Department of Pediatrics, Emory University School of Medicine, Atlanta, Georgia.
Children's Healthcare of Atlanta, Atlanta, Georgia.
Transfusion. 2019 Mar;59(3):981-988. doi: 10.1111/trf.15112. Epub 2018 Dec 30.
Prior studies have suggested an association between platelet transfusions (PTXs) and worse outcomes among infants with necrotizing enterocolitis (NEC), potentially mediated by proinflammatory factors released by platelets. However, the effects of storage on platelet proinflammatory factor release and the confounding role of illness severity on NEC outcomes have not been determined.
First, neuropeptide Y (a potent splanchnic vasoconstrictor released by platelets) was measured by enzyme-linked immunosorbent assay in fresh frozen plasma and in the supernatant of leukoreduced apheresis-derived platelets at different times during storage. Next, we evaluated the relationship between PTX rates and death in a multicenter cohort of very-low-birth-weight infants with NEC, adjusting for illness severity.
Neuropeptide Y levels increased over time in the supernatant of leukoreduced apheresis-derived platelets and were 4.4-fold and 8.9-fold higher than in fresh frozen plasma on Days 2 and 3 of storage, respectively (p < 0.001). Among 598 very-low-birth-weight infants, 44 developed NEC. In unadjusted analysis, PTX rate was 30.3 (95% confidence interval [CI], 11.5-80.1) per 100 infant-days among infants who died, compared to 6.0 (95% CI, 3.2-11.2) among survivors (incidence rate ratio, 5.1; 95% CI, 1.6-16.2; p = 0.006). In multivariable analysis, there was no association between PTX rate and mortality (incidence rate ratio, 3.0; 95% CI, 0.6-15.0; p = 0.18), although estimation was imprecise.
Proinflammatory mediators accumulate in platelet suspensions during storage. Although PTX rates were not associated with increased mortality among infants with NEC in our study, our estimates suggest the potential for such an association that needs evaluation in larger studies.
先前的研究表明,血小板输注(PTX)与坏死性小肠结肠炎(NEC)患儿的预后较差有关,这可能是由血小板释放的促炎因子介导的。然而,储存对血小板促炎因子释放的影响以及疾病严重程度对 NEC 结局的混杂作用尚未确定。
首先,通过酶联免疫吸附试验测量新神经肽 Y(一种由血小板释放的强烈内脏血管收缩剂)在不同储存时间的新鲜冷冻血浆和白细胞减少的单采衍生血小板上清液中的含量。其次,我们评估了 PTX 率与 NEC 极低出生体重儿多中心队列中死亡之间的关系,同时调整了疾病严重程度。
白细胞减少的单采衍生血小板上清液中的神经肽 Y 水平随时间推移而增加,在储存的第 2 天和第 3 天分别比新鲜冷冻血浆高 4.4 倍和 8.9 倍(p < 0.001)。在 598 例极低出生体重儿中,有 44 例发生了 NEC。在未调整的分析中,死亡患儿的 PTX 率为每 100 个婴儿日 30.3(95%置信区间[CI],11.5-80.1),而存活患儿为 6.0(95%CI,3.2-11.2)(发病率比,5.1;95%CI,1.6-16.2;p = 0.006)。在多变量分析中,PTX 率与死亡率之间没有关联(发病率比,3.0;95%CI,0.6-15.0;p = 0.18),尽管估计值不太准确。
促炎介质在储存过程中在血小板悬液中积累。尽管在我们的研究中,PTX 率与 NEC 患儿的死亡率增加无关,但我们的估计表明存在这种关联的可能性,需要在更大的研究中进行评估。