These results suggest that the implementation of CVVHDF with RCA using concentrated citrate solutions prolongs filter lifetime, achieves a longer effective hemodiafiltration time and is a safe and feasible method.
BackgroundThe presence of >94% classical monocytes (MO1, CD14++/CD16‐) in peripheral blood (PB) has an excellent performance for the diagnosis of chronic myelomonocytic leukemia (CMML). However, the monocyte gating strategy is not well defined. The objective of the study was to compare monocyte gating strategies and propose an optimal one.MethodsThis is a prospective, single center study assessing monocyte subsets in PB. First, we compared monocyte subsets using 13 monocyte gating strategies in 10 samples. Then we developed our own 10 color tube and tested it on 124 patients (normal white blood cell counts, reactive monocytosis, CMML and a spectrum of other myeloid malignancies). Both conventional and computational (FlowSOM) analyses were used.ResultsComparing different monocyte gating strategies, small but significant differences in %MO1 and percentually large differences in %MO3 (nonclassical monocytes) were found, suggesting that the monocyte gating strategy can impact monocyte subset quantification. Then, we designed a 10‐color tube for this purpose (CD45/CD33/CD14/CD16/CD64/CD86/CD300/CD2/CD66c/CD56) and applied it to 124 patients. This tube allowed proper monocyte gating even in highly abnormal PB. Computational analysis found a higher %MO1 and lower %MO3 compared to conventional analysis. However, differences between conventional and computational analysis in both MO1 and MO3 were globally consistent and only minimal differences were observed when comparing the ranking of patients according to %MO1 or %MO3 obtained with the conventional versus the computational approach.ConclusionsThe choice of monocyte gating strategy appears relevant for the monocyte subset distribution test. Our 10‐color proposal allowed satisfactory monocyte gating even in highly abnormal PB. Computational analysis seems promising to increase reproducibility in monocyte subset quantification.
variants: Class 1: relevant in the clinical management of myeloid hemopathies. It has been established as a pathogenic variant in myeloid hemopathies and alters an actionable gene. Class 2: it has been established as a pathogenic variant in solid tumors or non-myeloid hemopathies and alters an actionable gene. Class 3: variant not previously described, affects an actionable gene and in silico predictors or classifies mutations as:• Class 3A: likely pathogenic.• Class 3B: uncertain significance (VUS).• Class 3C: likely benign.† VAF: variant allele frequency.‡ This variant has not been previously described in public databases (either as somatic or germline) and in silico predictors classified it, some as benign and others as pathogenic. In this situation, NGS recommendations suggest to classify these variants as of uncertain significance. Chr = chromosome.
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