Hafenthyl 200 Hasan drugs for hypercholesteroline blood cholesterol (5 blisters x 10 tablets)

The three types of ppar participating in this process are α, β and γ. Fibrat associated with pparα mainly in the liver and adipose tissue, less in the kidneys, heart and skeletal muscles. Fibrat decreases triglycerides by stimulating through pparα intermediaries of fatty acid oxidation, increasing lipoprotein lipase synthesis, and reducing APOC-LLL's expression. The increase in lipoprotein lipase will increase the clearance of lipoprotein rich triglycerides.

The reduction of the APOC-LLL production in the liver will increase the clearance of lipoprotein very low density (VLDL) and low density lipoprotein (LDL).

High density fibrats increase lipoprotein levels (HDL) due to the activation of pparα, increasing the synthesis of APOA-L and APOA-LL.

Fenofibrat can reduce 20-25% of total cholesterol and 40-50% of triglycerides in the blood. Fenofibrat treatment needs to be continuous. There is a decrease in cholesterol of low density and very low density lipoprotein (LDL, VLDL) which are components that cause atherosclerosis and increase cholesterol of high density lipoprotein (HDL).

The relationship between blood cholesterol and atherosclerosis has been established, and the relationship between atherosclerosis and the risk of coronary artery. HDL concentration is associated with high coronary risk. High triglyceride concentration is also associated with increased cardiovascular risk.

There is evidence that the treatment of fibrats may reduce the risk of coronary artery events, but have not yet been found to decrease death in primary or secondary prevention of cardiovascular disease.

Although fibrats can reduce the risk of coronary events in humans with low HDL-cholesterol or high triglycerides, the first Statin (HMG-CoA Reductase inhibitor) should be used first.

Fibrats are only the leading treatment for patients with blood triglycerides higher than 10 mmol/iodine or non -tolerated persons.

Fenofibrat also reduces blood uric acid in normal people and people with hyperuricemiaemia due to increased urine elimination of urine.

Fenofibrat can also reduce platelet aggregation and reduce blood uric acid

pharmacokinetics

absorption:

Fenofibrat is well absorbed in the digestive tract. The maximum concentration in plasma (CMAX) reached 2-4 hours after taking the drug. The concentration of drugs in plasma is stable when treated continuously in all individuals.

The peak concentration in plasma and the total exposure of Fenofibrat does not depend on the meal. Therefore, it is possible to take the medicine regardless of the meal.

Distribution:

about 99% fenofibrate in the blood combined with plasma proteins.

Metabolism:

After drinking, Fenofibrat is quickly hydrolyzed by esterase into active metabolites of fenofibric acid, mainly in combination with glucuronic acid. Fenofibrat does not metabolize through the liver microsom. There is no metabolic form in plasma. Fenofibrat is not the substrate of CYP3A4.

Era:

Fenofibrat is eliminated in the urine (60%) in the form of metabolites and feces (about 25%) all drugs are eliminated within 6 days, in people with normal kidney function, the selling time is about 20 hours but this time increases greatly in patients with kidney disease and fenofibric acid accumulated in patients with fenofibrat drinks daily, in the elderly patient, the total amount Fenofibric in plasma does not change.

Research on dynamics after drinking single dose and continuous treatment shows that this drug is not accumulated.

What to do when overdose?

How to handle: There is no specific antidote. Symptomatic treatment should be treated and taken supportive measures in cases of overdose. Hemorrhage does not have the effect of eliminating the body from the body.

What to do when you forget a dose? However, if close to the next dose, skip the forgotten dose and take the next dose at the time as planned. Note that it should not be used double the prescribed dose.

Be cautious when using

necessarily explore the patient's liver and kidney function before starting Fibrat.

Secondary causes of hyperemia: secondary causes of hyperemia such as type 2 diabetes without control, hypothyroidism, nephrotic syndrome, blood protein disorders, clogged liver disease, drug or alcoholic treatment should be fully treated before using fenofibrat.

Secondary cause causes hyperchemical hyperkemin related to known drug treatment such as diuretics, beta, estrogen, progestogen, combined oral contraceptives, immune inhibitors and protease inhibitors. In these cases, it is necessary to determine the hyperlipidemia that is primary or secondary (can quantify the lipid values ​​caused by these treatment agents)

In patients with anticoagulant drugs: When starting to use fibrat, it is necessary to reduce the anticoagulant dose to only one third of the old dose and adjust the dose if necessary. Need to monitor more frequent amount of blood prothrombin. Adjust the anticoagulant dose during use and after stopping Fibrat 8 days.

Armor weakness can be a factor that increases the likelihood of side effects in muscle.

