Fenbrat 300 Overdose

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How long did you take this medication to work?

What happens if I overdose Fenbrat 300?

Contact 1-800-222-1222 (the American Association of Poison Control Centers), your local, or emergency room immediately.

Proper storage of Fenbrat 300 capsules:

Store Fenbrat 300 capsules at room temperature, between 59 and 86 degrees F (15 and 30 degrees C). Store away from heat, moisture, and light. Do not store in the bathroom. Keep Fenbrat 300 capsules out of the reach of children and away from pets.

Overdose of Fenbrat 300 in details

When a dose is taken in higher dose than the recommended doses, it is called Overdose. Overdose always needs a clinical supervision. Any medicine or drug when consumed in Overdose produces untoward side effects on one or various organs in the body. A medicine is excreted in the kidney or metabolized in the liver most of the times. This process goes without any hurdles when taken in normal dose, but when taken in an overdose, the body is not able to metabolize it or send it out properly which causes the effects of anoverdose.
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Only anecdotal cases of Fenbrat 300 overdosage have been reported. In the majority of cases, no overdose symptoms were reported.

There is no specific treatment for overdose with Fenbrat 300. General supportive care of the patient is indicated, including monitoring of vital signs and observation of clinical status, should an overdose occur. If indicated, elimination of unabsorbed drug should be achieved by emesis or gastric lavage; usual precautions should be observed to maintain the airway. Because Fenbrat 300 is highly bound to plasma proteins, hemodialysis should not be considered.

What should I avoid while taking Fenbrat 300?

If you also take cholestyramine, colesevelam, or colestipol: Wait 4 to 6 hours after taking any of these other medicines before you take Fenbrat 300. Avoid taking Fenbrat 300 within 1 hour before taking the other medicine.

Avoid drinking alcohol. It can raise triglyceride levels, and may also damage your liver while you are taking Fenbrat 300.

Fenbrat 300 warnings

Warnings are a mix of Precautions. Contraindications and interactions and serious harmful effects associated with the medicine intake. A diabetic or Hypertensive patient need to be warned about few drug interactions. A known hypersensitivity patient needs to be careful about the reactions or anaphylactic shock. A pregnant woman or a breastfeeding woman should be warned of certain medications. A Hepatitis [liver disease] patient or a cardiac patient should avoid few drugs.

Mortality and Coronary Heart Disease Morbidity

The effect of Fenbrat 300 on coronary heart disease morbidity and mortality and non-cardiovascular mortality has not been established. Because of similarities between Fenbrat 300 and Fenbrat 300, clofibrate, and gemfibrozil, the findings in the following large randomized, placebo-controlled clinical studies with these fibrate drugs may also apply to Fenbrat 300.

The Action to Control Cardiovascular Risk in Diabetes Lipid (ACCORD Lipid) trial was a randomized placebo-controlled study of 5518 patients with type 2 diabetes mellitus on background statin therapy treated with Fenbrat 300. The mean duration of follow-up was 4.7 years. Fenbrat 300 plus statin combination therapy showed a non-significant 8% relative risk reduction in the primary outcome of major adverse cardiovascular events (MACE), a composite of non-fatal myocardial infarction, non-fatal stroke, and cardiovascular disease death (hazard ratio [HR] 0.92, 95% CI 0.79-1.08) (p=0.32) as compared to statin monotherapy. In a gender subgroup analysis, the hazard ratio for MACE in men receiving combination therapy versus statin monotherapy was 0.82 (95% CI 0.69-0.99), and the hazard ratio for MACE in women receiving combination therapy versus statin monotherapy was 1.38 (95% CI 0.98-1.94) (interaction p=0.01). The clinical significance of this subgroup finding is unclear.

The Fenbrat 300 Intervention and Event Lowering in Diabetes (FIELD) study was a 5-year randomized, placebo-controlled study of 9795 patients with type 2 diabetes mellitus treated with Fenbrat 300. Fenbrat 300 demonstrated a non-significant 11% relative reduction in the primary outcome of coronary heart disease events (hazard ratio [HR] 0.89, 95% CI 0.75-1.05, p = 0.16) and a significant 11% reduction in the secondary outcome of total cardiovascular disease events (HR 0.89 [0.80-0.99], p = 0.04). There was a non-significant 11% (HR 1.11 [0.95, 1.29], p = 0.18) and 19% (HR 1.19 [0.90, 1.57], p = 0.22) increase in total and coronary heart disease mortality, respectively, with Fenbrat 300 as compared to placebo.

