Normal Platelet Function In Scurvy And Experimental Human Vitamin C Deficiency

Abstract

Mucocutaneous hemorrhage is a prominent feature of human scurvy. Platelet dysfunction has been observed in scorbutic guinea pigs and some humans with scurvy, but others have found normal platelet function in human scurvy. Since it is uncertain whether platelet dysfunction contributes to the hemorrhagic diathesis of scurvy, we studied platelet function in one patient with typical perifollicular hemorrhagic manifestations of scurvy and in five healthy human ascorbic acid (AA) deficient volunteers. Volunteers were hospitalized on a metabolic ward, and fed a diet providing 3-4mg AA per day. Platelet function studies were performed at the end of a) a 30 day control period of AA supplementation; b) a 60 day period of AA deficiency; and c) a 40 day period of AA supplementation. The patient with scurvy was studied before and 10 days after AA supplementation. The following platelet studies were performed: venous count, bleeding time (Ivy method), in vitro adhesiveness (Bowie method), in vivo adhesiveness (Johnson method), aggregation in response to ADP, collagen, epinephrine, sodium arachidonate and ristocetin, and 14C-serotonin release. Plasma and leukocyte AA were found to be normal in both periods of supplementation and markedly decreased (plasma mean 0.12 ± 0.02mg/dl; WBC mean 8.9 ± 1.8μg/108 cells) following the deficient diet. Plasma AA was 0.07mg/dl and WBC AA was 4.92μg/108 cells in the scurvy patient. Platelet count and all platelet function studies were within the normal range in the patient with scurvy and all volunteers during AA supplementation. In vivo platelet adhesiveness decreased in 4 of the 5 volunteers during AA deficiency, but it remained in the normal range in all but one. All other studies were normal in both AA deficient volunteers and the patient with scurvy. We conclude that significant platelet dysfunction does not accompany subclinical AA deficiency, and that platelet dysfunction is not primarily responsible for the hemorrhagic diathesis of scurvv.