Need to measure transaminase every 3 months, in the first 12 months of taking the drug and periodically. Pay attention to patients increasing transaminase concentrations and discontinuing treatment if AST (SGOT) and ALT (SGPT) concentration increases 3 times higher than the normal level of the above limit. When there are signs of hepatitis (jaundice, itching), and the diagnosis is confirmed through tests, should stop treatment with fenofibrat.

Do not combine fenofibrat with drugs that have a toxic effect with the liver.

File complications occur in patients with bile or gallstones.

Pancreatic glands: Pancreatitis has been reported in patients using fenofibrat. This event may be the result of failure in patients with severe hyperglyceremia, which is a direct effect of the drug, or a secondary phenomenon through the formation of fibers or sedimentation in bile ducts with bile duct obstruction.

muscle:

Mechanical poisoning, including rare cases such as pattern patterns, or no kidney failure, has been reported when using fibrats and other lipid medications. Muscle poisoning should be suspected in patients with signs of spreading muscle pain, muscle inflammation, cramps and muscle weakness and/ or increasing the CPK index (higher concentration than 5 times compared to the normal level of the upper limit). In these cases, Fenofibrat should be stopped.

The risk of muscle poisoning can increase when used simultaneously with other fibrat groups or HMG-Coa Reductase inhibitors, especially in the case of a history of muscle disease. Therefore, the combination of drugs should be reserved for patients with severe lipid disorders with high cardiovascular risks without a history of muscle disease, and need to closely monitor the possibility of muscle poisoning.

Periodically monitor the concentration of creatinine kinase in patients with side effects. Stop treatment if the high serum creatinine concentration is noticeable or the patient is diagnosed or suspected of muscle or muscle disease.

Kidney function: Hafenthyl 200 should adjust the dose in patients with estimated glomerular filtration (EGFR) 30-59 ml/min/1.73m2.

Colonel: The drug contains Lactose excipients. Patients with rare genetic problems in tolerance of galactose, deficiency of lactase or absorbent Glucose - Galactose should not use this drug.

If after a few months of taking the drug (3-6 months) that the amount of lipid in the blood changes is not significant, it is necessary to consider other therapy (supplemented or other)

The ability to drive and operate machines

fenofibrat does not have or have a significant impact on the ability to drive and operate machinery.

Pregnancy

should not be used for pregnant women. Animal research does not see teratogenic effects. However, observed signs of poison for pregnancy at the poisonous doses for the mother animal. However, it has not yet determined the potential risk in humans.

The period of breastfeeding

There is no data on the excretion of fenofibrat and or the metabolites of this drug through breast milk. However, because of safety, should not be used for breastfeeding women.

Interactive drug

anticoagulant, orally (warfarin): extends the time of PT/INR. It is necessary to reduce the anticoagulant dose (about one third of the original dose and adjust the next dose when necessary), and monitor PT/INR periodically until stable.

HMG-CAA Reductase inhibitors and other fibrats: The risk of serious muscle poisoning increases when using simultaneously fenofibrat with HMG-CAA Reductase inhibitors or other fibrats, need to be cautious when combining drugs and patients should be closely monitored by signs of muscle poisoning. Currently there is no evidence that Fenofibrat has an effect on the pharmacokinetics of Simvastatin.

Bile acid -mounted plastic (Cholestyramin, Colestipol): reduces fenofibrat absorption.

Cyclosporin: Increased risk of kidney toxicity (impaired renal function).

Glitazon: Some cases of reduced HDL-cholesterol paradox have been recovered when used simultaneously fenofibrat with Glitazon. Therefore, HDL -cholesterol should be monitored when combining drugs and stopping one of the two drugs if HDL -cholesterol concentration is too low.

Cytochrom P450 enzyme: In vitro studies use human liver microsom indicated that fenofibrat and fenofibric acid do not inhibit cytochrom (CYP) P450 such as CYP3A4, CYP2D6, CYP2E1 or CYP1A2; weak inhibitors CYP2C19 and CYP2A6; Mild to medium inhibition CYP2C9 at treatment concentration.

Patients with simultaneous use of fenofibrat with metabolic drugs through CYP2C19, CYP2A6 and especially CYP2C9 have a narrow treatment index, should be carefully monitored and adjusted if necessary.

Do not use a combination of poison with liver (Mao inhibitors, Perhexilin Maleat ...) with fenofibrat.

Similar to other fibrats, fenofibrat stimulates the multifunctional oxidation enzymes of mitochondria related to the metabolism of fatty acids in rodents and can interact with the drugs metabolized through these enzymes.