G-CSF-primed haplo-identical HSCT with intensive immunosuppressive and myelosuppressive treatments does not increase the risk of pre-engraftment bloodstream infection: a multicenter case-control study
G-CSF-primed haplo-identical HSCT with intensive immunosuppressive and myelosuppressive treatments does not increase the risk of pre-engraftment bloodstream infection: a multicenter case-control study
复制标题
G-CSF引发的单倍相合 HSCT 联合强化免疫抑制和骨髓抑制治疗不会增加植入前血流感染的风险：一项多中心病例对照研究
DOI：
10.1007/s10096-019-03482-6
复制
发表时间：
2019-05-01
影响因子：
4.5
通讯作者：
Yang, Ting
中科院分区：
文献类型：
--
作者：
Ren, Jinhua;Lin, Qiaoxian;Yang, Ting
2013年2月至2016年2月，对131例血液疾病患者（44例女性/87例男性）进行了一项多中心回顾性研究，这些患者接受了粒细胞集落刺激因子（G - CSF）动员的单倍体相合（Haplo - ID）（n = 76）或人类白细胞抗原（HLA）全相合（HLA - ID）造血干细胞移植（HSCT）（n = 55），以比较植入前血流感染（PE - BSI）的发生率和危险因素。在单倍体相合组中，71/76例高危（n = 28）或复发/难治性血液恶性肿瘤（n = 43）患者接受了FA5 - BUCY预处理（NCT02328950）。所有患者均接受复方磺胺甲恶唑（TMP - SMX）预防。获取血培养和导管尖端培养以确诊血流感染。在28次发热性中性粒细胞减少发作后，131例造血干细胞移植患者中有24例（单倍体相合组18/76例，HLA全相合组6/55例）检测到植入前血流感染。24例患者的28株分离菌中，21株（75%）为革兰阴性菌，6株（21.4%）为革兰阳性菌，1株（3.6%）为真菌。细菌来源为中心静脉导管感染（7/29.2%）、胃肠炎（6/25%）、下呼吸道感染（LRTI；5/20.8%）、肛周皮肤感染（4/16.7%）和不明原因（2/8.3%）。单因素分析显示，中性粒细胞减少持续时间（P = 0.046）和既往革兰阴性菌血症（P = 0.037）是重要危险因素，而造血干细胞移植类型不是。两组中均存在对复方磺胺甲恶唑耐药的血流感染趋势，可能是由于常规的抗菌预防策略所致。我们的数据表明，即使采用强化免疫抑制治疗，粒细胞集落刺激因子动员的单倍体相合造血干细胞移植也不会增加植入前血流感染的风险。
A multicenter retrospective study in 131 patients (44 females/87 males) with hematological disorders who underwent G-CSF-primed/haplo-identical (Haplo-ID) (n = 76) or HLA-identical (HLA-ID) HSCT (n = 55) from February 2013 to February 2016 was conducted to compare the incidence and risk factors for pre-engraftment bloodstream infection (PE-BSI). In the Haplo-ID group, 71/76 patients with high-risk (n=28) or relapsed/refractory hematological malignancies (n=43) received FA5-BUCY conditioning (NCT02328950). All received trimethoprim-sulfamethoxazole (TMP-SMX) prophylaxis. Blood cultures and catheter tip cultures were obtained to confirm the BSI. PE-BSI was detected in 24/131 HSCT patients (18/76 in Haplo-ID and 6/55 in HLA-ID) after 28 febrile neutropenic episodes. Among 28 isolates for the 24 patients, 21 (75%) were G(neg) bacteria, 6 (21.4%) G(pos) and 1 (3.6%) fungi. Bacteria sources were central venous line infection (7/29.2%), gastroenteritis (6/25%), lower respiratory tract infection (LRTI; 5/20.8%), perianal skin infection (4/16.7%), and unknown (2/8.3%). The duration of neutropenia (P=0.046) and previous G(neg) bacteremia (P=0.037) were important risk factors by univariate analysis, while the type of HSCT was not. A trend of TMP-SMX-resistant BSI in both groups may be due to routine antibacterial prophylaxis strategies. Our data show that G-CSF-primed Haplo-ID HSCT did not increase the risk of PE-BSI, even with intensive immunosuppressive treatments.