In the Coronary Drug Project, a large study of post-myocardial infarction patients treated for 5 years with clofibrate, there was no difference in mortality seen between the clofibrate group and the placebo group. There was, however, a difference in the rate of cholelithiasis and cholecystitis requiring surgery between the two groups (3.0% vs. 1.8%).

In a study conducted by the World Health Organization (WHO), 5000 subjects without known coronary artery disease were treated with placebo or clofibrate for 5 years and followed for an additional one year. There was a statistically significant, higher age-adjusted all-cause mortality in the clofibrate group compared with the placebo group (5.70% vs. 3.96%, p = < 0.01). Excess mortality was due to a 33% increase in non-cardiovascular causes, including malignancy, post-cholecystectomy complications, and pancreatitis. This appeared to confirm the higher risk of gallbladder disease seen in clofibrate-treated patients studied in the Coronary Drug Project.

The Helsinki Heart Study was a large (N = 4081) study of middle-aged men without a history of coronary artery disease. Subjects received either placebo or gemfibrozil for 5 years, with a 3.5 year open extension afterward. Total mortality was numerically higher in the gemfibrozil randomization group but did not achieve statistical significance (p = 0.19, 95% confidence interval for relative risk G:P = 0.91-1.64). Although cancer deaths trended higher in the gemfibrozil group (p = 0.11), cancers (excluding basal cell carcinoma) were diagnosed with equal frequency in both study groups. Due to the limited size of the study, the relative risk of death from any cause was not shown to be different than that seen in the 9 year follow-up data from WHO study (RR = 1.29). A secondary prevention component of the Helsinki Heart Study enrolled middle-aged men excluded from the primary prevention study because of known or suspected coronary heart disease. Subjects received gemfibrozil or placebo for 5 years. Although cardiac deaths trended higher in the gemfibrozil group, this was not statistically significant (hazard ratio 2.2, 95% confidence interval: 0.94-5.05).

Skeletal Muscle

Fibrates increase the risk of myositis or myopathy and have been associated with rhabdomyolysis. The risk for serious muscle toxicity appears to be increased in elderly patients and in patients with diabetes, renal failure, or hypothyroidism.

Myopathy should be considered in any patient with diffuse myalgias, muscle tenderness or weakness, and/or marked elevations of CPK levels. Patients should promptly report unexplained muscle pain, tenderness or weakness, particularly if accompanied by malaise or fever. CPK levels should be assessed in patients reporting these symptoms, and Fenbrat 300 should be discontinued if markedly elevated CPK levels occur or myopathy or myositis is suspected or diagnosed.

Data from observational studies suggest that the risk for rhabdomyolysis is increased when fibrates are co-administered with a statin.

Cases of myopathy, including rhabdomyolysis, have been reported with fenofibrates co-administered with colchicine, and caution should be exercised when prescribing Fenbrat 300 with colchicine.

Liver Function

Fenbrat 300 at a dose of 135 mg once daily has been associated with increases in serum transaminases [AST (SGOT) or ALT (SGPT)]. In a pooled analysis of three 12-week, double-blind, controlled studies of Fenbrat 300, increases in ALT and AST to > 3 times the upper limit of normal on two consecutive occasions occurred in 1.9% and 0.2%, respectively, of patients receiving Fenbrat 300 without other lipid-altering drugs. Increases in ALT and/or AST were not accompanied by increases in bilirubin or clinically significant increases in alkaline phosphatase.

In a pooled analysis of 10 placebo-controlled trials of Fenbrat 300, increases to > 3 times the upper limit of normal in ALT occurred in 5.3% of patients taking Fenbrat 300 versus 1.1% of patients treated with placebo. The incidence of increases in transaminases observed with Fenbrat 300 therapy may be dose related. In an 8-week dose-ranging study of Fenbrat 300 in hypertriglyceridemia, the incidence of ALT or AST elevations ≥ 3 times the upper limit of normal was 13% in patients receiving dosages equivalent to 90 mg to 135 mg Fenbrat 300 once daily and was 0% in those receiving dosages equivalent to 45 mg Fenbrat 300 once daily or less, or placebo. Hepatocellular, chronic active, and cholestatic hepatitis observed with Fenbrat 300 therapy have been reported after exposures of weeks to several years. In extremely rare cases, cirrhosis has been reported in association with chronic active hepatitis.

