“…(Hill, et al, 2010, Risitano, et al, 2009 Critically, it has also been found that the intensity of complement deposition in PNH-E inversely correlates with the levels of the complement regulator CR1 (CD35) on erythrocytes, which are determined by genetic variants at the CR1 locus; (Rodriguez de Cordoba andRubinstein, 1986, Wilson, et al, 1986) individuals carrying the low expression allele CR1-L being particularly susceptible to experience extravascular hemolysis under eculizumab treatment. (Rondelli, et al, 2014) In addition to this extravascular removal of heavily opsonized PNH-E, one study has recently indicated that the residual low-level hemolysis could, in some patients, be related to incomplete C5 blockade and recommended close supervision of free eculizumab levels and terminal pathway activity to prevent this possibility. (Peffault de Latour, et al, 2015) Here, we searched for correlations between hemolysis parameters, complement determinations (including CR1 H/L genotypes) and plasma levels of free eculizumab in our cohort of eculizumab-treated patients.…”