Can you take Metoclopramide with Vitamin D2?

The ergocalciferol in Vitamin D2 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 Vitamin D2 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.

Metoclopramide has a moderate potential interaction with Cirrhosis.

Metoclopramide produces a transient increase in plasma aldosterone and may cause fluid retention and volume overload in susceptible patients. Therapy with metoclopramide should be administered cautiously in patients with or at risk for fluid overload (e.g., cirrhosis, congestive heart failure). If these side effects occur at any time during metoclopramide therapy, the drug should be discontinued.

Metoclopramide has a major potential interaction with Depression.

Metoclopramide has been reported to cause mental depression in patients with and without a prior history of depression. Symptoms have ranged from mild to severe and have included suicidal ideation and suicide. Therapy with metoclopramide in patients with a history of mental depression, especially suicidal tendencies, should be administered cautiously, and only if benefits are anticipated to outweigh the potential risks. Some patients who experience depression with metoclopramide have improved following temporary discontinuation of the drug and reinstitution at a lower dosage with gradual titration.

Metoclopramide has a moderate potential interaction with Fluid Retention.

Metoclopramide produces a transient increase in plasma aldosterone and may cause fluid retention and volume overload in susceptible patients. Therapy with metoclopramide should be administered cautiously in patients with or at risk for fluid overload (e.g., cirrhosis, congestive heart failure). If these side effects occur at any time during metoclopramide therapy, the drug should be discontinued.

Metoclopramide has a major potential interaction with Gastrointestinal Hemorrhage.

The use of metoclopramide is contraindicated in patients with conditions where stimulation of gastrointestinal motility might be harmful, such as mechanical bowel obstruction, bowel perforation, or gastrointestinal hemorrhage.

Metoclopramide has a major potential interaction with Gastrointestinal Perforation.

The use of metoclopramide is contraindicated in patients with conditions where stimulation of gastrointestinal motility might be harmful, such as mechanical bowel obstruction, bowel perforation, or gastrointestinal hemorrhage.

Metoclopramide has a moderate potential interaction with Heart Failure.

Metoclopramide produces a transient increase in plasma aldosterone and may cause fluid retention and volume overload in susceptible patients. Therapy with metoclopramide should be administered cautiously in patients with or at risk for fluid overload (e.g., cirrhosis, congestive heart failure). If these side effects occur at any time during metoclopramide therapy, the drug should be discontinued.

Metoclopramide has a moderate potential interaction with High Blood Pressure.

In a study involving patients with essential hypertension, intravenously administered metoclopramide was shown to induce the release of catecholamines. Therapy with metoclopramide should be administered cautiously in patients with hypertension because of potential increases in blood pressure.

The ergocalciferol in Vitamin D2 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.

Metoclopramide has a major potential interaction with Intestinal Obstruction.

The use of metoclopramide is contraindicated in patients with conditions where stimulation of gastrointestinal motility might be harmful, such as mechanical bowel obstruction, bowel perforation, or gastrointestinal hemorrhage.

The ergocalciferol in Vitamin D2 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 Vitamin D2 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.

Metoclopramide has a major potential interaction with Neuroleptic Malignant Syndrome.

Although not a neuroleptic agent, metoclopramide has antidopaminergic effects and may rarely precipitate or aggravate a potentially fatal symptom complex known as Neuroleptic Malignant Syndrome (NMS). Clinical manifestations of NMS include hyperpyrexia, muscle rigidity, involuntary movements, altered mental status and autonomic instability (irregular pulse or blood pressure, tachycardia, diaphoresis and cardiac arrhythmias). Metoclopramide therapy should not be initiated in patients with active NMS and should be immediately discontinued if currently being administered in such patients. In patients with a history of NMS, introduction or reintroduction of metoclopramide or other antidopaminergic therapy should be carefully considered, since NMS may recur.

Metoclopramide has a moderate potential interaction with Parkinsonism.

Metoclopramide has antidopaminergic effects and may cause parkinsonian-like symptoms such as akinesia, bradykinesia, tremors, pill-rolling motion, cogwheel rigidity, and postural abnormalities including stooped posture and shuffling gait. The onset is usually within the first six months following initiation of therapy but occasionally after longer periods. Symptoms generally subside within 2 to 3 months after drug discontinuation. Therapy with metoclopramide should be administered cautiously, if at all, in patients with Parkinson's disease or parkinsonian symptoms.

Metoclopramide has a major potential interaction with Pheochromocytoma.

The use of metoclopramide is contraindicated in patients with pheochromocytoma. In a study involving patients with essential hypertension, intravenously administered metoclopramide was shown to induce the release of catecholamines. Hypertensive crises may occur in patients with pheochromocytoma due to induction of catecholamine release from the tumor.

The ergocalciferol in Vitamin D2 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.

Metoclopramide has a moderate potential interaction with Renal Dysfunction.

Renal function affects the clearance of metoclopramide. In patients with varying degrees of renal impairment, a reduction in creatinine clearance was correlated with a reduction in plasma clearance, renal clearance, and non-renal clearance, and increase in elimination half-life of metoclopramide. Therapy with metoclopramide should be administered cautiously in patients with impaired renal function. A dosage reduction may be appropriate to avoid drug accumulation.

The ergocalciferol in Vitamin D2 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.

Metoclopramide has a major potential interaction with Seizures.

The use of metoclopramide is contraindicated in patients with seizure disorders. Metoclopramide may increase the frequency and severity of seizures.

The ergocalciferol in Vitamin D2 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.

Metoclopramide has a major potential interaction with Tardive Dyskinesia.

Metoclopramide may precipitate symptoms of tardive dyskinesia (TD) following chronic administration. Elderly patients, particularly women, are most susceptible. Both the risk of developing TD and the likelihood that it will become irreversible increase with the duration and total cumulative dose of metoclopramide or other antidopaminergic therapy administered. Metoclopramide therapy should be discontinued in patients who develop signs or symptoms of tardive dyskinesia. There is no known treatment for tardive dyskinesia. In some patients, symptoms may lessen or resolve after metoclopramide treatment is stopped. Treatment with metoclopramide for longer than 12 weeks should be avoided in all but rare cases where therapeutic benefit is thought to outweigh the risk of developing tardive dyskinesia. In patients with preexisting drug-induced TD, initiating or increasing the dosage of metoclopramide therapy may temporarily mask the symptoms of TD but may eventually worsen the condition.