

Rare: episodes of hepatitis. When symptoms (e.g. jaundice, pruritus) indicative of hepatitis occur, laboratory tests are to be conducted for verification and fenofibrate discontinued, if applicable.

Skin and subcutaneous tissue disorders

Uncommon: rashes, pruritus, urticaria.

Rare: alopecia, cutaneous photosensitivity reactions with erythema, vesiculation or nodulation on parts of the skin exposed to sunlight or artificial UV light (e.g. sunlamp) in individual cases (even after many months of uncomplicated use)

Musculoskeletal, connective tissue and bone disorders

Uncommon: diffuse myalgia, myositis, muscular cramps and weakness

Not known: rhabdomyolysis

Cardiovascular system

Uncommon: thromboembolism (pulmonary embolism, deep vein thrombosis)

Blood and lymphatic system disorders

Rare: decrease in haemoglobin and leukocytes

Nervous system disorders

Uncommon: sexual asthenia, headache

Respiratory, thoracic and mediastinal disorders

Now known: interstitial pneumopathies

Hepatobiliary disorders

Jaundice, complications of cholelithiasis (e.g. cholecystitis, cholangitis, biliary colic)

Investigation:

Uncommon: increases in serum creatinine and urea.

Skin and Subcutaneous Tissue Disorders: severe cutaneous reactions (e.g. erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis)

See the package insert about the details below:

Oral anticoagulants

Cyclosporin

HMG-CoA reductase inhibitors and other fibrates

Glitazones

CYP450 enzymes

Pregnancy

There are no adequate data from the use of fenofibrate in pregnant women.

Fenofibrate should only be used during pregnancy after a careful benefit/risk assessment.

Lactation

Fenofibrate should not be used during breast-feeding.

Secondary cause of hypercholesterolemia, such as uncontrolled type 2 diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinemia, obstructive liver disease, pharmacological treatment, alcoholism, should be adequately treated before fenofibrate therapy is initiated.

Response to therapy should be monitored by determination of serum lipid values (total cholesterol, LDL-cholesterol, triglycerides), if an adequate response has not been achieved after several months (e.g. 3 months) complementary or different therapeutic measures should be considered.

For hyperlipidaemic patients taking estrogens or contraceptives containing oestrogens it should be ascertained whether the hyperlipidaemia is of primary or secondary nature (possible hyperlipidaemia is of primary or secondary nature (possible elevation of lipid values caused by oral oestrogen).

See the package insert about the details below:

Liver function

Pancreatitis

Muscle

Serum Lipid Reducing Agents/Cholesterol and Triglycerides Reducers/Fibrates

Fenofibrate is a fibric acid derivative whose lipid modifying effects reported in humans are mediated via activation of Peroxisome Proliferator Activated Receptor type alpha (PPARα).

Through activation of PPARα, fenofibrate increases the lipolysis and elimination of atherogenic triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apoprotein CⅢ. Activation of PPARα also induces an increase in the synthesis of apoproteins AⅠand AⅡ.

The above stated effects of fenofibrate on lipoproteins lead to a reduction in very low- and low density fractions (VLDL and LDL) containing apoprotein B and an increase in the high density lipoprotein fraction (HDL) containing apoprotein AⅠand AⅡ.

In addition, through modulation of the synthesis and the catabolism of VLDL fractions, fenofibrate increases the LDL clearance and reduces small and dense LDL, the levels of which are elevated in the atherogenic lipoprotein phenotype, a common disorder in patients at risk for coronary heart disease.

At the present time, no results of long-term controlled clinical trials are available to demonstrate the efficacy of fenofibrate in the primary or secondary prevention of atherosclerotic complications.

Extravascular deposits of cholesterol (tendinous and tuberous xanthoma) may be markedly reduced or even entirely eliminated during fenofibrate therapy.

Patients with raised levels of fibrinogen treated with fenofibrate have shown significant reductions in this parameter, as have those with raised levels of Lp(a).

Other inflammatory markers such as C Reactive Protein are reduced with fenofibrate treatment.

The uricosuric effect of fenofibrate leading to reduction in uric acid levels of approximately 25% should be of additional benefit in those dyslipidaemic patients with hyperuricaemia.

Fenofibrate has been shown to possess an anti-aggregatory effect on platelets in animas and in a clinical study, which showed a reduction in platelet aggregation induced by ADP, arachidonic acid and epinephrine.