Vitamin C deficiency in patients with acute myeloid leukemia: a case series and review of the literature

Vitamin C (Vc) deficiency is characterized by an array of mucocutaneous findings, including ecchymoses, petechiae, perifollicular hemorrhage, oral ulcerations, gingival hypertrophy, and corkscrew hairs.In addition, it can cause cardiovascular, pulmonary, and neuropsychiatric effects and may be fatal if left untreated.1,2 Also known as ascorbic acid, Vc acts as an essential cofactor to enzymes prolyl hydroxylase and lysyl hydroxylase, which crosslink propeptides to stabilize the structure of collagen.Scurvy, the clinical disease caused by Vc deficiency, is primarily seen in patients with restrictive diets, resource limitations, substance abuse, and malabsorption syndromes.2 Currently defined as Vc concentrations <11 μmol/L, many consider hypovitaminosis C to be represented by serum concentrations of <30 μmol/L.