Baseline and regular monitoring of liver function, including serum ALT (SGPT) should be performed for the duration of therapy with Fenbrat 300, and therapy discontinued if enzyme levels persist above 3 times the upper limit of normal.

Serum Creatinine

Reversible elevations in serum creatinine have been reported in patients receiving Fenbrat 300 as well as patients receiving Fenbrat 300. In the pooled analysis of three 12-week, double-blind, controlled studies of Fenbrat 300, increases in creatinine to > 2 mg/dL occurred in 0.8% of patients treated with Fenbrat 300 without other lipid-altering drugs. 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. The clinical significance of these observations is unknown. Monitoring renal function in patients with renal impairment taking Fenbrat 300 is suggested. Renal monitoring should be considered for patients at risk for renal insufficiency, such as the elderly and those with diabetes.

Cholelithiasis

Fenbrat 300, like Fenbrat 300, clofibrate, and gemfibrozil, may increase cholesterol excretion into the bile, potentially leading to cholelithiasis. If cholelithiasis is suspected, gallbladder studies are indicated. Fenbrat 300 therapy should be discontinued if gallstones are found.

Coumarin Anticoagulants

Caution should be exercised when Fenbrat 300 is given in conjunction with oral coumarin anticoagulants. Fenbrat 300 may potentiate the anticoagulant effects of these agents resulting in prolongation of the prothrombin time/International Normalized Ratio (PT/INR). Frequent monitoring of PT/INR and dose adjustment of the oral anticoagulant are recommended until the PT/INR has stabilized in order to prevent bleeding complications.

Pancreatitis

Pancreatitis has been reported in patients taking drugs of the fibrate class, including Fenbrat 300. 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 with obstruction of the common bile duct.

Hematological Changes

Mild to moderate hemoglobin, hematocrit, and white blood cell decreases have been observed in patients following initiation of Fenbrat 300 and Fenbrat 300 therapy. However, these levels stabilize during long-term administration. Thrombocytopenia and agranulocytosis have been reported in individuals treated with fenofibrates. Periodic monitoring of red and white blood cell counts are recommended during the first 12 months of Fenbrat 300 administration.

Hypersensitivity Reactions

Acute hypersensitivity reactions such as Stevens-Johnson syndrome and toxic necrolysis requiring patient hospitalization and treatment with steroids have been reported in individuals treated with fenofibrates.

Venothromboembolic Disease

In the FIELD trial, pulmonary embolus (PE) and deep vein thrombosis (DVT) were observed at higher rates in the Fenbrat 300- than the placebo-treated group. Of 9,795 patients enrolled in FIELD, there were 4,900 in the placebo group and 4,895 in the Fenbrat 300 group. For DVT, there were 48 events (1%) in the placebo group and 67 (1%) in the Fenbrat 300 group (p = 0.074); and for PE, there were 32 (0.7%) events in the placebo group and 53 (1%) in the Fenbrat 300 group (p = 0.022).

In the Coronary Drug Project, a higher proportion of the clofibrate group experienced definite or suspected fatal or nonfatal PE or thrombophlebitis than the placebo group (5.2% vs. 3.3% at five years; p < 0.01).

Paradoxical Decreases in HDL Cholesterol Levels

There have been postmarketing and clinical trial reports of severe decreases in HDL cholesterol levels (as low as 2 mg/dL) occurring in diabetic and non-diabetic patients initiated on fibrate therapy. The decrease in HDL-C is mirrored by a decrease in apolipoprotein A1. This decrease has been reported to occur within 2 weeks to years after initiation of fibrate therapy. The HDL-C levels remain depressed until fibrate therapy has been withdrawn; the response to withdrawal of fibrate therapy is rapid and sustained. The clinical significance of this decrease in HDL-C is unknown. It is recommended that HDL-C levels be checked within the first few months after initiation of fibrate therapy. If a severely depressed HDL-C level is detected, fibrate therapy should be withdrawn, and the HDL-C level monitored until it has returned to baseline, and fibrate therapy should not be re-initiated.

