McCloy Mary P, Roberts Irene A G, Howarth Lucy J, Watts Timothy L, Murray Neil A
Department of Paediatrics and Neonatal Medicine, Faculty of Medicine, Imperial College, Hammersmith Hospital Campus, London W12 ONN, UK.
Pediatr Res. 2002 Jun;51(6):756-60. doi: 10.1203/00006450-200206000-00016.
Thrombocytopenia is common in sick neonates, and affected neonates have adverse outcomes compared with those without thrombocytopenia. As impaired platelet production underlies many neonatal thrombocytopenias, affected neonates are potential candidates for hemopoietic growth factor therapy. Although recombinant human (rh) thrombopoietin remains under therapeutic development, rhIL-11, which stimulates megakaryocytopoiesis and increases platelet counts after chemotherapy, is already licensed for clinical use. However, nothing is known about IL-11 in neonates. We therefore measured plasma IL-11 by ELISA in healthy term neonates, stable preterm neonates with or without thrombocytopenia, and preterm neonates with sepsis or necrotizing enterocolitis (NEC) with or without thrombocytopenia. At birth IL-11 was undetectable (<10 pg/mL) in healthy term neonates (n = 20) and 27 of 31 (87%) stable preterm neonates. Three stable preterm neonates with detectable IL-11 (mean+/-SD, 11.3 +/- 0.4 pg/mL; median, 11.6 pg/mL) suffered chorioamnionitis, the remaining neonate (IL-11, 14 pg/mL) being one of nine with early onset thrombocytopenia (present by <72 h of age). IL-11 was also measured in 58 preterm neonates with suspected sepsis or NEC. In 25 of 58, sepsis or NEC was unconfirmed and IL-11 was undetectable. By contrast, 14 of 33 with proven sepsis or NEC had elevated IL-11 (median, 14.9 pg/mL; range, 11.2-92.2 pg/mL). Of these 33 neonates, 19 developed thrombocytopenia: nine of 19 (47%) had detectable IL-11 and 10 of 19 (53%) did not (p > 0.05). Although its role in platelet production in neonates remains unclear, these data suggest that IL-11 is involved in the endogenous cytokine response to sepsis or NEC in preterm neonates. Further studies of IL-11 in neonates are warranted to assess its role both in platelet production and in mediation of the endogenous inflammatory response.
血小板减少症在患病新生儿中很常见，与无血小板减少症的新生儿相比，受影响的新生儿会出现不良后果。由于血小板生成受损是许多新生儿血小板减少症的基础，因此受影响的新生儿是造血生长因子治疗的潜在候选者。尽管重组人（rh）血小板生成素仍处于治疗研发阶段，但rhIL-11已获临床使用许可，它可刺激巨核细胞生成并在化疗后增加血小板计数。然而，关于新生儿体内的IL-11情况却一无所知。因此，我们采用酶联免疫吸附测定法（ELISA）对健康足月儿、有无血小板减少症的稳定早产儿以及有无血小板减少症的患败血症或坏死性小肠结肠炎（NEC）的早产儿的血浆IL-11进行了检测。出生时，健康足月儿（n = 20）和31例稳定早产儿中的27例（87%）的IL-11检测不到（<10 pg/mL）。3例IL-11可检测到的稳定早产儿（平均值±标准差，11.3±0.4 pg/mL；中位数，11.6 pg/mL）患有绒毛膜羊膜炎，其余1例新生儿（IL-11，14 pg/mL）是9例早发型血小板减少症（出生后<72小时出现）患儿之一。我们还对58例疑似患败血症或NEC的早产儿进行了IL-11检测。58例中有25例败血症或NEC未得到证实且IL-11检测不到。相比之下，33例确诊患败血症或NEC的患儿中有14例IL-11升高（中位数，14.9 pg/mL；范围，11.2 - 92.2 pg/mL）。在这33例新生儿中，19例出现了血小板减少症：19例中有9例（47%）IL-11可检测到，19例中有10例（53%）检测不到（p>0.05）。尽管IL-11在新生儿血小板生成中的作用仍不清楚，但这些数据表明，IL-11参与了早产儿对败血症或NEC的内源性细胞因子反应。有必要对新生儿的IL-11进行进一步研究，以评估其在血小板生成以及内源性炎症反应介导中的作用。
