Can you take Caltrate 600+D with Pravastatin?

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.

Pravastatin has a major potential interaction with Alcoholism.

The use of most HMG-CoA reductase inhibitors is contraindicated in patients with active liver disease, decompensated cirrhosis, or unexplained persistent elevations of serum transaminases. HMG-CoA reductase inhibitors are extensively metabolized by the liver. Decreased drug metabolism may lead to accumulation and increased risk of toxicity, including biochemical abnormalities of liver function and, rarely, jaundice, hepatitis, cirrhosis, fatty change in the liver, and fulminant hepatic necrosis. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with a history of liver disease and/or heavy alcohol use. A lower initial dosage may be appropriate, and clinical monitoring of liver transaminase levels according to the individual manufacturer product information is recommended. Patients who develop elevated ALT or AST levels during therapy should be monitored until abnormalities resolve. If an increase above 3 times the upper limit of normal persists, consideration should be given to a reduction in dosage or withdrawal of 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.

Pravastatin has a moderate potential interaction with Central Nervous System Disorders.

Cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion) have been observed in patients receiving statins. The reports are usually not serious, and reversible upon statin discontinuation. Caution is recommended when using these agents in patients with cognitive impairment.

Pravastatin has a moderate potential interaction with Diabetes Mellitus.

Increases in hemoglobin A1c and fasting serum glucose levels have been reported with the use of certain HMG-CoA reductase inhibitors. Caution should be exercised when using these agents in diabetic patients and close monitoring is recommended.

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.

Pravastatin has a major potential interaction with Liver Disease.

The use of most HMG-CoA reductase inhibitors is contraindicated in patients with active liver disease, decompensated cirrhosis, or unexplained persistent elevations of serum transaminases. HMG-CoA reductase inhibitors are extensively metabolized by the liver. Decreased drug metabolism may lead to accumulation and increased risk of toxicity, including biochemical abnormalities of liver function and, rarely, jaundice, hepatitis, cirrhosis, fatty change in the liver, and fulminant hepatic necrosis. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with a history of liver disease and/or heavy alcohol use. A lower initial dosage may be appropriate, and clinical monitoring of liver transaminase levels according to the individual manufacturer product information is recommended. Patients who develop elevated ALT or AST levels during therapy should be monitored until abnormalities resolve. If an increase above 3 times the upper limit of normal persists, consideration should be given to a reduction in dosage or withdrawal of therapy.

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 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 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.

Pravastatin has a moderate potential interaction with Myoneural Disorder.

HMG-CoA reductase inhibitors may cause myopathy and rhabdomyolysis; acute renal failure secondary to myoglobinuria and rare fatalities have occurred due to rhabdomyolysis in patients treated with statins. The myopathy may be dose-related and is characterized by unexplained muscle weakness, pain, or tenderness accompanied by increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with preexisting myopathy, in those with predisposing factors for myopathy, or with a history of myoneural disorder, since it may delay the recognition or confound the diagnosis of a drug-induced musculoskeletal effect. Patients should be advised to report promptly any unusual muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever. Periodic CPK determinations may be considered in some patients, although the value of such monitoring is uncertain. HMG-CoA reductase inhibitor therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.

Pravastatin has a moderate potential interaction with Myopathy.

HMG-CoA reductase inhibitors may cause myopathy and rhabdomyolysis; acute renal failure secondary to myoglobinuria and rare fatalities have occurred due to rhabdomyolysis in patients treated with statins. The myopathy may be dose-related and is characterized by unexplained muscle weakness, pain, or tenderness accompanied by increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with preexisting myopathy, in those with predisposing factors for myopathy, or with a history of myoneural disorder, since it may delay the recognition or confound the diagnosis of a drug-induced musculoskeletal effect. Patients should be advised to report promptly any unusual muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever. Periodic CPK determinations may be considered in some patients, although the value of such monitoring is uncertain. HMG-CoA reductase inhibitor therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.

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.

Pravastatin has a major potential interaction with Renal Dysfunction.

Pravastatin is partially eliminated by the kidney. Drug and/or metabolite accumulation may occur in patients with significant renal impairment, which may increase the risk of adverse effects, including hepatic and musculoskeletal toxicities. Therapy with pravastatin should be administered cautiously in patients with severely impaired renal function. A lower initial dosage may be appropriate, accompanied by close clinical monitoring.

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.

Pravastatin has a moderate potential interaction with Renal Dysfunction.

Some HMG-CoA reductase inhibitors (e.g., fluvastatin) have not been studied in patients with severe renal dysfunction or end-stage renal disease. Some others (e.g., pitavastatin, simvastatin) require a dose reduction when used in this group of patients. Caution and close monitoring are advised when using these drugs in patients with renal dysfunction.

Pravastatin has a moderate potential interaction with Renal Dysfunction.

HMG-CoA reductase inhibitors may cause myopathy and rhabdomyolysis; acute renal failure secondary to myoglobinuria and rare fatalities have occurred due to rhabdomyolysis in patients treated with statins. The myopathy may be dose-related and is characterized by unexplained muscle weakness, pain, or tenderness accompanied by increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with preexisting myopathy, in those with predisposing factors for myopathy, or with a history of myoneural disorder, since it may delay the recognition or confound the diagnosis of a drug-induced musculoskeletal effect. Patients should be advised to report promptly any unusual muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever. Periodic CPK determinations may be considered in some patients, although the value of such monitoring is uncertain. HMG-CoA reductase inhibitor therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.

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.

Pravastatin has a moderate potential interaction with Underactive Thyroid.

HMG-CoA reductase inhibitors may cause myopathy and rhabdomyolysis; acute renal failure secondary to myoglobinuria and rare fatalities have occurred due to rhabdomyolysis in patients treated with statins. The myopathy may be dose-related and is characterized by unexplained muscle weakness, pain, or tenderness accompanied by increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with preexisting myopathy, in those with predisposing factors for myopathy, or with a history of myoneural disorder, since it may delay the recognition or confound the diagnosis of a drug-induced musculoskeletal effect. Patients should be advised to report promptly any unusual muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever. Periodic CPK determinations may be considered in some patients, although the value of such monitoring is uncertain. HMG-CoA reductase inhibitor therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.