[Classification and clinical findings of myelodysplastic syndromes].

Myelodysplastic syndromes (MDS) are a group of related disorders in which bone marrow stem cells malfunction, while the type is diagnosed based on the WHO classification revised in 2008. Although the diagnosis largely depends on the cytomorphology, it is difficult to diagnose MDS based on the morphology alone, particularly in patients with < 5% blasts in the bone marrow and a normal karyotype. In Japan, a grading system for the diagnostic accuracy of MDS was proposed in 2007, and evaluation of dysplasia (high, intermediate, low, minimal) is a characteristic part. Morphologic dysplastic changes are classified into highly specific category A (pseudo-Pelger-Huet anomaly, degranulation of neutrophils, micro-megakaryocytes, ringed sideroblasts) and less specific category B (dysplasia other than category A). With the use of this grading system, diagnostic problems should be reduced. Flow cytometry has also been proposed as a tool to improve the evaluation of marrow dysplasia, because immunophenotyping is an accurate method for quantitative and qualitative evaluations of hematopoietic cells, and MDS specimens have been found to exhibit abnormal expressions of several cellular antigens. In addition, the molecular classification of MDS has received marked attention in recent years. New molecular markers including RPS14, TET2, IDH1/2, SF3B1, ASXL1, RUNX1, TP53, EZH2, JAK2, and WT1 have been revealed to be important for the prognosis, as well as diagnosis and classification. In this report, we review MDS diagnostic approaches from the viewpoints of cytomorphology, immunophenotyping, and cytogenetics.

Pulmonary Nodular Lymphoid Hyperplasia Evaluated with Bronchoalveolar Lavage Fluid Findings: A Case Report and Review of the Literature on Japanese Patients.

Pulmonary nodular lymphoid hyperplasia (PNLH) is a very rare disease, and it is difficult to diagnose PNLH and distinguish it from mucosa-associated lymphoid tissue (MALT) lymphoma. In addition, information on bronchoalveolar lavage fluid (BALF) analyses is lacking. We herein report a 36-year-old Japanese woman diagnosed with PLNH by a surgical biopsy and analysis of BALF. The BALF showed an increase in B-cell marker-positive lymphocytes, normal patterns of B-cell clonality, mucosa-associated lymphoid tissue 1 gene, and immunoglobulin heavy chain at 14q32 translocations. We also reviewed Japanese cases of PNLH described in Japanese or English to explore the characteristics of such cases.

Corrigendum: The Contribution of Serum Complement Component 3 Levels to 90-Day Mortality in Living Donor Liver Transplantation.

[This corrects the article DOI: 10.3389/fimmu.2021.652677.].

The Contribution of Serum Complement Component 3 Levels to 90-Day Mortality in Living Donor Liver Transplantation.

The contributions of the complement system have been elucidated in the process of solid organ transplantation, including kidney transplantation. However, the role of complement in liver transplantation is unknown. We sought to elucidate the time-dependent changes of peritransplantational serum complement levels and the relationships with posttransplant outcomes and other immunological biomarkers. We enrolled 82 patients who underwent living-related donor liver transplantation (LDLT). Nine patients (11%) died within 90 days after LDLT (non-survivors). The following immunomarkers were collected preoperatively and at 1, 2, and 4 week(s) after LDLT: serum C3, C4, immunoglobulin G (IgG), and peripheral blood leukocyte populations characterized by CD3, CD4, CD8, CD16, CD19, CD20, CD22, and CD56. Consequently, C3 and C4 increased time-dependently after LDLT. Preoperatively, C3 was negatively correlated with the MELD score, Child-Pugh score, CD16-positive leukocyte percentage, and the CD56-positive leukocyte percentage. Non-survivors had lower levels of C3 at 2 weeks in comparison to survivors (median [interquartile range]: 56 [49-70] mg/dL vs. 88 [71-116] md/dL, p=0.0059). When the cutoff value of C3 at 2 weeks to distinguish non-survivors was set to 71 mg/dL, the sensitivity, specificity, and area under the ROC curve were 87.5%, 75.0%, and 0.80, respectively. A principal component analysis showed an inverse relationship between the C3 and C4 levels and the percentage of CD8-, CD16-, and CD56-positive leukocytes at 1 and 2 week(s). All non-survivors were included in the cluster that showed higher percentages of CD8-, CD16-, and CD56-positive leukocytes at 2 weeks. In conclusion, we demonstrated the relationship between complement, outcomes, and other immunomarkers in LDLT and suggested the usefulness of C3 at 2 weeks after LDLT in distinguishing the mortality.