STORAGE POOL DEFICIENCY IN NEONATAL PLATELETS

Abstract

It is recognized that newborns exhibit a transient thrombocyropathy. Some investigators have described this as an “aspirin-like” defect, while others have ascribed it to a “storage-pool” abnormality. In an attempt to resolve this discrepancy platelets (plts.) from IP normal newborns, 10 normal adults and 10 aspirin created adults were studied. None of the mothers of the newborn infants had ingested drugs known to interfere with plt. function. Plt. aggregations with ADP (3uM), epinephrine (5uM) and collagen demonstrated abormal 2nd phase aggregation in both the newborns and in the aspirin treated adults. When mixtures of equal volumes of pits, from newborn and aspirin treated controls were tested, normal, irreversible aggregation was observed. Mutual correction was not observed on preincubation of newborn plts, with aspirin prior to mixing. When plt. malonaldehyde production was measured, PS an index of prostaglandin synthesis, in the presence of thrombin, or MEM, no differences were observed between normal adults and newborn plts. Malonaldehyde production was markedly reduced in the aspirin treated controls. Storage-pool deficient plts., when combined with aspirinized plts., prove mutually corrective in aggregation studies since storage pool deficient plts, overcome the abnormality in prostaglandin synthesis of the aspirin treated cells. These latter cells in turn provide the necessary storage-pool nucleotides to cause mutual correction and irreversible aggregation of the mixture. Our findings indicate that newborn pits, have a “storage-pool” defect.

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