Can you take Caltrate 600+D with Ticlopidine?

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.

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.

Ticlopidine has a major potential interaction with Bleeding Disorder.

The use of ticlopidine is contraindicated in patients with hemostatic disorders such as vascular defect or coagulation dysfunction or active pathological bleeding such as peptic ulcer disease or intracranial hemorrhage. Ticlopidine induces an irreversible inhibition of platelet aggregation resulting in a prolongation of bleeding time.

Ticlopidine has a major potential interaction with Coagulation Defects and Disorders.

The use of ticlopidine is contraindicated in patients with hemostatic disorders such as vascular defect or coagulation dysfunction or active pathological bleeding such as peptic ulcer disease or intracranial hemorrhage. Ticlopidine induces an irreversible inhibition of platelet aggregation resulting in a prolongation of bleeding time.

Ticlopidine has a moderate potential interaction with High Cholesterol.

Ticlopidine can induce increases in serum cholesterol and triglycerides. Serum total cholesterol levels have increased 8% to 10% in some patients within 1 month of initiation of ticlopidine therapy and have persisted at those levels. Clinical monitoring of lipid profiles is recommended during ticlopidine therapy in patients at risk for hyperlipidemia-associated adverse events.

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.

Ticlopidine has a major potential interaction with Liver Disease.

The use of ticlopidine is contraindicated in patients with severe hepatic impairment. Ticlopidine is extensively metabolized to inactive forms by the liver. Therapy with ticlopidine should be administered cautiously in patients with mild to moderate hepatic impairment and dosage modifications should be considered. Clinical monitoring of hepatic function and bleeding activity is recommended.

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.

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.

Ticlopidine has a major potential interaction with Neutropenia.

The use of ticlopidine is contraindicated in patients with hematopoietic disorders such as neutropenia and/or thrombocytopenia or a past history of thrombotic thrombocytopenic purpura (TTP) or aplastic anemia. Ticlopidine can cause life-threatening hematological adverse reactions, including neutropenia/agranulocytosis, TTP and aplastic anemia. Clinical monitoring of hematopoietic function is required for all patients receiving ticlopidine, since severe hematopoietic disorders may develop suddenly, usually within the first 3 weeks to 3 months of therapy. CBCs (including differential and platelet count) should be performed prior to initiation of ticlopidine and every 2 weeks through the first 3 months or as often as necessary.

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.

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.

Ticlopidine has a moderate potential interaction with Renal Dysfunction.

Ticlopidine is primarily eliminated by the kidney, and there is limited experience in patients with renal impairment. Elevated serum concentration of ticlopidine and prolonged half-live have been noted in patients with mild and moderate renal impairment. Prolonged bleeding times have been reported in patients with moderate renal impairment. Therapy with ticlopidine should be administered cautiously in patients with compromised renal function and dosage modifications may be necessary.

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.

Ticlopidine has a major potential interaction with Thrombocytopathy.

The use of ticlopidine is contraindicated in patients with hemostatic disorders such as vascular defect or coagulation dysfunction or active pathological bleeding such as peptic ulcer disease or intracranial hemorrhage. Ticlopidine induces an irreversible inhibition of platelet aggregation resulting in a prolongation of bleeding time.

Ticlopidine has a major potential interaction with Thrombocytopenia.

The use of ticlopidine is contraindicated in patients with hematopoietic disorders such as neutropenia and/or thrombocytopenia or a past history of thrombotic thrombocytopenic purpura (TTP) or aplastic anemia. Ticlopidine can cause life-threatening hematological adverse reactions, including neutropenia/agranulocytosis, TTP and aplastic anemia. Clinical monitoring of hematopoietic function is required for all patients receiving ticlopidine, since severe hematopoietic disorders may develop suddenly, usually within the first 3 weeks to 3 months of therapy. CBCs (including differential and platelet count) should be performed prior to initiation of ticlopidine and every 2 weeks through the first 3 months or as often as necessary.