| Literature DB >> 31932840 |
Sonata Jodele1,2, Christopher E Dandoy1,2, Adam Lane1,2, Benjamin L Laskin3, Ashley Teusink-Cross4, Kasiani C Myers1,2, Gregory Wallace1,2, Adam Nelson1,2, Jack Bleesing1,2, Ranjit S Chima2,5, Russel Hirsch2,6, Thomas D Ryan2,6, Stefanie Benoit1,2,7, Kana Mizuno2,8, Mikako Warren9,10, Stella M Davies1,2.
Abstract
Overactivated complement is a high-risk feature in hematopoietic stem cell transplant (HSCT) recipients with transplant-associated thrombotic microangiopathy (TA-TMA), and untreated patients have dismal outcomes. We present our experience with 64 pediatric HSCT recipients who had high-risk TA-TMA (hrTA-TMA) and multiorgan injury treated with the complement blocker eculizumab. We demonstrate significant improvement to 66% in 1-year post-HSCT survival in treated patients from our previously reported untreated cohort with same hrTA-TMA features that had 1-year post-HSCT survival of 16.7%. Responding patients benefited from a brief but intensive course of eculizumab using pharmacokinetic/pharmacodynamic-guided dosing, requiring a median of 11 doses of eculizumab (interquartile range [IQR] 7-20). Treatment was discontinued because TA-TMA resolved at a median of 66 days (IQR 41-110). Subjects with higher complement activation measured by elevated blood sC5b-9 at the start of treatment were less likely to respond (odds ratio, 0.15; P = .0014) and required more doses of eculizumab (r = 0.43; P = .0004). Patients with intestinal bleeding had the fastest eculizumab clearance, required the highest number of eculizumab doses (20 vs 9; P = .0015), and had lower 1-year survival (44% vs 78%; P = .01). Over 70% of survivors had proteinuria on long-term follow-up. The best glomerular filtration rate (GFR) recovery in survivors was a median 20% lower (IQR, 7.3%-40.3%) than their pre-HSCT GFR. In summary, complement blockade with eculizumab is an effective therapeutic strategy for hrTA-TMA, but some patients with severe disease lacked a complete response, prompting us to propose early intervention and search for additional targetable endothelial injury pathways.Entities:
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Year: 2020 PMID: 31932840 PMCID: PMC7099329 DOI: 10.1182/blood.2019004218
Source DB: PubMed Journal: Blood ISSN: 0006-4971 Impact factor: 22.113