Can you take Caltrate 600+D with Lisinopril?

The calcium carbonate in Caltrate 600+D has a major potential interaction with Achlorhydria.

Calcium is absorbed from the intestinal tract by active transport and passive diffusion. Malabsorption syndromes (celiac disease, GI resection), deficiency of vitamin D, parathyroid hormone, or calcitonin, or an alkaline gastric pH (achlorhydria, carbonate or phosphate salts) can decrease the absorption of oral formulations of calcium. Calcium is available in oral and parenteral formulations.

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.

The calcium carbonate in Caltrate 600+D has a major potential interaction with Arrhythmia.

Calcium is involved in cardiac muscle contraction and electrical impulse conduction. Therapy with calcium salt formulations (particularly IV) should be administered cautiously to patients with cardiac disease. Patients receiving cardiac glycosides and concomitant IV calcium may experience arrhythmias. Therapy with IV calcium should be administered slowly and at reduced dosages in patients with cardiac disease.

The ergocalciferol in Caltrate 600+D has a moderate potential interaction with Arrhythmia.

Vitamin D analogs function to increase serum calcium concentrations and can exacerbate arrhythmias, particularly in patients receiving cardiac glycosides. Therapy with vitamin D analogs should be administered cautiously in patients with or predisposed to cardiac arrhythmias. Clinical monitoring of serum electrolyte concentrations and cardiac function is recommended.

The ergocalciferol in Caltrate 600+D has a moderate potential interaction with Biliary Obstruction.

Vitamin D analogs are fat soluble and oral formulations require bile for adequate intestinal absorption. Hepatic and/or biliary dysfunction decrease the absorption of vitamin D analogs. Metabolites of vitamin D analogs are primarily excreted in bile and feces. Ergocalciferol, cholecalciferol, and dihydrotachysterol undergo hepatic hydroxylation during metabolic activation. Hepatic impairment can alter the metabolic and therapeutic activity of certain vitamin D analogs. Alternative vitamin D analogs such as calcitriol (active form) may be considered in patients with compromised hepatic function.

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.

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.

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.

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.

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.

The ergocalciferol in Caltrate 600+D has a major potential interaction with Hypercalcemia.

Vitamin D analogs such as calciferol and ergocalciferol should not be given to patients with hypercalcemia, malabsorption syndrome, or evidence of vitamin D toxicity.

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.

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.

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 ergocalciferol in Caltrate 600+D has a moderate potential interaction with Liver Disease.

Vitamin D analogs are fat soluble and oral formulations require bile for adequate intestinal absorption. Hepatic and/or biliary dysfunction decrease the absorption of vitamin D analogs. Metabolites of vitamin D analogs are primarily excreted in bile and feces. Ergocalciferol, cholecalciferol, and dihydrotachysterol undergo hepatic hydroxylation during metabolic activation. Hepatic impairment can alter the metabolic and therapeutic activity of certain vitamin D analogs. Alternative vitamin D analogs such as calcitriol (active form) may be considered in patients with compromised hepatic function.

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 calcium carbonate in Caltrate 600+D has a major potential interaction with Malabsorption Syndrome.

Calcium is absorbed from the intestinal tract by active transport and passive diffusion. Malabsorption syndromes (celiac disease, GI resection), deficiency of vitamin D, parathyroid hormone, or calcitonin, or an alkaline gastric pH (achlorhydria, carbonate or phosphate salts) can decrease the absorption of oral formulations of calcium. Calcium is available in oral and parenteral formulations.

The ergocalciferol in Caltrate 600+D has a major potential interaction with Malabsorption Syndrome.

Vitamin D analogs such as calciferol and ergocalciferol should not be given to patients with hypercalcemia, malabsorption syndrome, or evidence of vitamin D toxicity.

The calcium carbonate in Caltrate 600+D has a major potential interaction with Phosphate Imbalance.

Elevated serum concentrations of calcium and phosphate can exceed the solubility level and result in calcium- phosphate precipitates that deposit in vascular and renal systems as well as other soft tissues of the body. Therapy with calcium should be administered with extreme caution in patients with hyperphosphatemia (hypoparathyroidism or severe renal impairment). Administration of oral calcium acetate or calcium carbonate, in addition to providing calcium, complexes phosphates within the GI tract. These complexes are eliminated in the feces. Clinical monitoring of serum calcium and phosphate concentrations is necessary.

The ergocalciferol in Caltrate 600+D has a moderate potential interaction with Phosphate Imbalance.

Vitamin D analogs administered in the presence of hyperphosphatemia can result in precipitation of calcium-phosphate deposits within the vascular or renal systems or other soft tissue calcifications. A solubility product (Serum Calcium X Phosphate) should not exceed 70. Serum electrolyte concentrations should be corrected prior to vitamin D analog therapy and monitored during therapy.

The calcium carbonate in Caltrate 600+D has a major potential interaction with Renal Dysfunction.

Absorption of oral calcium formulations may be altered and elimination of calcium by the kidney decreased with renal impairment. Hyperphosphatemia occurs during renal failure. Calcium acetate or calcium carbonate, in addition to providing calcium, complexes phosphates within the GI tract. Calcium carbonate can partially correct metabolic acidosis associated with chronic renal failure. Clinical monitoring of renal function and serum calcium and phosphate concentrations is necessary.

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.

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.

The ergocalciferol in Caltrate 600+D has a moderate potential interaction with Renal Dysfunction.

Ergocalciferol and cholecalciferol undergo renal biotransformation during metabolic activation. Renal impairment can alter metabolic and therapeutic activity of certain vitamin D analogs. Alternative vitamin D analogs such as dihydrotachysterol (hepatic activation) and calcitriol (active form) may be considered in patients with compromised renal function.

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 calcium carbonate in Caltrate 600+D has a major potential interaction with Sarcoidosis.

Hypercalciuria, with or without hypercalcemia, may occasionally occur in patients with sarcoidosis. Elevated calcium levels may result from increased intestinal absorption of calcium, which is related to the extrarenal production of vitamin D by mononuclear phagocytes present within the sarcoid granuloma. Therapy with calcium salts should be administered cautiously and only if necessary in patients with sarcoidosis.

The ergocalciferol in Caltrate 600+D has a major potential interaction with Tachyarrhythmia.

The amine ergot alkaloids, ergonovine and methylergonovine, can cause serious cardiovascular complications because of their vasospastic effects. Hypertension (more often with ergonovine) has been most commonly reported, particularly when administered IV undiluted or at an excessive rate or when used in conjunction with regional anesthesia or vasoconstrictors. Headaches, seizures, cerebrovascular accidents and death have been associated with the hypertensive episodes. Other, less common adverse effects include acute myocardial infarction, transient chest pains, thrombophlebitis, tachycardia and palpitations. Therapy with ergot alkaloids should generally be avoided, except under special circumstances, in patients with chronic hypertension, preeclampsia or eclampsia, cardiovascular disease, cerebrovascular disease, or peripheral vascular disease. Caution is advised when these agents are administered to patients with venoatrial shunts, mitral valve stenosis, or sepsis. Close monitoring of cardiovascular status is highly recommended during therapy.

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.