Platelet dysfunction in the neonate with essential fatty acid deficiency.
Platelet aggregation in response to ADP was studied in five EFA-deficient sick premature newborn infants who were receiving fat-free parenteral nutrition. EFA deficiency was diagnosed by analysis of plasma lipid fatty acid values. The deficient infants had impaired platelet aggregation when compared to other low-birth-weight infants fed orally who served as control subjects (maximum 18.1% versus 43.4% at 2.5 muM ADP; 34.5% versus 52.2% at 5.0 muM ADP). In addition, the platelets from EFA-deficient infants demonstrated clearly evident disaggregation. On recovery from their deficient state, the low-birth-weight infants had platelet functions similar to those of apparently healthy premature infants. Clinical hemorrhage occurred in four of the EFA-deficient infants. Thus a deficiency of arachidonic acid, the precursor of thromboxane A2, is correlated with an impairment of the aggregation of platelets, a phenomenon mediated by thromboxane A2. This correlation provides the basis for a hypothesis that the observed EFA deficiency is causally related to the platelet dysfunction.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D005228:Fatty Acids, Essential / Q000172:deficiency*; D006801:Humans; D007231:Infant, Newborn; D007235:Infant, Premature, Diseases / Q000097:blood; D008055:Lipids / Q000032:analysis; D010289:Parenteral Nutrition, Total / Q000009:adverse effects; D010974:Platelet Aggregation / Q000187:drug effects
D005228:Fatty Acids, Essential; D008055:Lipids; D000244:Adenosine Diphosphate