What should I discuss with my healthcare provider before taking Fenbrat 300?

Some medical conditions may interact with Fenbrat 300 capsules. Tell your doctor or pharmacist if you have any medical conditions, especially if any of the following apply to you:

  • if you are pregnant, planning to become pregnant, or are breast-feeding
  • if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement
  • if you have allergies to medicines or other substances
  • if you have a history of diabetes, an underactive thyroid, heart problems (eg, heart blood vessel problems), gallbladder problems (eg, gallstones), pancreatitis, kidney or liver problems, or muscle problems
  • if you have a history of blood clots in your veins (deep vein thrombosis or pulmonary embolism)
  • if you are very overweight, have an inactive lifestyle, have a poor diet, or you drink alcohol or have a history of alcohol abuse
  • if you have trouble swallowing
  • if you are taking a beta-blocker (eg, propranolol), estrogen, or thiazide diuretic (eg, hydrochlorothiazide)

Some MEDICINES MAY INTERACT with Fenbrat 300 capsules. Tell your health care provider if you are taking any other medicines, especially any of the following:

  • Colchicine or HMG-CoA reductase inhibitors (statins) (eg, simvastatin) because the risk of serious muscle problems may be increased
  • Immunosuppressants (eg, cyclosporine) or other medicines that may harm the kidney (eg, aminoglycoside antibiotics [eg, gentamicin], amphotericin B, nonsteroidal anti-inflammatory drugs [NSAIDs] [eg, ibuprofen], tacrolimus, vancomycin) because they may increase the risk of Fenbrat 300 capsules's side effects. Ask your doctor if you are unsure if any of your medicines might harm the kidney
  • Anticoagulants (eg, warfarin) because the risk of their side effects may be increased by Fenbrat 300 capsules

This may not be a complete list of all interactions that may occur. Ask your health care provider if Fenbrat 300 capsules may interact with other medicines that you take. Check with your health care provider before you start, stop, or change the dose of any medicine.

Fenbrat 300 precautions

Certain people who are very sick or very old or who are sensitive show an exacerbation of side effect of the drug which can turn dangerous at times. So, it is very important to remember the precautions while taking the medicine. Pregnancy and Breastfeeding are also special categories wherein extra care or precaution is needed when taking a drug. Few patients may have a hypersensitivity reaction to few medications, and that can be life-threatening rarely. Penicillin hypersensitivity is one example. Diarrhea, rashes are few other symptoms which need a watch. A patient with other co-existing diseases like liver disease, heart disease, kidney disease should take special precautions.
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Mortality And Coronary Heart Disease Morbidity

The effect of Fenbrat 300 on coronary heart disease morbidity and mortality and non-cardiovascular mortality has not been established. Because of similarities between Fenbrat 300 and Fenbrat 300, clofibrate, and gemfibrozil, the findings in the following large randomized, placebo-controlled clinical studies with these fibrate drugs may also apply to Fenbrat 300.

The Action to Control Cardiovascular Risk in Diabetes Lipid (ACCORD Lipid) trial was a randomized placebo-controlled study of 5518 patients with type 2 diabetes mellitus on background statin therapy treated with Fenbrat 300. The mean duration of follow-up was 4.7 years. Fenbrat 300 plus statin combination therapy showed a non-significant 8% relative risk reduction in the primary outcome of major adverse cardiovascular events (MACE), a composite of non-fatal myocardial infarction, non-fatal stroke, and cardiovascular disease death (hazard ratio [HR] 0.92, 95% CI 0.79-1.08) (p=0.32) as compared to statin monotherapy. In a gender subgroup analysis, the hazard ratio for MACE in men receiving combination therapy versus statin monotherapy was 0.82 (95% CI 0.69-0.99), and the hazard ratio for MACE in women receiving combination therapy versus statin monotherapy was 1.38 (95% CI 0.98-1.94) (interaction p=0.01). The clinical significance of this subgroup finding is unclear.

