Interactions between Proguanil and TriCor

The fenofibrate in TriCor has a moderate potential interaction with Anemia.

Mild to moderate hemoglobin, hematocrit and white blood cell decreases have been observed in patients following initiation of fibric acid derivatives therapy. However, these levels stabilize during long-term administration. Thrombocytopenia and agranulocytosis have been reported in individuals treated with these agents. Caution is recommended when treating patients predisposed to hematologic changes. Periodic monitoring of red and white blood cell counts is recommended during the first 12 months of therapy.

The fenofibrate in TriCor has a major potential interaction with Gallbladder Disease.

The use of fibric acid derivatives is contraindicated in patients with gallbladder disease. A significantly increased incidence of cholelithiasis has been observed in patients treated with the fibric acid derivative, clofibrate, presumably because of increased cholesterol excretion into the bile. Based on two separate studies (the WHO study and the Coronary Drug Project study), clofibrate use was associated with twice the risk of developing cholelithiasis and cholecystitis requiring surgery. Due to their structural and pharmacologic similarities, use of other fibric acid derivatives may be expected to carry the same risk.

The fenofibrate in TriCor has a major potential interaction with Liver Disease.

The use of fibric acid derivatives is contraindicated in patients with active liver disease or unexplained, persistent elevations of serum transaminases. Fibric acid derivatives therapy is associated with dose-related hepatotoxicity, including biochemical abnormalities of liver function, hepatitis (hepatocellular, chronic active, as well as cholestatic) and, rarely, cirrhosis. Postmarketing cases of severe drug-induced liver injury, including liver transplantation and death, have been reported. Therapy with these agents should be administered cautiously in patients with a history of liver disease and/or heavy alcohol use. Liver function tests, including serum transaminase levels and total bilirubin, should be performed at baseline and periodically throughout the duration of therapy. Therapy should be discontinued if signs or symptoms of liver injury develop or if elevated enzyme levels persist (ALT or AST greater than 3 times the upper limit of normal, or if accompanied by elevation of bilirubin). Do not restart therapy if there is no alternative explanation for the liver injury.

Proguanil has a moderate potential interaction with Liver Disease.

No proguanil dosage adjustments are needed in patients with mild or moderate hepatic impairment, however, no trials have been conducted in patients with severe hepatic impairment. Caution is advised, as elevated liver laboratory tests and cases of hepatitis and hepatic failure requiring liver transplantation have been reported with prophylactic use of atovaquone and proguanil hydrochloride tablets.

The fenofibrate in TriCor has a major potential interaction with Myoneural Disorder.

Severe myopathy, including rhabdomyolysis with acute renal failure secondary to myoglobinuria, has been reported rarely with the use of fibric acid derivatives. The myopathy may be dose-related and is characterized by muscle aches and/or weakness in conjunction with increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with fibric acid derivatives should be administered cautiously in patients with preexisting myopathy or a myoneural disorder, since it may delay the recognition or confound the diagnosis of a drug-induced musculoskeletal effect. Patients should be advised to report promptly any unusual muscle pain, tenderness or weakness, particularly if accompanied by malaise or fever. Periodic CPK determinations may be considered in some patients, although the value of such monitoring is uncertain. Therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.

The fenofibrate in TriCor has a major potential interaction with Myopathy.

Severe myopathy, including rhabdomyolysis with acute renal failure secondary to myoglobinuria, has been reported rarely with the use of fibric acid derivatives. The myopathy may be dose-related and is characterized by muscle aches and/or weakness in conjunction with increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with fibric acid derivatives should be administered cautiously in patients with preexisting myopathy or a myoneural disorder, since it may delay the recognition or confound the diagnosis of a drug-induced musculoskeletal effect. Patients should be advised to report promptly any unusual muscle pain, tenderness or weakness, particularly if accompanied by malaise or fever. Periodic CPK determinations may be considered in some patients, although the value of such monitoring is uncertain. Therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.

The fenofibrate in TriCor has a major potential interaction with Primary Biliary Cholangitis.

The use of fibric acid derivatives is contraindicated in patients with primary biliary cirrhosis. These agents may further raise the already elevated cholesterol in these patients.

Proguanil has a major potential interaction with Renal Dysfunction.

Atovaquone and Proguanil tablets are contraindicated for prophylaxis of P. falciparum malaria in patients with severe renal impairment (creatinine clearance <30 mL/min) because of pancytopenia in patients with severe renal impairment treated with proguanil. Use with caution for the treatment of malaria in patients with severe renal impairment, only if the benefits of the 3-day treatment regimen outweigh the potential risks associated with increased drug exposure. No dosage adjustments are needed in patients with mild (creatinine clearance 50 to 80 mL/min) or moderate (creatinine clearance 30 to 50 mL/min) renal impairment.

The fenofibrate in TriCor has a major potential interaction with Renal Dysfunction.

The use of fibric acid derivatives is contraindicated in patients with significantly impaired renal function. The rate of clearance of fenofibric acid has been shown to decrease substantially when CrCl is below 50 mL/min, with drug accumulation during chronic dosing. Increased adverse effects, including rhabdomyolysis (with or without secondary renal failure) and severe hyperkalemia, have been associated with the use of fibric acid derivatives in patients with renal insufficiency. Therapy with these agents should be administered cautiously in patients with mild or moderate renal impairment. Close clinical monitoring is recommended during therapy.