Nephrocaps (folic acid/vitamin B complex and vitamin C)
Last reviewed · Source: First Databank (FDB) drug data
Overview
Ascorbic acid is the functional and principal in vivo form of vitamin C, an essential water-soluble vitamin.
Folic acid is a water-soluble, B complex vitamin.
Folic acid is used for the treatment of megaloblastic and macrocytic anemias resulting from folate deficiency. The drug is usually indicated in the treatment of nutritional macrocytic anemia; megaloblastic anemias of pregnancy, infancy, and childhood; and megaloblastic anemia associated with primary liver disease, alcoholism and alcoholic cirrhosis, intestinal strictures, anastomoses, or sprue. Folate deficiency may also result from increased loss of folate secondary to renal dialysis or the administration of some drugs such as phenytoin, primidone, barbiturates, methotrexate, nitrofurantoin, or sulfasalazine.
Generic name: folic acid/vitamin B complex and vitamin C
Reference product & biosimilars
No reference, biosimilar or interchangeable associated with this drug.
Today’s intelligence on Nephrocaps
Indications
The following indications are listed for Nephrocaps:
- Vitamin Deficiency
- Vitamin Deficiency Prevention
Also known as: Vitamin Deficiency Prophylaxis.
Dosing
Dosage of folic acid injection (sodium folate) is expressed in terms of folic acid. In general, although patient response to folic acid therapy depends on the degree and nature of the deficiency, once proper corrective measures are undertaken, folate-deficient patients generally respond rapidly. During the first 24 hours of treatment, the patient experiences an improved sense of well-being, and within 48 hours, the bone marrow begins to become normoblastic. Reticulocytosis generally begins within 2-5 days following initiation of folic acid therapy.
Ascorbic acid is usually administered orally. When oral administration is not feasible or when malabsorption is suspected, the drug may be administered IM, IV, or subcutaneously. When given parenterally, utilization of the vitamin reportedly is best after IM administration and that is the preferred parenteral route.
Folic acid is usually administered orally. When oral administration is not feasible or when malabsorption is suspected, the drug may be administered by deep IM, subcutaneous, or IV injection. However, most patients with malabsorption are able to absorb oral folic acid.
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Drug interactions
Concurrent administration of more than 200 mg of ascorbic acid per 30 mg of elemental iron increases absorption of iron from the GI tract; however, most individuals are able to absorb orally ingested iron adequately without concurrent administration of ascorbic acid.
Increased urinary excretion of ascorbic acid and decreased excretion of aspirin occur when the drugs are administered concurrently.
Salicylates inhibit uptake of ascorbic acid by leukocytes and platelets. As a result, leukocyte and plasma concentrations of ascorbic acid are decreased to concentrations slightly higher than those associated with tissue depletion of the vitamin; however, there is no evidence to date that salicylate therapy precipitates ascorbic acid deficiency. Although concomitant administration of ascorbic acid supplements in patients receiving salicylates increases plasma ascorbic acid concentrations, leukocyte ascorbic acid concentrations are not increased and tissue stores of the vitamin may not be increased. Therefore, routine administration of ascorbic acid supplements to patients receiving salicylates is not warranted; however, patients receiving high dosages of salicylates who exhibit any signs or symptoms of ascorbic acid deficiency should be evaluated for such a deficiency.
Ascorbic acid has reportedly decreased the anticoagulant effect of warfarin; however, other investigators have failed to show this effect. Concurrent administration of ascorbic acid and fluphenazine reportedly resulted in decreased fluphenazine plasma concentration. Acidification of the urine following administration of ascorbic acid may result in altered excretion of other drugs.
In folate-deficient patients, folic acid therapy may increase phenytoin metabolism, resulting in decreased phenytoin serum concentrations. Although this interaction is not usually clinically important, an increase in seizure frequency may occur in some patients.
It has been reported that concurrent administration of chloramphenicol and folic acid in folate-deficient patients may result in antagonism of the hematopoietic response to folic acid. Although the importance and mechanism of the interaction is unclear, the hematologic response to folic acid in patients receiving both drugs should be carefully monitored.
There are no contraindication interactions for this drug.
There are no severe interactions for this drug.
There are no moderate interactions for this drug.
Contraindications
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There are no contraindication contraindications for this drug.
There are no severe contraindications for this drug.
There are no moderate contraindications for this drug.
Adverse reactions
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There are no severe adverse reactions for this drug.
There are no less severe adverse reactions for this drug.
Precautions
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ICD codes
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Formulary status
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Last reviewed · Source: First Databank (FDB) drug data
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