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Vitamin C

Vitamin C is also known as ascorbic acid. Humans do not synthesize, or store vitamin C. They require regular and adequate exogenous intake for the biosynthesis and hydroxylation of hormones, neurotransmitters, and mature collagen. Vitamin C is present in many fruits and vegetables, but proper food preparation is necessary to avoid degrading the vitamin C content. The absorption of vitamin C occurs in the ileum.

Several patient groups are at increased risk for developing vitamin C deficiency including patients with; colitis, alcohol use disorder and cancer treated with chemotherapy. The third National Health and Nutrition Examination Survey estimated that 14% of men and 10% of women in the United States have vitamin C deficiency.

Vitamin C deficiency results in scurvy. Generalized symptoms of scurvy include fatigue, myalgias, arthralgias, weakness, anorexia, weight loss, and irritability. Dermatologic manifestations include follicular hyperkeratosis with perifollicular hemorrhage surrounding twisted, brittle hairs, ecchymoses, poor wound healing, and swelling in the legs. Soft-tissue or subperiosteal hemorrhage usually occurs in the legs and may cause pain so severe that affected persons are unwilling to walk. Left untreated, scurvy may result in cardiorespiratory failure and death. Vitamin C must be completely absent from the diet for 60 to 90 days for these symptoms to occur.

Vitamin C is a cofactor in collagen synthesis. Vitamin C deficiency results in structural instability of collagen, resulting in blood vessel fragility and impaired wound healing. Low levels of vitamin C within red cells may causes low grade chronic hemolysis. Vitamin C stabilizes vitamin E, folate and iron. Therefore, vitamin C deficiency predisposes to additional deficiencies.

Anemia occurs in 75% of patients with scurvy and is the only routine laboratory abnormality. Multifactorial causes of the anemia include blood loss into tissues or from the gastrointestinal tract, intravascular hemolysis, and coexisting folate and iron deficiencies. Vitamin C deficiency does not cause coagulation abnormalities.

The diagnosis of scurvy depends on history, physical examination, and clinical improvement after the administration of ascorbic acid. Although a low plasma vitamin C level is specific for the diagnosis of scurvy, plasma vitamin C levels quickly normalize with enteral intake of ascorbic acid and do not reflect tissue levels. Leukocytes serve as a storage pool for ascorbic acid. The measurement of ascorbic acid levels in leukocytes may be considered, although such levels may not be easily obtainable and may also be affected by dietary intake.

Reference range for plasma vitamin C is 23-100 umoles/L.


Hampl JS, Taylor CA, Johnston CS. Vita- min C deficiency and depletion in the Unit- ed States: the Third National Health and Nutrition Examination Survey, 1988 to 1994. Am J Public Health 2004;94:870-5.

Hirschmann JV, Raugi GJ. Adult scurvy. J Am Acad Dermatol 1999;41:895-906

Reuler JB, Broudy VC, Cooney TG. Adult scurvy. JAMA 1985;253:805-807

Wilson CW. Clinical pharmacological aspects of ascorbic acid. Ann N Y Acad Sci 1975;258:355-376

Van Baalen E, et al. A patient with psychiatric illness and multiple hemorrhages. JAMA 2019;322:2437-2438.

Bennet SE. et al. Case 22-2018: A 64-year-old man with progressive leg weakness, recurrent falls and anemia. New Engl J Med 2018;379:282-

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