Can you take Lisinopril with Proben-C?

The probenecid in Proben-C has a major potential interaction with Anemia.

The manufacturer does not recommend the use of probenecid in patients with known blood dyscrasias. Aplastic anemia, leukopenia, hemolytic anemia and other anemia have been reported infrequently during administration of probenecid. Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency may increase the risk of probenecid-induced hemolytic anemia.

Lisinopril 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.

Lisinopril 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.

The probenecid in Proben-C has a major potential interaction with Bone Marrow Depression/Low Blood Counts.

The manufacturer does not recommend the use of probenecid in patients with known blood dyscrasias. Aplastic anemia, leukopenia, hemolytic anemia and other anemia have been reported infrequently during administration of probenecid. Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency may increase the risk of probenecid-induced hemolytic anemia.

The colchicine in Proben-C has a major potential interaction with Bone Marrow Depression/Low Blood Counts.

The use of colchicine should be used with caution in patients with bone marrow suppression. Patients on long term therapy may require periodic blood counts.

The colchicine in Proben-C has a major potential interaction with Cardiovascular Conditions and Disorders.

The use of colchicine should be used with caution in patients with cardiac dysfunction. The possibility of cumulative effects of colchicine is increased in these patients.

Lisinopril 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.

Lisinopril 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.

Lisinopril 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.

The probenecid in Proben-C has a major potential interaction with Dehydration.

Probenecid may promote lithiasis by increasing uric acid concentration in the renal tubules. Adequate hydration is necessary during therapy. Patients who are dehydrated (e.g., due to severe diarrhea or vomiting) may be at increased risk for the development of uric acid kidney stones and should be encouraged to consume additional amounts of liquid or given intravenous fluid. In general, fluid intake sufficient to yield a daily urinary output of at least 2 liters is recommended. Maintenance of a slightly alkaline or neutral urine is also desirable.

Lisinopril 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.

Lisinopril 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.

The probenecid in Proben-C has a major potential interaction with Diarrhea.

Probenecid may promote lithiasis by increasing uric acid concentration in the renal tubules. Adequate hydration is necessary during therapy. Patients who are dehydrated (e.g., due to severe diarrhea or vomiting) may be at increased risk for the development of uric acid kidney stones and should be encouraged to consume additional amounts of liquid or given intravenous fluid. In general, fluid intake sufficient to yield a daily urinary output of at least 2 liters is recommended. Maintenance of a slightly alkaline or neutral urine is also desirable.

The colchicine in Proben-C has a major potential interaction with Disseminated Intravascular Coagulation.

Colchicine should be used with caution in patients with disseminated intravascular coagulation. Debilitated patients have an increased risk of developing colchicine toxicity.

The colchicine in Proben-C has a major potential interaction with Electrolyte Abnormalities.

Electrolyte imbalances including hypokalemia and hyponatremia may worsen in patients taking colchicine as the most common adverse effects of colchicine include nausea and vomiting. Therapy with colchicine should be administered with caution in patients with electrolyte imbalances. Monitoring serum electrolytes is recommended in these patients.

The probenecid in Proben-C has a major potential interaction with Gouty Nephropathy.

The use of probenecid is not recommended in patients with a history of uric acid nephrolithiasis or a urinary urate excretion greater than 750 mg/24 hr. Probenecid may promote lithiasis by increasing uric acid concentration in the renal tubules. Adequate hydration is necessary during treatment. In general, a fluid intake sufficient to yield a daily urinary output of at least 2 liters is recommended. Maintenance of a slightly alkaline urine is also desirable.

Lisinopril 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.

Lisinopril 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.

The probenecid in Proben-C has a major potential interaction with History, Nephrolithiasis.

The use of probenecid is not recommended in patients with a history of uric acid nephrolithiasis or a urinary urate excretion greater than 750 mg/24 hr. Probenecid may promote lithiasis by increasing uric acid concentration in the renal tubules. Adequate hydration is necessary during treatment. In general, a fluid intake sufficient to yield a daily urinary output of at least 2 liters is recommended. Maintenance of a slightly alkaline urine is also desirable.

The probenecid in Proben-C has a moderate potential interaction with History, Peptic Ulcer.

