Ascorbic Acid (Antiscorbutic Vitamin- Vitamin C): Clinical Manifestations Of Deficiency, Treatment And Prevention

James Lind, a scotish naval physician, recognized the antiscorbutic properties of citrous fruits in 1753 and this was considered an important discovery with far- reaching effects.

Dietary sources: Ascorbic acid is present in a wide variety of foods. In the process of cooking, about 50% of vitamin C passes into water and 20% is destroyed. Fresh fruits, green leafy vegetables and germinating pulses are rich in ascorbic acid. The Indian gooseberry and guavas are particularly rich sources. Animal foods like milk and meat contain only small amounts of this vitamin. The vitamin is present in potato in the layer just below the skin. If the potatoes are boiled whole with the skin, the vitamin diffuses into the deeper layers. The minimum daily requirement for an adult is 30 to 40 mg and for infants, is 5 mg per Kg body weight. Normal plasma levels vary between 0.7 to 1.5 mg per dl. Leucocytes, platelets and adrenal glands contain large amounts of vitamin C. Deficiency of vitamin C causes scurvy.

Physiological actions: Vitamin C is a strong reducing agent. It takes part in biological oxidation- reduction reactions. Vitamin C is required for the formation of collagen by the hydroxylation of proline. It takes part in the formation of hemoglobin, erythrocyte maturation and the conversion of folic acid to tetrahydrofolate. Ascorbic acid reduces ferric iron to ferrous iron which is more easily absorbed. Body stores of ascorbic acid are small and therefore dietary deficiency leads to the development of scurvy. The condition is fatal if untreated.

Manifestations of scurvy vary in children and adults. Early symptoms include weakness, lassitude and normocytic normochromic anemia. In infancy and childhood, subperiosteal hemorrhages occur, which lead to painful swellings over long bones. Scurvy in infancy produces pseudoparalysis owing to pain. This condition may mimic arthritis, osteomyelitis, or poliomyelitis. X-ray abnormalities may develop over the sterna ends of ribs, and ends of long bones. Bleeding from the gums occurs commonly at the sites of erupted teeth. Retrobulbar, subarachnoid and cerebral bleeding may develop in a few cases.

In adults, early manifestation is follicular hyperkeratosis over the skin of the lower limbs. The lesions are popular with perifollicular hemorrhages which appear as purpura. Hemorrhage into the deep tissues of the thighs and legs cause tense induration (“woody legs”). Other sites of hemorrhage include joints, nail beds and viscera. The gums are hypertrophied and the inter- dental papillae are red and prominent (scurvy- buds). They bleed easily. Edentulous subjects do not get gingival abnormalities. The gum changes are aggravated by infection. The teeth become loose and may fall off. The hair assumes cork- screw shape since the follicles are obstructed by keratin plugs. Wound healing is delayed and resistance to infection is reduced.

Scurvy is a potentially fatal disease and sudden death may occur unexpectedly. Treatment should be started without delay. In infants and children, 25 to 50 mg of ascorbic acid three times daily is sufficient to replete the body stores. In adults, 500 mg is given daily in divided doses up to a total of 4 g. A diet rich in vitamin C should be given to prevent relapse.

Prevention: Infant foods should contain fruit juices or vitamin C supplements. Children, convalescent subjects and elderly people who are liable to be neglected, should receive 25 mg of vitamin C daily. As an alternative, 500 mg may be given once a month.

Adverse effects of vitamin C: Side effects like digestive upsets and hypoglycemia occur if the drug is given in doses exceeding 3g/day. Oxaluria and oxalate stone formation in the urinary tract may result from prolonged overdosage.