The Fenbrat 300 Intervention and Event Lowering in Diabetes (FIELD) study was a 5-year randomized, placebo-controlled study of 9795 patients with type 2 diabetes mellitus treated with Fenbrat 300. Fenbrat 300 demonstrated a non-significant 11% relative reduction in the primary outcome of coronary heart disease events (hazard ratio [HR] 0.89, 95% CI 0.75-1.05, p = 0.16) and a significant 11% reduction in the secondary outcome of total cardiovascular disease events (HR 0.89 [0.80-0.99], p = 0.04). There was a non-significant 11% (HR 1.11 [0.95, 1.29], p = 0.18) and 19% (HR 1.19 [0.90, 1.57], p = 0.22) increase in total and coronary heart disease mortality, respectively, with Fenbrat 300 as compared to placebo.

In the Coronary Drug Project, a large study of post-myocardial infarction patients treated for 5 years with clofibrate, there was no difference in mortality seen between the clofibrate group and the placebo group. There was, however, a difference in the rate of cholelithiasis and cholecystitis requiring surgery between the two groups (3.0% vs. 1.8%).

In a study conducted by the World Health Organization (WHO), 5000 subjects without known coronary artery disease were treated with placebo or clofibrate for 5 years and followed for an additional one year. There was a statistically significant, higher age-adjusted all-cause mortality in the clofibrate group compared with the placebo group (5.70% vs. 3.96%, p = < 0.01). Excess mortality was due to a 33% increase in non-cardiovascular causes, including malignancy, postcholecystectomy complications, and pancreatitis. This appeared to confirm the higher risk of gallbladder disease seen in clofibrate-treated patients studied in the Coronary Drug Project.

The Helsinki Heart Study was a large (N = 4081) study of middle-aged men without a history of coronary artery disease. Subjects received either placebo or gemfibrozil for 5 years, with a 3.5 year open extension afterward. Total mortality was numerically higher in the gemfibrozil randomization group but did not achieve statistical significance (p = 0.19, 95% confidence interval for relative risk G:P = 0.91-1.64). Although cancer deaths trended higher in the gemfibrozil group (p = 0.11), cancers (excluding basal cell carcinoma) were diagnosed with equal frequency in both study groups. Due to the limited size of the study, the relative risk of death from any cause was not shown to be different than that seen in the 9 year follow-up data from WHO study (RR = 1.29). A secondary prevention component of the Helsinki Heart Study enrolled middle-aged men excluded from the primary prevention study because of known or suspected coronary heart disease. Subjects received gemfibrozil or placebo for 5 years. Although cardiac deaths trended higher in the gemfibrozil group, this was not statistically significant (hazard ratio 2.2, 95% confidence interval: 0.94-5.05).

Skeletal Muscle

Fibrates increase the risk of myositis or myopathy and have been associated with rhabdomyolysis. The risk for serious muscle toxicity appears to be increased in elderly patients and in patients with diabetes, renal failure, or hypothyroidism.

Myopathy should be considered in any patient with diffuse myalgias, muscle tenderness or weakness, and/or marked elevations of CPK levels. Patients should promptly report unexplained muscle pain, tenderness or weakness, particularly if accompanied by malaise or fever. CPK levels should be assessed in patients reporting these symptoms, and Fenbrat 300 should be discontinued if markedly elevated CPK levels occur or myopathy or myositis is suspected or diagnosed.

Data from observational studies suggest that the risk for rhabdomyolysis is increased when fibrates are co-administered with a statin.

Cases of myopathy, including rhabdomyolysis, have been reported with fenofibrates coadministered with colchicine, and caution should be exercised when prescribing Fenbrat 300 with colchicine.

Liver Function

Fenbrat 300 at a dose of 135 mg once daily has been associated with increases in serum transaminases [AST (SGOT) or ALT (SGPT)]. In a pooled analysis of three 12-week, doubleblind, controlled studies of Fenbrat 300, increases in ALT and AST to > 3 times the upper limit of normal on two consecutive occasions occurred in 1.9% and 0.2%, respectively, of patients receiving Fenbrat 300 without other lipid-altering drugs. Increases in ALT and/or AST were not accompanied by increases in bilirubin or clinically significant increases in alkaline phosphatase.

