Can you take Caltrate 600+D with Eltrombopag?

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.

Eltrombopag has a moderate potential interaction with Cataract.

In clinical trials, eltrombopag developed or worsened cataracts in 7% of the patients receiving treatment. A baseline ocular examination prior to administration of eltrombopag is recommended, and regular monitoring for signs and symptoms of cataracts should be performed regularly during treatment.

Eltrombopag has a moderate potential interaction with History, Thrombotic/Thromboembolic Disorder.

Thromboembolic complications may result from increases in platelet counts with TPO receptor agonists such as avatrombopag, lusutrombopag, and eltrombopag. Consider the potential for increased risk of thromboembolism when administering these medications to patients with known risk factors for thromboembolism, including genetic prothrombotic conditions (Factor V Leiden, Prothrombin 20210 A, Antithrombin deficiency or Protein C or S deficiency).

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.

Eltrombopag has a major potential interaction with Infectious Hepatitis.

Eltrombopag has shown to increase the risk of hepatic decompensation in patients with chronic hepatitis C in treatment with interferon and ribavirin. Clinical trials reported that ascites and encephalopathy occurred more frequently on these patients than in the placebo arm. Patients with chronic hepatitis and receiving antiviral treatment should be closely monitored. The manufacturers also recommend to discontinue eltrombopag if the antiviral therapy is discontinued.

Eltrombopag has a major potential interaction with Liver Disease.

Eltrombopag can cause liver enzyme elevations. Monitor ALT, AST and bilirubin prior to treatment initiation, and every 2 weeks during dose adjustment phase and then monthly. If abnormalities are confirmed, monitor serum liver tests weekly until resolved or stabilized. Treatment should be discontinued if ALT levels increase to greater than or equal to 3 x ULN in patients with normal liver function, or greater or equal to 3 x baseline in patients with pretreatment transaminase elevations that are progressively increasing, persist for 4 weeks or more, also have an increase in bilirubin, or also have clinical symptoms of liver injury or hepatic decompensation.

Hepatic impairment influences the exposure to eltrombopag. The initial dose should be reduced in patients with chronic ITP or severe aplastic anemia who have hepatic impairment. No dose adjustment is required on patients with chronic hepatitis C and hepatic impairment.

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.

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.

Eltrombopag has a moderate potential interaction with Protein C Deficiency.

Thromboembolic complications may result from increases in platelet counts with TPO receptor agonists such as avatrombopag, lusutrombopag, and eltrombopag. Consider the potential for increased risk of thromboembolism when administering these medications to patients with known risk factors for thromboembolism, including genetic prothrombotic conditions (Factor V Leiden, Prothrombin 20210 A, Antithrombin deficiency or Protein C or S deficiency).

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.

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.

Eltrombopag has a moderate potential interaction with Thrombotic/Thromboembolic Disorder.

Thromboembolic complications may result from increases in platelet counts with TPO receptor agonists such as avatrombopag, lusutrombopag, and eltrombopag. Consider the potential for increased risk of thromboembolism when administering these medications to patients with known risk factors for thromboembolism, including genetic prothrombotic conditions (Factor V Leiden, Prothrombin 20210 A, Antithrombin deficiency or Protein C or S deficiency).