Interactions between Trandolapril and Trimethoprim

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.

Trandolapril has a major potential interaction with Angioedema.

The use of these agents is contraindicated in patients with hereditary angioedema or a history of idiopathic angioedema. Patients with a history of angioedema unrelated to ACE inhibitors may be at increased risk of angioedema while receiving an ACE inhibitor. Patients should be advised to immediately report any signs or symptoms suggestive of angioedema (swelling of face, extremities, eyes, lips, or tongue, or difficulty swallowing or breathing) and to stop taking the medication until otherwise directed by their physician. Emergency therapy and/or measures to prevent airway obstruction are required for angioedema involving the tongue, glottis, or larynx. Treatment with ACE inhibitors should be discontinued permanently if angioedema develops in association with therapy.

Trandolapril has a major potential interaction with Bone Marrow Depression/Low Blood Counts.

ACE inhibitors may cause bone marrow suppression, rarely in uncomplicated individuals but more frequently in patients with renal impairment, especially if they also have a collagen-vascular disease such as systemic lupus erythematosus or scleroderma. Neutropenia, agranulocytosis, aplastic anemia, hemolytic anemia, eosinophilia and thrombocytopenia have been reported, mostly with captopril. Therapy with ACE inhibitors should be administered cautiously in patients with preexisting blood dyscrasias or complications that may increase the risk of bone marrow depression during ACE inhibitor therapy. Monitoring of blood counts, particularly white blood cells, should be considered.

Trandolapril has a major potential interaction with Cerebrovascular Insufficiency.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.

Trandolapril has a major potential interaction with Collagen Vascular Disease.

ACE inhibitors may cause bone marrow suppression, rarely in uncomplicated individuals but more frequently in patients with renal impairment, especially if they also have a collagen-vascular disease such as systemic lupus erythematosus or scleroderma. Neutropenia, agranulocytosis, aplastic anemia, hemolytic anemia, eosinophilia and thrombocytopenia have been reported, mostly with captopril. Therapy with ACE inhibitors should be administered cautiously in patients with preexisting blood dyscrasias or complications that may increase the risk of bone marrow depression during ACE inhibitor therapy. Monitoring of blood counts, particularly white blood cells, should be considered.

Trandolapril has a major potential interaction with Dehydration.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.

Trandolapril has a major potential interaction with Diabetes Mellitus.

In patients with hyperkalemia, especially those associated with impaired renal function or congestive heart failure, ACE inhibitors may further raise serum potassium levels. Therapy with ACE inhibitors should be administered cautiously in patients with or predisposed to hyperkalemia, and serum potassium levels should be carefully monitored. Risk factors for the development of hyperkalemia during ACE inhibitor therapy include renal insufficiency, diabetes mellitus, and the concomitant use of potassium-sparing diuretics, potassium supplements, and/or potassium-containing salt substitutes.

Trandolapril has a major potential interaction with Diarrhea.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.

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.

Trandolapril has a major potential interaction with Hemodialysis.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.

Trandolapril has a major potential interaction with Hemodialysis.

Anaphylactoid reactions have been reported in patients undergoing hemodialysis with high-flux polyacrylonitrile membranes and treated concomitantly with an ACE inhibitor. The frequency and mechanism of this interaction have not been established, and it is not known whether the interaction occurs with other membrane types. Therapy with ACE inhibitors should be administered cautiously in patients requiring hemodialysis.

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.

Trandolapril has a major potential interaction with Hyperkalemia.

In patients with hyperkalemia, especially those associated with impaired renal function or congestive heart failure, ACE inhibitors may further raise serum potassium levels. Therapy with ACE inhibitors should be administered cautiously in patients with or predisposed to hyperkalemia, and serum potassium levels should be carefully monitored. Risk factors for the development of hyperkalemia during ACE inhibitor therapy include renal insufficiency, diabetes mellitus, and the concomitant use of potassium-sparing diuretics, potassium supplements, and/or potassium-containing salt substitutes.

Trandolapril has a major potential interaction with Hyponatremia.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.

Trandolapril has a major potential interaction with Ischemic Heart Disease.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.

Trandolapril has a major potential interaction with Liver Disease.

The clearance of trandolapril and its active metabolite, trandolaprilat, may be decreased in patients with hepatic cirrhosis. Following oral administration in patients with mild to moderate alcoholic cirrhosis, plasma concentrations of trandolapril and trandolaprilat were 9-fold and 2-fold greater, respectively, than in normal subjects. However, the inhibition of ACE activity was not affected. The manufacturer states that lower initial dosages should be considered in patients with hepatic insufficiency.

Trandolapril has a moderate potential interaction with Liver Disease.

Rarely, elevations of liver enzymes and/or serum bilirubin have occurred with the use of ACE inhibitors. Patients receiving ACE inhibitors who develop jaundice or marked elevations of hepatic enzymes should discontinue the ACE inhibitor and receive appropriate medical follow-up.

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.

Trandolapril has a major potential interaction with Renal Dysfunction.

In patients with hyperkalemia, especially those associated with impaired renal function or congestive heart failure, ACE inhibitors may further raise serum potassium levels. Therapy with ACE inhibitors should be administered cautiously in patients with or predisposed to hyperkalemia, and serum potassium levels should be carefully monitored. Risk factors for the development of hyperkalemia during ACE inhibitor therapy include renal insufficiency, diabetes mellitus, and the concomitant use of potassium-sparing diuretics, potassium supplements, and/or potassium-containing salt substitutes.

Trandolapril has a major potential interaction with Renal Dysfunction.

ACE inhibitors may cause bone marrow suppression, rarely in uncomplicated individuals but more frequently in patients with renal impairment, especially if they also have a collagen-vascular disease such as systemic lupus erythematosus or scleroderma. Neutropenia, agranulocytosis, aplastic anemia, hemolytic anemia, eosinophilia and thrombocytopenia have been reported, mostly with captopril. Therapy with ACE inhibitors should be administered cautiously in patients with preexisting blood dyscrasias or complications that may increase the risk of bone marrow depression during ACE inhibitor therapy. Monitoring of blood counts, particularly white blood cells, should be considered.

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.

Trandolapril has a moderate potential interaction with Renal Dysfunction.

With the exception of fosinopril, ACE inhibitors (and/or their active metabolites in some cases) are primarily eliminated by the kidney and may accumulate in patients with renal impairment. ACE inhibitors can also worsen renal function in some patients by blocking the effect of angiotensin II-mediated efferent arteriolar vasoconstriction, thereby decreasing glomerular filtration. Therapy with ACE inhibitors should be administered cautiously in patients with preexisting renal dysfunction, particularly those with renovascular disease. Patients with moderate to severe renal impairment usually require lower or less frequent doses and smaller increments in dose. In addition, a dosage reduction or discontinuation of any concomitantly administered diuretics may be helpful. Fosinopril probably does not require dosage adjustments unless hepatic function is also significantly impaired.

In patients with bilateral renal artery stenosis or renal artery stenosis in a solitary kidney, ACE inhibitors may reduce renal perfusion to a critically low level. Renal function should be monitored closely for the first few weeks of therapy.

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.

Trandolapril has a major potential interaction with Vomiting.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.