In a pooled analysis of 10 placebo-controlled trials of Fenbrat 300, increases to > 3 times the upper limit of normal in ALT occurred in 5.3% of patients taking Fenbrat 300 versus 1.1% of patients treated with placebo. The incidence of increases in transaminases observed with Fenbrat 300 therapy may be dose related. In an 8-week dose-ranging study of Fenbrat 300 in hypertriglyceridemia, the incidence of ALT or AST elevations ≥ 3 times the upper limit of normal was 13% in patients receiving dosages equivalent to 90 mg to 135 mg Fenbrat 300 once daily and was 0% in those receiving dosages equivalent to 45 mg Fenbrat 300 once daily or less, or placebo. Hepatocellular, chronic active, and cholestatic hepatitis observed with Fenbrat 300 therapy have been reported after exposures of weeks to several years. In extremely rare cases, cirrhosis has been reported in association with chronic active hepatitis.

Baseline and regular monitoring of liver function, including serum ALT (SGPT) should be performed for the duration of therapy with Fenbrat 300, and therapy discontinued if enzyme levels persist above 3 times the upper limit of normal.

Serum Creatinine

Reversible elevations in serum creatinine have been reported in patients receiving Fenbrat 300 as well as patients receiving Fenbrat 300. In the pooled analysis of three 12-week, double-blind, controlled studies of Fenbrat 300, increases in creatinine to > 2 mg/dL occurred in 0.8% of patients treated with Fenbrat 300 without other lipid-altering drugs. 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. The clinical significance of these observations is unknown. Monitoring renal function in patients with renal impairment taking Fenbrat 300 is suggested. Renal monitoring should be considered for patients at risk for renal insufficiency, such as the elderly and those with diabetes.

Cholelithiasis

Fenbrat 300, like Fenbrat 300, clofibrate, and gemfibrozil, may increase cholesterol excretion into the bile, potentially leading to cholelithiasis. If cholelithiasis is suspected, gallbladder studies are indicated. Fenbrat 300 therapy should be discontinued if gallstones are found.

Coumarin Anticoagulants

Caution should be exercised when Fenbrat 300 is given in conjunction with oral coumarin anticoagulants. Fenbrat 300 may potentiate the anticoagulant effects of these agents resulting in prolongation of the prothrombin time/International Normalized Ratio (PT/INR). Frequent monitoring of PT/INR and dose adjustment of the oral anticoagulant are recommended until the PT/INR has stabilized in order to prevent bleeding complications.

Pancreatitis

Pancreatitis has been reported in patients taking drugs of the fibrate class, including Fenbrat 300. 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 with obstruction of the common bile duct.

Hematological Changes

Mild to moderate hemoglobin, hematocrit, and white blood cell decreases have been observed in patients following initiation of Fenbrat 300 and Fenbrat 300 therapy. However, these levels stabilize during long-term administration. Thrombocytopenia and agranulocytosis have been reported in individuals treated with fenofibrates. Periodic monitoring of red and white blood cell counts are recommended during the first 12 months of Fenbrat 300 administration.

Hypersensitivity Reactions

Acute hypersensitivity reactions such as Stevens-Johnson syndrome and toxic necrolysis requiring patient hospitalization and treatment with steroids have been reported in individuals treated with fenofibrates.

Venothromboembolic Disease

In the FIELD trial, pulmonary embolus (PE) and deep vein thrombosis (DVT) were observed at higher rates in the Fenbrat 300- than the placebo-treated group. Of 9,795 patients enrolled in FIELD, there were 4,900 in the placebo group and 4,895 in the Fenbrat 300 group. For DVT, there were 48 events (1%) in the placebo group and 67 (1%) in the Fenbrat 300 group (p = 0.074); and for PE, there were 32 (0.7%) events in the placebo group and 53 (1%) in the Fenbrat 300 group (p = 0.022).

In the Coronary Drug Project, a higher proportion of the clofibrate group experienced definite or suspected fatal or nonfatal PE or thrombophlebitis than the placebo group (5.2% vs. 3.3% at five years; p < 0.01).

