Vitamin C Other names: l-ascorbic acid Ascorbic acid

Ascorbic acid should be used with caution in scorbutic patients with a history of or risk of developing renal oxalate stones or evidence of renal impairment or other issues (e.g., patients on dialysis, patients with diabetic nephropathy, and renal transplant recipients). These patients may be at increased risk of developing acute or chronic oxalate nephropathy following high dose ascorbic acid administration.

Patients known to be at risk of hyperoxaluria should not ingest ascorbic acid doses exceeding 1 g daily as there may be increased urinary oxalate excretion. However, such risk has not been demonstrated in normal, non-hyper oxaluric individuals.

Concomitant administration of aluminium-containing antacids may increase urinary aluminium elimination. Concurrent administration of antacids and ascorbic acid is not recommended, especially in patients with renal insufficiency.

Ascorbic acid increases the absorption of iron.

The plasma concentration of ascorbate is decreased by oral contraceptives.

Concomitant administration of acetylsalicylic acid and ascorbic acid may interfere with absorption of ascorbic acid. Renal excretion of acetylsalicylic acid is not affected and does not lead to reduced anti-inflammatory effects of acetylsalicylic acid.

Ascorbic acid may acidify the urine and lower serum concentrations of amphetamine by increasing renal excretion (as reflected by changes in amphetamine urine recovery rates). In case of decreased amphetamine efficacy discontinue ascorbic acid administration. Standard monitoring of therapy is warranted.

Concurrent administration of ascorbic acid with desferrioxamine enhances urinary iron excretion. Cases of cardiomyopathy and congestive heart failure have been reported in patients with idiopathic haemochromatosis and thalassaemias receiving desferrioxamine who were subsequently given ascorbic acid. Ascorbic acid should be used with caution in these patients and cardiac function monitored.

Ascorbic acid may decrease activities of erythromycin, kanamycin, streptomycin, doxycycline, and lincomycin. Bleomycin is inactivated in vitro by ascorbic acid. If the antibiotic efficacy is suspected to be decreased by concomitant administration of ascorbic acid, discontinue ascorbic acid administration.

Acidification of urine by ascorbic acid will alter the excretion of certain drugs affected by the pH of the urine (e.g., fluphenazine) when administered concurrently. It has been reported that concurrent administration of ascorbic acid and fluphenazine has resulted in decreased fluphenazine plasma concentrations. Standard monitoring of therapy is warranted.

Limited case reports have suggested interference of ascorbic acid with the anticoagulation effects of warfarin, however, patients on warfarin therapy treated with ascorbic acid doses up to 1000 mg/day (5 times the largest recommended single dose) for 2 weeks (twice the maximum recommended duration), no effect was observed. Standard monitoring for anti-coagulation therapy should continue during ascorbic acid treatment, as per standard of care.

Hemolysis has been reported with administration of ascorbic acid in patients with glucose-6-phosphate dehydrogenase deficiency. Patients with glucose-6-phosphate dehydrogenase deficiency may be at increased risk for severe hemolysis during treatment with ascorbic acid. Monitor hemoglobin and blood count and use a reduced dose of ascorbic acid in patients with glucose-6-phosphate dehydrogenase deficiency. Discontinue treatment with ascorbic acid if hemolysis is suspected and treat as needed.

Patients with glucose-6-dehydrogenase deficiency should not exceed the daily Adequate Intake (AI) level for ascorbic acid for their age group and condition.

The plasma concentration of ascorbate is decreased by smoking.

Co-administration of ascorbic acid with amygdalin (a complementary medicine) can cause cyanide toxicity.

For ascorbic acid no clinical data on exposed pregnancies are available. Animal studies do not indicate direct or harmful effects with respect to pregnancy, embryonal/foetal development, parturition or postnatal development. Pregnant women should exercise caution.

Ascorbic acid is excreted in breast milk. Though again caution should be exercised, no evidence exists suggesting such excretion is hazardous to the infant.

On the basis of the product’s pharmacodynamic profile and reported adverse events, ascorbic acid has no known effect on an individual’s ability to drive or operate machinery.

Nervous system disorders: headache.

Vascular disorders: flushing.

Gastrointestinal disorders: nausea, vomiting and stomach cramps. Large doses of ascorbic acid may cause diarrhoea.

Skin and subcutaneous tissue disorders: redness of skin.

Renal and urinary disorders: Patients known to be at risk of hyperoxaluria should not ingest ascorbic acid doses exceeding 1 g daily as there may be increased urinary oxalate excretion. However, such risk has not been demonstrated in normal, non-hyper oxaluric individuals. Ascorbic acid has been implicated in precipitating haemolytic anaemia in certain individuals deficient of glucose-6-phosphate dehydrogenase.

Increased intake of ascorbic acid over a prolonged period may result in increased renal clearance of ascorbic acid, and deficiency may result if the intake is reduced or withdrawn rapidly. Doses of more than 600 mg daily have a diuretic effect.