A consistent clinical feature of human scurvy is mucocutaneous hemorrhage which has been attributed to abnormal blood vessel structure secondary to deficient collagen synthesis. Quantitative and qualitative platelet abnormalities have also been implicated in the pathogenesis of scorbutic bleeding in some studies; however, the presence of other nutritional deficiencies has clouded interpretation of these results. To further evaluate the effect of vitamin C deficiency on platelet number and function, we studied one patient with typical perifollicular hemorrhagic manifestations of scurvy and five normal subjects fed a diet deficient only in ascorbic acid. Markedly decreased plasma (0.07 mg/dl) and leukocyte (4.92 μg/108 cells) ascorbic acid was found in the scurvy patient, and similar levels developed in the normal subjects fed the ascorbic acid deficient diet (mean plasma level 0.12 mg/dl; mean leukocyte level 8.1 μg/108 cells). Platelet number; glass bead column retention; aggregation in response to ADP, collagen, epinephrine, sodium arachidonate and ristocetin; serotonin release; bleeding time and platelet retention during bleeding were all normal in the patient with scurvy. Platelet retention during bleeding decreased in all five normal subjects when they became vitamin C deficient, but none became abnormal. The bleeding time remained normal in all five subjects. Slight thrombocytopenia developed in one subject, but otherwise platelet number and all of the above platelet functions were normal in the ascorbic acid deficient control subjects. We conclude that mucocutaneous hemorrhage in scurvy is not a consequence of impaired platelet function. Previously reported abnormal platelet function in scurvy is probably not the result of vitamin C deficiency per se, but may be the consequence of other coexisting nutritional deficiencies.
- Human platelets
- vitamin C