Paradoxical Decreases In HDL Cholesterol Levels

There have been postmarketing and clinical trial reports of severe decreases in HDL cholesterol levels (as low as 2 mg/dL) occurring in diabetic and non-diabetic patients initiated on fibrate therapy. The decrease in HDL-C is mirrored by a decrease in apolipoprotein A1. This decrease has been reported to occur within 2 weeks to years after initiation of fibrate therapy. The HDL-C levels remain depressed until fibrate therapy has been withdrawn; the response to withdrawal of fibrate therapy is rapid and sustained. The clinical significance of this decrease in HDL-C is unknown. It is recommended that HDL-C levels be checked within the first few months after initiation of fibrate therapy. If a severely depressed HDL-C level is detected, fibrate therapy should be withdrawn, and the HDL-C level monitored until it has returned to baseline, and fibrate therapy should not be re-initiated.

Patient Counseling Information

Patient Counseling

Patients should be advised:

  • of the potential benefits and risks of Fenbrat 300.
  • to read the Medication Guide before starting Fenbrat 300 therapy and to reread it each time the prescription is renewed.
  • of medications that should not be taken in combination with Fenbrat 300.
  • to continue to follow an appropriate lipid-modifying diet while taking Fenbrat 300.
  • to take Fenbrat 300 once daily, without regard to food, at the prescribed dose, swallowing each capsule whole.
  • to return for routine monitoring.
  • to inform their physician of all medications, supplements, and herbal preparations they are taking and any change to their medical condition. Patients should also be advised to inform their physicians prescribing a new medication that they are taking Fenbrat 300.
  • to inform their physician of any muscle pain, tenderness, or weakness; onset of abdominal pain; or any other new symptoms.

Nonclinical Toxicology

Carcinogenesis, Mutagenesis, Impairment Of Fertility

Fenbrat 300 (fenofibric acid)

No carcinogenicity and fertility studies have been conducted with choline Fenbrat 300 or fenofibric acid. However, because Fenbrat 300 is rapidly converted to its active metabolite, fenofibric acid, either during or immediately following absorption both in animals and humans, studies conducted with Fenbrat 300 are relevant for the assessment of the toxicity profile of fenofibric acid. A similar toxicity spectrum is expected after treatment with either Fenbrat 300 or Fenbrat 300.

Fenbrat 300

Two dietary carcinogenicity studies have been conducted in rats with Fenbrat 300. In the first 24- month study, Wistar rats were dosed with Fenbrat 300 at 10, 45, and 200 mg/kg/day, approximately 0.3, 1, and 6 times the maximum recommended human dose (MRHD), based on body surface area comparisons (mg/m²). At a dose of 200 mg/kg/day (6 times the MRHD), the incidence of liver carcinomas was significantly increased in both sexes. A statistically significant increase in pancreatic carcinomas was observed in males at 1 and 6 times the MRHD; an increase in pancreatic adenomas and benign testicular interstitial cell tumors was observed at 6 times the MRHD in males. In a second 24-month rat carcinogenicity study in a different strain of rats (Sprague-Dawley), (doses of 10 and 60 mg/kg/day (0.3 and 2 times the MRHD), produced significant increases in the incidence of pancreatic acinar adenomas in both sexes and increases in interstitial cell tumors of the testes at 2 times the MRHD.

A 117-week carcinogenicity study was conducted in rats comparing three drugs: Fenbrat 300 10 and 60 mg/kg/day (0.3 and 2 times the MRHD), clofibrate (400 mg/kg/day; 2 times the human dose), and gemfibrozil (250 mg/kg/day; 2 times the MRHD). Fenbrat 300 increased pancreatic acinar adenomas in both sexes. Clofibrate increased hepatocellular carcinoma and pancreatic acinar adenomas in males and hepatic neoplastic nodules in females. Gemfibrozil increased hepatic neoplastic nodules in males and females, while all three drugs increased testicular interstitial cell tumors in males.

In a 21-month study in CF-1 mice, Fenbrat 300 10, 45, and 200 mg/kg/day (approximately 0.2, 1, and 3 times the MRHD on the basis of mg/m² surface area) significantly increased the liver carcinomas in both sexes at 3 times the MRHD. In a second 18-month study at 10, 60, and 200 mg/kg/day, Fenbrat 300 significantly increased the liver carcinomas in male and female mice at 3 times the MRHD.

Electron microscopy studies have demonstrated peroxisomal proliferation following Fenbrat 300 administration to the rat. An adequate study to test for peroxisome proliferation in humans has not been done, but changes in peroxisome morphology and numbers have been observed in humans after treatment with other members of the fibrate class when liver biopsies were compared before and after treatment in the same individual.

