Infuvite Adult Vial 1 (multivitamin infusion adult no.4,vit K,component vial 1 of 2)

Dose, frequency of administration, and duration of treatment with phytonadione depend on the severity of the prothrombin deficiency and the response of the patient; the lowest effective dose of phytonadione should be used.

Phytonadione may be administered orally or parenterally (IV, IM, or subcutaneously). The parenteral preparation also has been administered orally+ in neonates. The route of administration of phytonadione depends on the severity of the prothrombin deficiency and the risks associated with administration by each route. The manufacturers state that because of the possibility of severe adverse reactions (see Cautions: Adverse Effects), IV or IM administration is indicated only when other routes of administration are not feasible and the serious risk is justified. However, the effects of phytonadione have been reported to be delayed and/or unpredictable following subcutaneous injection, and subcutaneous administration may be less effective for reversal of excessive anticoagulation than IV or oral administration. The American College of Chest Physicians (ACCP) and other clinicians recommend IV administration of phytonadione in emergency situations for major bleeding due to vitamin K-antagonist anticoagulants because of its more rapid onset; these clinicians recommend that subcutaneous administration be avoided.

Oral administration of phytonadione usually reduces international normalized ratio (INR) levels in 24-48 hours and generally is recommended over parenteral administration in selected asymptomatic (nonbleeding) patients with hypoprothrombinemia due to vitamin K-antagonist anticoagulants. In patients with decreased bile secretion, bile salts (e.g., ox bile extract 300 mg or dehydrocholic acid 500 mg) should be given with each oral dose of phytonadione to ensure absorption. Parenteral administration is indicated in patients who are unable to retain or absorb the drug from the GI tract.

When phytonadione injection is administered IV, it should be injected at a rate not exceeding 1 mg/minute. The drug may be diluted for infusion with 0.9% sodium chloride, 5% dextrose, or 5% dextrose in 0.9% sodium chloride injection; other diluents that may contain benzyl alcohol should not be used. (See Cautions: Pediatric Precautions.) The drug should be administered immediately after dilution, and any unused portion of the dilution and the unused contents of the ampul or vial should be discarded. The infusion container must be protected from light at all times. (See Chemistry and Stability: Stability.)

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Because vitamin K1 is a pharmacologic antagonist to coumarin and indandione derivatives, patients being treated with these anticoagulants should not receive phytonadione except for the treatment of excessive hypoprothrombinemia. Phytonadione does not antagonize the anticoagulant effects of heparin, low molecular weight heparins, fondaparinux, or direct-acting oral anticoagulants.

Orlistat may result in decreased GI absorption of fat-soluble vitamins such as phytonadione (vitamin K1). At least 2 hours should elapse between (before or after) any orlistat dose and phytonadione administration; administering fat-soluble vitamins at bedtime may be a convenient time. Although the manufacturer of orlistat recommends that a vitamin supplement containing fat-soluble vitamins (A, D, E, and K) be used during orlistat therapy, such vitamin concentrations in clinical studies with the drug remained within the normal range for most patients despite decreases, and vitamin supplementation was only occasionally needed.

Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.

Vitamin A/Selected Retinoids

SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.

MECHANISM OF ACTION: The retinoids are structurally related to vitamin A. (1-6)

CLINICAL EFFECTS: Concurrent use of retinoids with vitamin A supplements may result in signs of vitamin A toxicity.(1-6) Symptoms of vitamin A toxicity include nausea, vomiting, loss of appetite, weakness, dry or itchy skin or lips, irritability, and hair loss.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: The manufacturer of acitretin states that concomitant use of vitamin A supplements should be avoided.(1) The manufacturer of bexarotene states that patients should be advised to limit vitamin A supplements. In clinical studies, patients were advised to limit their vitamin A intake to less than or equal to 15,000 International Units/day.(2) The manufacturer of isotretinoin states that patients should be advised against taking vitamin A supplements.(3) The manufacturer of palovarotene states that concomitant use of vitamin A must be avoided.(4) The manufacturer of tretinoin states that tretinoin must not be administered in combination with vitamin A.(5) The UK manufacturer of alitretinoin states that tretinoin must not be administered in combination with vitamin A.(6)

DISCUSSION: The retinoids are structurally related to vitamin A. The concurrent use of retinoids with vitamin A may result in signs and symptoms of vitamin A toxicity.(1-6)

Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

Ascorbic Acid (VITAMIN C)/Bortezomib

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Vitamin C can form a complex with the boronic acid moiety of the bortezomib molecule, preventing its absorption into cells.(1-4) This may protect normal tissue in the body, which may have higher levels of Vitamin C.(5)

CLINICAL EFFECTS: Concurrent administration of Vitamin C may result in decreased bortezomib activity.(1-4)

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Instruct patients receiving bortezomib therapy not to begin taking vitamin C supplements without consulting their oncologist first. Patients who are instructed to take vitamin C should follow their oncologist's instructions on how to separate dosages and should be carefully monitored for bortezomib efficacy.

