Drug Interaction Report

Trimethoprim has a major potential interaction with Alcoholism.

The use of trimethoprim is contraindicated in patients with documented megaloblastic anemia due to folate deficiency. Trimethoprim inhibits dihydrofolate reductase, an enzyme necessary in the synthesis of tetrahydrofolic acid, or the metabolically active form of folic acid. Thrombocytopenia, neutropenia, megaloblastic anemia, and methemoglobinemia have been reported rarely. However, the risk is increased in the presence of folate deficiency, chronic hemolytic anemia and/or renal impairment, as well as during prolonged therapy (e.g., > 6 months) with high dosages. Therapy with trimethoprim should be administered cautiously under these conditions and in patients with suspected folate depletion (e.g., elderly, alcoholic, malnourished or debilitated patients). Folic acid supplementation, if necessary, may be administered concomitantly without interfering with the antibacterial action of trimethoprim. Patients should be instructed to immediately report any signs or symptoms suggestive of hematologic toxicity such as fever, sore throat, local infection, bleeding, pallor, dizziness, or jaundice. Leucovorin (folinic acid) should be administered if bone marrow depression is detected.

Trimethoprim has a major potential interaction with Anemia, Folate Deficiency.

The use of trimethoprim is contraindicated in patients with documented megaloblastic anemia due to folate deficiency. Trimethoprim inhibits dihydrofolate reductase, an enzyme necessary in the synthesis of tetrahydrofolic acid, or the metabolically active form of folic acid. Thrombocytopenia, neutropenia, megaloblastic anemia, and methemoglobinemia have been reported rarely. However, the risk is increased in the presence of folate deficiency, chronic hemolytic anemia and/or renal impairment, as well as during prolonged therapy (e.g., > 6 months) with high dosages. Therapy with trimethoprim should be administered cautiously under these conditions and in patients with suspected folate depletion (e.g., elderly, alcoholic, malnourished or debilitated patients). Folic acid supplementation, if necessary, may be administered concomitantly without interfering with the antibacterial action of trimethoprim. Patients should be instructed to immediately report any signs or symptoms suggestive of hematologic toxicity such as fever, sore throat, local infection, bleeding, pallor, dizziness, or jaundice. Leucovorin (folinic acid) should be administered if bone marrow depression is detected.

The rosuvastatin in Crestor has a moderate potential interaction with Central Nervous System Disorders.

Cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion) have been observed in patients receiving statins. The reports are usually not serious, and reversible upon statin discontinuation. Caution is recommended when using these agents in patients with cognitive impairment.

The rosuvastatin in Crestor has a moderate potential interaction with Diabetes Mellitus.

Increases in hemoglobin A1c and fasting serum glucose levels have been reported with the use of certain HMG-CoA reductase inhibitors. Caution should be exercised when using these agents in diabetic patients and close monitoring is recommended.

Trimethoprim has a major potential interaction with Folic Acid/Cyanocobalamin Deficiency.

The use of trimethoprim is contraindicated in patients with documented megaloblastic anemia due to folate deficiency. Trimethoprim inhibits dihydrofolate reductase, an enzyme necessary in the synthesis of tetrahydrofolic acid, or the metabolically active form of folic acid. Thrombocytopenia, neutropenia, megaloblastic anemia, and methemoglobinemia have been reported rarely. However, the risk is increased in the presence of folate deficiency, chronic hemolytic anemia and/or renal impairment, as well as during prolonged therapy (e.g., > 6 months) with high dosages. Therapy with trimethoprim should be administered cautiously under these conditions and in patients with suspected folate depletion (e.g., elderly, alcoholic, malnourished or debilitated patients). Folic acid supplementation, if necessary, may be administered concomitantly without interfering with the antibacterial action of trimethoprim. Patients should be instructed to immediately report any signs or symptoms suggestive of hematologic toxicity such as fever, sore throat, local infection, bleeding, pallor, dizziness, or jaundice. Leucovorin (folinic acid) should be administered if bone marrow depression is detected.

The rosuvastatin in Crestor has a moderate potential interaction with Hematuria.

An association between rosuvastatin and the development of proteinuria and microscopic hematuria was observed among treated patients during clinical trials. Patients with unexplained persistent proteinuria and/or hematuria during routine urinalysis testing should be instructed to reduce the dose of rosuvastatin according to clinical standards. Therapy with rosuvastatin should be administered cautiously in patients showing abnormal urinalysis. Monitoring for proteinuria and hematuria is recommended.

Trimethoprim has a moderate potential interaction with Hemodialysis.

Trimethoprim is moderately removed by hemodialysis. Doses should either be scheduled for administration after dialysis or supplemental doses be given after dialysis.

Trimethoprim has a major potential interaction with Hemolytic Anemia.

The use of trimethoprim is contraindicated in patients with documented megaloblastic anemia due to folate deficiency. Trimethoprim inhibits dihydrofolate reductase, an enzyme necessary in the synthesis of tetrahydrofolic acid, or the metabolically active form of folic acid. Thrombocytopenia, neutropenia, megaloblastic anemia, and methemoglobinemia have been reported rarely. However, the risk is increased in the presence of folate deficiency, chronic hemolytic anemia and/or renal impairment, as well as during prolonged therapy (e.g., > 6 months) with high dosages. Therapy with trimethoprim should be administered cautiously under these conditions and in patients with suspected folate depletion (e.g., elderly, alcoholic, malnourished or debilitated patients). Folic acid supplementation, if necessary, may be administered concomitantly without interfering with the antibacterial action of trimethoprim. Patients should be instructed to immediately report any signs or symptoms suggestive of hematologic toxicity such as fever, sore throat, local infection, bleeding, pallor, dizziness, or jaundice. Leucovorin (folinic acid) should be administered if bone marrow depression is detected.

