Moh-Klaren Julia, Bodivit Gwellaouen, Jugie Myriam, Chadebech Philippe, Chevret Laurent, Mokhtari Mostafa, Chamillard Xavier, Gallon Philippe, Tissières Pierre, Bierling Philippe, Djoudi Rachid, Pirenne France, Burin-des-Roziers Nicolas
Etablissement Français du Sang (EFS) Ile-de-France, Paris.
INSERM U955, Équipe 2 "Transfusion et Maladies du Globule Rouge"; Institut Mondor de Recherche Biomédicale (IMRB) and Université Paris-Est-Créteil Val-de-Marne (UPEC), Créteil; Laboratoire d'Excellence GR-Ex, Paris.
Transfusion. 2017 Nov;57(11):2571-2577. doi: 10.1111/trf.14196. Epub 2017 Jun 22.
Red blood cell (RBC) Thomsen-Friedenreich antigen exposure (T activation) in infants with necrotizing enterocolitis (NEC) has occasionally been associated with posttransfusional intravascular hemolysis thought to be due to anti-T antibodies in the donor plasma.
We describe an infant with NEC and Clostridium perfringens infection complicated by severe hemolysis after plasma transfusion. After this case, infants with confirmed NEC were prospectively evaluated for T activation. We checked for hemolysis in patients with T activation receiving plasma-containing blood products.
The infant had received 80 mL of fresh-frozen plasma (FFP). His RBCs displayed strong T activation, and agglutination was observed with four of six ABO-compatible FFP units. A direct antiglobulin test was negative. IgM-class anti-T antibodies were present in small amounts (titer of 8) in the transfused FFP. Anti-T antibodies from the blood donor were not hemolytic in vitro. In the prospective study, T activation was observed in three of 28 infants with NEC (11%). One infant presented moderate T activation and two infants presented very strong T activation but only moderate decreases in sialic acid expression on the RBC membrane. These three infants presented no signs of hemolysis after transfusion with unwashed blood products or FFP.
Anti-T antibodies are unlikely to be the etiologic factor for the hemolytic reactions observed in infants with NEC and T activation. Massive RBC desialylation and the direct action of bacterial toxins are more probable causes. Strict avoidance of plasma-containing blood products does not seem justified in these infants.
坏死性小肠结肠炎(NEC)婴儿的红细胞(RBC)暴露于汤姆森 - 弗里德赖希抗原(T激活)偶尔与输血后血管内溶血有关,这种溶血被认为是由于供体血浆中的抗T抗体所致。
我们描述了一名患有NEC和产气荚膜梭菌感染的婴儿,在输注血浆后并发严重溶血。在此病例之后,对确诊为NEC的婴儿进行了T激活的前瞻性评估。我们检查了接受含血浆血液制品的T激活患者的溶血情况。
该婴儿接受了80毫升新鲜冰冻血浆(FFP)。他的红细胞显示出强烈的T激活,并且在六个ABO相容的FFP单位中有四个观察到凝集。直接抗球蛋白试验为阴性。在输注的FFP中存在少量(滴度为8)的IgM类抗T抗体。来自献血者的抗T抗体在体外无溶血作用。在前瞻性研究中,28名NEC婴儿中有3名(11%)观察到T激活。一名婴儿表现为中度T激活,两名婴儿表现为非常强烈的T激活,但红细胞膜上唾液酸表达仅中度降低。这三名婴儿在输注未洗涤的血液制品或FFP后均未出现溶血迹象。
抗T抗体不太可能是NEC和T激活婴儿中观察到的溶血反应的病因。大量红细胞去唾液酸化和细菌毒素的直接作用更可能是原因。在这些婴儿中严格避免使用含血浆的血液制品似乎没有道理。