DISCUSSION: An in vitro study with human plasma and multiple myeloma cells found that high levels of vitamin C (following 1 gram/day of ascorbic acid for 4 days) decreased bortezomib effectiveness by 26%. An in vivo study in mice found that vitamin C administration with bortezomib completely blocked the response of bortezomib.(6) An in vitro study in rat Schwann cells and myeloma cells(4) and an in vivo study in mice(7) found that delayed administration of vitamin C had no effect on bortezomib effects. In an in vivo study in multiple myeloma patients, concurrent ascorbic acid, arsenic trioxide, bortezomib, and high-dose melphalan in which ascorbic acid was administered close to bortezomib, the combination was safe and well tolerated, but produced no changes in response rates.(8) In another in vivo study in multiple myeloma patients, a regimen of ascorbic acid, bortezomib, and melphalan in which bortezomib was administered in the morning and ascorbic acid in the evening was found to be safe and efficacious, with 74% of patients responding to therapy.(9)

Serum Phosphate Level-Altering Drugs/Erdafitinib

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Medications that alter serum phosphate may interfere with interpretation of phosphate levels that are needed to determine initial erdafitinib dose.(1)

CLINICAL EFFECTS: Serum phosphate levels that are elevated by concomitant medications may result in an inappropriately low dose and decreased effectiveness of erdafitinib. Serum phosphate levels that are decreased by concomitant medications may result in an inappropriately high dose and increased toxicity from erdafitinib.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: The manufacturer of erdafitinib states that agents that alter serum phosphate levels should be avoided before the initial dose increase period for erdafitinib based on serum phosphate levels (days 14 to 21).(1)

DISCUSSION: Concomitant administration of serum phosphate level-altering agents during the initial dose increase period of erdafitinib based on serum phosphate levels (days 14 to 21) may interfere with serum phospate levels and lead to incorrect dosing of erdafitinib.(1) Agents that may alter serum phosphate levels linked to this monograph include: aluminum carbonate, aluminum hydroxide, calcium acetate, calcium carbonate, calcium citrate, cod liver oil, ferric citrate, lanthanum, magnesium carbonate, magnesium hydroxide, potassium phosphate, sevelamer, sodium phosphate, sucroferric oxyhydroxide, tenapanor, and vitamin D.(1)

Vitamin K/Selected Anticoagulants (VITAMIN K ANTAGONISTS)

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Anticoagulants interfere with the activation of vitamin K-dependent clotting factors. Vitamin K administration may reverse this effect.

CLINICAL EFFECTS: The pharmacological effect of anticoagulants may be reversed resulting in thrombus formation.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Patients receiving anticoagulants should avoid eating unusual increases in foods high in vitamin K content. The time of highest risk for a coumarin-type drug interaction is when the precipitant drug is initiated or discontinued. Contact the prescriber before initiating, altering the dose or discontinuing either drug.

DISCUSSION: Numerous reports have demonstrated that vitamin K interferes with the hypoprothrombinemic effects of anticoagulants. However, reports of clinically important consequences are uncommon. A clearer understanding of the mechanism by which these drugs act has made it possible to use vitamin K to control bleeding side effects of warfarin therapy. One should be aware of the vitamin K content of enteral feeding products being administered to patients on anticoagulant therapy. Prothrombin time should be monitored when these products are given.

Moderate Interaction: Assess the risk to the patient and take action as needed.

Ascorbic Acid (VITAMIN C)/Deferoxamine

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: It is believed that ascorbic acid increases the iron available for chelation from an labile intracellular iron pool. Ascorbic acid may then facilitate iron-induced oxidative tissue damage.(1)

CLINICAL EFFECTS: Dietary ascorbic acid may increase the absorption of dietary iron. Supplemental ascorbic acid therapy given during chelation therapy may improve iron output;(1-9) however, excessive dosages may result in cardiac toxicity from iron-induced oxidative tissue damage.(1,2,11-13)

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Ascorbic acid intake is often restricted in patients with iron overload; however, it has been used in conjunction with deferoxamine to increase iron excretion.(2) Supplemental ascorbic acid therapy should only be initiated after one month of deferoxamine therapy. Ascorbic acid therapy should only be given in patients receiving deferoxamine regularly and the dose should be given after the infusion has started. The dosage of ascorbic acid should be limited to 50 mg daily in children under 10 years of age; 100 mg daily in older children; and 200 mg daily, in divided doses, in adults.(2) Cardiac function should be monitored in patients receiving concurrent therapy. Discontinue ascorbic acid therapy in patients who develop cardiac dysfunction.(2)

DISCUSSION: Supplemental ascorbic acid therapy given during chelation therapy has been shown to improve iron output,(1-9) possibly by increasing iron available for chelation from an labile intracellular iron pool.(1) However, dosages in excess of 500 mg daily have been associated with cardiac dysfunction.(1,2,11-13)

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There are no contraindication contraindications for this drug.

• Hemophilia

• Increased risk of bleeding due to coagulation disorder
• Vitamin K deficiency induced hypoprothrombinemia

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Rare or Very Rare

• Anaphylaxis
• Cyanosis
• Dizziness
• Hyperbilirubinemia
• Hyperhidrosis
• Hypersensitivity drug reaction
• Hypotension
• Skin lesion

Less Frequent

• Dysgeusia
• Flushing
• Injection site sequelae
• Skin swelling

Rare or Very Rare

• Dyspnea
• Eczema
• Erythema
• Erythema dyschromicum perstans
• Pseudoscleroderma
• Tachycardia
• Urticaria

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Reproduction studies have not been conducted in animals, and it is not known if phytonadione has teratogenic effects.

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