Cytometry Part B: Clinical Cytometry最新文献

Implementing a new laboratory information system (LIS) presents an opportunity to improve operational efficiency and streamline reporting by refining workflows by utilizing LIS functionality. Flow cytometry laboratories face unique challenges because the specimen and test results may be categorized under clinical pathology (CP), anatomic pathology (AP), or both. We describe the design and implementation of reporting flow cytometry results within the Epic Beaker CP module, its interface with the Epic Beaker AP module, and integrated reporting for AP/CP cases at an academic institution. This manuscript emphasizes the challenges and steps needed to integrate anatomic and clinical pathology workflows by leveraging LIS functionality to implement electronic and predominantly paperless workflows within a flow cytometry laboratory.

Blast quantification in the bone marrow (BM) is crucial for evaluating myeloid neoplasms, with cytomorphology being the only recognized analysis. The CD34 myeloid cell (CD34M) count by flow cytometry is promising but impaired by BM hemodilution. A modified version of the Holdrinet index (mHI) is routinely used to assess it, though not yet validated. By analyzing two differently hemodiluted BM samples from 51 patients with suspicion of myelodysplasia, this study confirms mHI accuracy in assessing BM white blood cell purity. mHI-adjusted count by flow cytometry of BM-exclusive cell subsets, such as CD34 myeloid cells, may offer a reliable and practical alternative to cytomorphology analysis, independently from hemodilution.

A reduced proportion of peripheral class-switched memory B cells (CSM-B cells) is presumed to indicate ineffective germinal activity. The extent that this finding corresponds to a plausible germinal center failure pathophysiology in patients not diagnosed with CVID or hyper IgM syndrome is not known. We asked if patients with low CSM-B cells are more likely to demonstrate failure to produce serum IgA and IgG than counterparts with nonreduced class-switched memory B cell levels, regardless of diagnosis. Patients with low CSM-B cell levels regardless of diagnosis were retrospectively compared with their counterparts without CSM-B cell reductions for demographics and serum immunoglobulin levels. Patients were further divided based on whether CSM-B cell levels remained low over time or fluctuated, and these groups were compared for serum immunoglobulin levels and diagnoses. Of 305 patients, those with CSM-B cell (n = 50) reductions were more likely to have low serum IgA and IgG than those without reductions. Of the 78 patients in whom CSM-B cells were measured repeatedly over time, 21 patients had low CSM-B cell levels, but this finding was persistent in only 10. Patients with persistent CSM-B cell reductions universally had severe serum IgA and IgG deficiencies and patients with transient CSM-B cell reduction often did not. These two groups contained divergent diagnoses and likely represent separate pathophysiologic groups. Quantifying CSM-B cells as a percentage of CD27+ B cells repeatedly over time is a robust approach to identifying patients with a plausible germinal center failure endotype.

The clinical and immunophenotypic attributes of reactive γδ T-cell expansions are less well characterized than their malignant counterparts, which can pose diagnostic challenges. This study aims to investigate the characteristics and long-term clinical outcomes of reactive γδ T-cell expansions. A retrospective review was performed to identify patients with expanded γδ T-cell population (>15% of T-cells) by flow cytometry in peripheral blood and/or bone marrow specimens over a 17-year period. The cases were divided into reactive and malignant categories and their clinical and immunophenotypic findings were compared. Clinical follow-up was performed. 97 patients were identified including 19 malignant and 78 reactive cases with a variety of underlying conditions. The median absolute γδ T-cell count and median percentage of γδ T-cells per total T-cells were significantly lower in reactive vs. malignant cases (p = 0.0001 and p < 0.00001, respectively). Reactive cases showed more frequent brighter surface CD3 expression (87.1% vs. 42.1%; p < 0.0001), no discrete loss of CD7 (0% vs. 36.9%; p < 0.0001), less frequent lack of CD5 (25.7% vs. 42.4%; p < 0.0001), and no homogeneous CD56 expression (0% vs. 31.6%; p > 0.0001) as compared with malignant cases. Upon long-term follow-up, none of the reactive cases showed clinical evidence of malignant evolution. Reactive expansions of γδ T-cells can be seen in a variety of conditions including hematologic neoplasms, autoimmune and post-transplant states, and infections. Such cases have significantly lower γδ T-cell counts and percentages and no discrete loss of CD7. Lack of CD5 on its own is not an indication of immunophenotypic aberrancy in γδ T-cells. Upon long-term clinical follow-up, such reactive expansions show no evidence of evolution to γδ T-cell malignancies.