The manufacturer states that probenecid should be used with caution in patients with a history of peptic ulcer. Uricosuric agents can cause upper gastrointestinal irritation and aggravate or reactivate peptic ulcer. However, these effects have primarily been reported with another uricosuric agent, sulfinpyrazone. GI effects associated with probenecid are usually limited to nausea, vomiting, and anorexia.

Lisinopril 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.

The colchicine in Proben-C has a major potential interaction with Hypokalemia.

Electrolyte imbalances including hypokalemia and hyponatremia may worsen in patients taking colchicine as the most common adverse effects of colchicine include nausea and vomiting. Therapy with colchicine should be administered with caution in patients with electrolyte imbalances. Monitoring serum electrolytes is recommended in these patients.

Lisinopril 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.

The colchicine in Proben-C has a major potential interaction with Hyponatremia.

Electrolyte imbalances including hypokalemia and hyponatremia may worsen in patients taking colchicine as the most common adverse effects of colchicine include nausea and vomiting. Therapy with colchicine should be administered with caution in patients with electrolyte imbalances. Monitoring serum electrolytes is recommended in these patients.

Lisinopril 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.

The colchicine in Proben-C has a major potential interaction with Liver Disease.

The clearance of colchicine may be significantly reduced and plasma half-life prolonged in patients with chronic hepatic impairment compared to healthy subject. No pharmacokinetic data are available for patients with severe hepatic impairment (Child-Pugh C). Caution is recommended when prescribing colchicine to these patients.

Lisinopril 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.

The colchicine in Proben-C has a moderate potential interaction with Liver Disease.

Colchicine-induced neuromuscular toxicity and rhabdomyolysis have been reported with chronic treatment in therapeutic doses. Patients with renal dysfunction and elderly patients, even those with normal renal and hepatic function, are at increased risk. Caution must be exercised when colchicine therapy is instituted in these patients.

The probenecid in Proben-C has a moderate potential interaction with Peptic Ulcer.

The manufacturer states that probenecid should be used with caution in patients with a history of peptic ulcer. Uricosuric agents can cause upper gastrointestinal irritation and aggravate or reactivate peptic ulcer. However, these effects have primarily been reported with another uricosuric agent, sulfinpyrazone. GI effects associated with probenecid are usually limited to nausea, vomiting, and anorexia.

Lisinopril 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.

Lisinopril 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.

The colchicine in Proben-C has a major potential interaction with Renal Dysfunction.

Colchicine is significantly excreted in urine in healthy subjects. Clearance of colchicine is decreased in patients with impaired renal function. Colchicine dosing must be individualized according to the patient's renal function. Caution must be exercised when colchicine therapy is instituted in these patients. Monitoring creatinine function is recommended in patients on long term therapy.

Lisinopril 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.

The colchicine in Proben-C has a moderate potential interaction with Renal Dysfunction.

Colchicine-induced neuromuscular toxicity and rhabdomyolysis have been reported with chronic treatment in therapeutic doses. Patients with renal dysfunction and elderly patients, even those with normal renal and hepatic function, are at increased risk. Caution must be exercised when colchicine therapy is instituted in these patients.

The probenecid in Proben-C has a moderate potential interaction with Renal Dysfunction.

Probenecid may not be effective in patients with chronic renal insufficiency, particularly when glomerular filtration rate is 30 mL/min or less. Probenecid has been used in patients with some renal impairment but dosage requirements may be increased.

The probenecid in Proben-C has a major potential interaction with Uric Acid Nephrolithiasis.

The use of probenecid is not recommended in patients with a history of uric acid nephrolithiasis or a urinary urate excretion greater than 750 mg/24 hr. Probenecid may promote lithiasis by increasing uric acid concentration in the renal tubules. Adequate hydration is necessary during treatment. In general, a fluid intake sufficient to yield a daily urinary output of at least 2 liters is recommended. Maintenance of a slightly alkaline urine is also desirable.

Lisinopril 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.

The probenecid in Proben-C has a major potential interaction with Vomiting.

Probenecid may promote lithiasis by increasing uric acid concentration in the renal tubules. Adequate hydration is necessary during therapy. Patients who are dehydrated (e.g., due to severe diarrhea or vomiting) may be at increased risk for the development of uric acid kidney stones and should be encouraged to consume additional amounts of liquid or given intravenous fluid. In general, fluid intake sufficient to yield a daily urinary output of at least 2 liters is recommended. Maintenance of a slightly alkaline or neutral urine is also desirable.