Mutagenesis

Fenbrat 300 has been demonstrated to be devoid of mutagenic potential in the following tests: Ames, and micronucleus in vivo/rat. In addition, fenofibric acid, has been demonstrated to be devoid of mutagenic potential in the following tests: Ames, mouse lymphoma, chromosomal aberration and sister chromatid exchange in human lymphocytes, and unscheduled DNA synthesis in primary rat hepatocytes.

Impairment of Fertility

In a fertility study, rats were given oral dietary doses of Fenbrat 300. Males received doses for 61 days prior to mating and females for 15 days prior to mating through weaning, which resulted in no adverse effect on fertility at doses up to 300 mg/kg/day (~10 times the MRHD, based on mg/m² surface area comparisons).

Use In Specific Populations

Pregnancy

Pregnancy Category: C

The safety of Fenbrat 300 in pregnant women has not been established. There are no adequate and well controlled studies of Fenbrat 300 in pregnant women. Fenbrat 300 should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

In pregnant rats given oral dietary doses of 14, 127, and 361 mg/kg/day from gestation day 6-15 during the period of organogenesis, adverse developmental findings were not observed at 14 mg/kg/day (less than 1 times the maximum recommended human dose [MRHD], based on body surface area comparisons; mg/m²). At higher multiples of human doses evidence of maternal toxicity was observed.

In pregnant rabbits given oral gavage doses of 15, 150, and 300 mg/kg/day from gestation day 6- 18 during the period of organogenesis and allowed to deliver, aborted litters were observed at 150 mg/kg/day (10 times the MRHD, based on body surface area comparisons; mg/m²). No developmental findings were observed at 15 mg/kg/day (at less than 1 times the MRHD, based on body surface area comparisons; mg/m²).

In pregnant rats given oral dietary doses of 15, 75, and 300 mg/kg/day from gestation day 15 through lactation day 21 (weaning), maternal toxicity was observed at less than 1 times the MRHD, based on body surface area comparisons; mg/m².

Nursing Mothers

Fenbrat 300 should not be used in nursing mothers. A decision should be made whether to discontinue nursing or to discontinue the drug taking into account the importance of the drug to the mother.

Pediatric Use

The safety and effectiveness of Fenbrat 300 in pediatric patients have not been established.

Geriatric Use

Fenbrat 300 is substantially excreted by the kidney as fenofibric acid and fenofibric acid glucuronide, and the risk of adverse reactions to this drug may be greater in patients with impaired renal function. Fenofibric acid exposure is not influenced by age. Since elderly patients have a higher incidence of renal impairment, dose selection for the elderly should be made on the basis of renal function. Elderly patients with normal renal function should require no dose modifications. Consider monitoring renal function in elderly patients taking Fenbrat 300.

Renal Impairment

The use of Fenbrat 300 should be avoided in patients who have severe renal impairment. Dose reduction is required in patients with mild to moderate renal impairment.

Monitoring renal function in patients with renal impairment is recommended.

Hepatic Impairment

The use of Fenbrat 300 has not been evaluated in subjects with hepatic impairment.

What happens if I miss a dose of Fenbrat 300?

When you miss a dose, you should take it as soon as you remember, but you should take care that it should be well spaced from the next dose. You should not take an extra dose at the time of the second dose as it will become a double dose. The double dose can give unwanted side effects, so be careful. In chronic conditions or when you have a serious health issue, if you miss a dose, you should inform your health care provider and ask his suggestion.

Take the missed dose as soon as you remember. If it is almost time for your next dose, skip the missed dose and take the medicine at the next regularly scheduled time. Do not take extra medicine to make up the missed dose.


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References

  1. DailyMed. "FENOFIBRATE: DailyMed provides trustworthy information about marketed drugs in the United States. DailyMed is the official provider of FDA label information (package inserts).". https://dailymed.nlm.nih.gov/dailyme... (accessed September 17, 2018).
  2. DrugBank. "fenofibrate". http://www.drugbank.ca/drugs/DB01039 (accessed September 17, 2018).
  3. MeSH. "Hypolipidemic Agents". https://www.ncbi.nlm.nih.gov/mesh/68... (accessed September 17, 2018).

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