Trimethoprim has a major potential interaction with Malnourishment.

The use of trimethoprim is contraindicated in patients with documented megaloblastic anemia due to folate deficiency. Trimethoprim inhibits dihydrofolate reductase, an enzyme necessary in the synthesis of tetrahydrofolic acid, or the metabolically active form of folic acid. Thrombocytopenia, neutropenia, megaloblastic anemia, and methemoglobinemia have been reported rarely. However, the risk is increased in the presence of folate deficiency, chronic hemolytic anemia and/or renal impairment, as well as during prolonged therapy (e.g., > 6 months) with high dosages. Therapy with trimethoprim should be administered cautiously under these conditions and in patients with suspected folate depletion (e.g., elderly, alcoholic, malnourished or debilitated patients). Folic acid supplementation, if necessary, may be administered concomitantly without interfering with the antibacterial action of trimethoprim. Patients should be instructed to immediately report any signs or symptoms suggestive of hematologic toxicity such as fever, sore throat, local infection, bleeding, pallor, dizziness, or jaundice. Leucovorin (folinic acid) should be administered if bone marrow depression is detected.

The rosuvastatin in Crestor has a moderate potential interaction with Myoneural Disorder.

HMG-CoA reductase inhibitors may cause myopathy and rhabdomyolysis; acute renal failure secondary to myoglobinuria and rare fatalities have occurred due to rhabdomyolysis in patients treated with statins. The myopathy may be dose-related and is characterized by unexplained muscle weakness, pain, or tenderness accompanied by increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with preexisting myopathy, in those with predisposing factors for myopathy, or with a history of 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. HMG-CoA reductase inhibitor therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.

The rosuvastatin in Crestor has a moderate potential interaction with Myopathy.

HMG-CoA reductase inhibitors may cause myopathy and rhabdomyolysis; acute renal failure secondary to myoglobinuria and rare fatalities have occurred due to rhabdomyolysis in patients treated with statins. The myopathy may be dose-related and is characterized by unexplained muscle weakness, pain, or tenderness accompanied by increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with preexisting myopathy, in those with predisposing factors for myopathy, or with a history of 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. HMG-CoA reductase inhibitor therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.

The rosuvastatin in Crestor has a moderate potential interaction with Proteinuria.

An association between rosuvastatin and the development of proteinuria and microscopic hematuria was observed among treated patients during clinical trials. Patients with unexplained persistent proteinuria and/or hematuria during routine urinalysis testing should be instructed to reduce the dose of rosuvastatin according to clinical standards. Therapy with rosuvastatin should be administered cautiously in patients showing abnormal urinalysis. Monitoring for proteinuria and hematuria is recommended.

Trimethoprim has a major potential interaction with Renal Dysfunction.

The use of trimethoprim is contraindicated in patients with documented megaloblastic anemia due to folate deficiency. Trimethoprim inhibits dihydrofolate reductase, an enzyme necessary in the synthesis of tetrahydrofolic acid, or the metabolically active form of folic acid. Thrombocytopenia, neutropenia, megaloblastic anemia, and methemoglobinemia have been reported rarely. However, the risk is increased in the presence of folate deficiency, chronic hemolytic anemia and/or renal impairment, as well as during prolonged therapy (e.g., > 6 months) with high dosages. Therapy with trimethoprim should be administered cautiously under these conditions and in patients with suspected folate depletion (e.g., elderly, alcoholic, malnourished or debilitated patients). Folic acid supplementation, if necessary, may be administered concomitantly without interfering with the antibacterial action of trimethoprim. Patients should be instructed to immediately report any signs or symptoms suggestive of hematologic toxicity such as fever, sore throat, local infection, bleeding, pallor, dizziness, or jaundice. Leucovorin (folinic acid) should be administered if bone marrow depression is detected.

The rosuvastatin in Crestor has a moderate potential interaction with Renal Dysfunction.

HMG-CoA reductase inhibitors may cause myopathy and rhabdomyolysis; acute renal failure secondary to myoglobinuria and rare fatalities have occurred due to rhabdomyolysis in patients treated with statins. The myopathy may be dose-related and is characterized by unexplained muscle weakness, pain, or tenderness accompanied by increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with preexisting myopathy, in those with predisposing factors for myopathy, or with a history of 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. HMG-CoA reductase inhibitor therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.

The rosuvastatin in Crestor has a moderate potential interaction with Renal Dysfunction.

Some HMG-CoA reductase inhibitors (e.g., fluvastatin) have not been studied in patients with severe renal dysfunction or end-stage renal disease. Some others (e.g., pitavastatin, simvastatin) require a dose reduction when used in this group of patients. Caution and close monitoring are advised when using these drugs in patients with renal dysfunction.

Trimethoprim has a moderate potential interaction with Renal Dysfunction.

Trimethoprim is primarily eliminated by the kidney. The serum concentration of trimethoprim may be increased and the half-life prolonged in patients with impaired renal function. Dosage adjustments may be necessary and modifications should be based on the degree of renal impairment as well as severity of infection. The manufacturers recommend a dosage of 50 mg every 12 hours in patients with creatinine clearance between 15 to 30 mL/min and not using the drug in patients with creatinine clearance below 15 mL/min.

The rosuvastatin in Crestor has a moderate potential interaction with Underactive Thyroid.

HMG-CoA reductase inhibitors may cause myopathy and rhabdomyolysis; acute renal failure secondary to myoglobinuria and rare fatalities have occurred due to rhabdomyolysis in patients treated with statins. The myopathy may be dose-related and is characterized by unexplained muscle weakness, pain, or tenderness accompanied by increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with preexisting myopathy, in those with predisposing factors for myopathy, or with a history of 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. HMG-CoA reductase inhibitor therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.