Friedman Z, Lamberth E L, Stahlman M T, Oates J A
J Pediatr. 1977 Mar;90(3):439-43. doi: 10.1016/s0022-3476(77)80712-9.
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.
对五名接受无脂肠外营养的患重病早产新生儿进行了血小板对二磷酸腺苷（ADP）的聚集反应研究。通过分析血浆脂质脂肪酸值诊断出必需脂肪酸（EFA）缺乏。与作为对照的其他经口喂养的低体重婴儿相比，缺乏必需脂肪酸的婴儿血小板聚集受损（在2.5微摩尔ADP时，最大聚集率分别为18.1%和43.4%；在5.0微摩尔ADP时，分别为34.5%和52.2%）。此外，必需脂肪酸缺乏婴儿的血小板表现出明显的解聚。从缺乏状态恢复后，低体重婴儿的血小板功能与明显健康的早产婴儿相似。四名必需脂肪酸缺乏的婴儿发生了临床出血。因此，血栓素A2的前体花生四烯酸缺乏与血小板聚集受损相关，这是一种由血栓素A2介导的现象。这种相关性为一个假说提供了基础，即观察到的必需脂肪酸缺乏与血小板功能障碍存在因果关系。
