中国实验血液学杂志最新文献

Objective: To analyze the anti-HCV (hepatitis C virus) screening results and confirmatory test results of blood samples in our laboratory, so as to provide a basis for the selection of blood screening strategies.

Methods: 946 anti-HCV ELISA screening non-conforming samples from volunteer blood donors at our center between 2015 and 2023 were randomly selected. Statistical analysis was performed on ELISA results and Western blot (WB) confirmatory test results. The ELISA retest concordance rate, proportion of confirmed positive samples, true positive detection rate and optimal shielding threshold value of four reagents (A, B, C and D) were analyzed.

Results: The overall retesting concordance rates of the initial screening non-conforming specimens for the four reagents were 69.88%, 27.54%, 84.00% and 69.08%, respectively. Results of WB confirmatory tests showed that the true positive detection rates of the four reagents were 99.49% (391/393), 98.00% (49/50), 93.88% (92/98), and 97.20% (382/393), respectively. The S/CO (sample/cut-off ratio) values of non-conforming samples detected by the four reagents were positively correlated with WB results: the higher the S/CO value, the higher the proportion of confirmed positive samples (r=0.99, 0.95, 0.87, and 0.99, respectively). The receiver operating characteristic (ROC) curves for the detection performance of the four reagents were drawn according to the WB results, and the areas under the curves (AUC) were 0.946, 0.909, 0.934, and 0.967, respectively. The optimal shielding threshold value of S/CO were 5.64, 1.61, 1.58, and 2.42, with corresponding positive predictive values (PPV) of 93.50%, 100%, 100%, and 92.66%, respectively.

Conclusion: There are certain differences in the detection capabilities of different anti-HCV ELISA screening reagents. Each laboratory can choose different reagent combinations for complementary advantages or set the optimal shielding threshold value of S/CO according to its own needs, so as to improve the accuracy of detection, ensure blood safety, and avoid waste of blood and reagents.

Objective: To explore the clinical features and prognosis of patients with Epstein-Barr virus (EBV)-positive diffuse large B-cell lymphoma (DLBCL).

Methods: The clinical data of 152 patients with DLBCL in Jixi Road Hospital District, Gaoxin Hospital District, North District of the First Affiliated Hospital and the Second Affiliated Hospital of Anhui Medical University from January 2017 to March 2024 were collected and retrospectively analyzed to determine the clinical characteristics and the impact of EBV positivity on prognosis.

Results: Among 152 DLBCL cases, there were only 15 cases of EBV-positive DLBCL, with a positivity rate of about 9.87% (15/152). Among the patients with EBV-positive DLBCL, the median age at onset was 75 years old, there were 8 males and 7 females, all of them were immunophenotyped as ABC (15/15), all of the 15 EBV-positive patients were treated with R-CHOP, the recent efficacy assessment was progressive disease in all of them (15/15). Ann Arbor staging, ECOG score, lactate dehydrogenase (LDH), IPI score, immunophenotyping, and MYC expression were correlated with the expression of EBER (P< 0.05). The prognosis of patients with EBV-positive DLBCL was significantly worse than that of patients with EBV-negative DLBCL, and the ECOG score and EBER positivity were independent prognostic factors in patients with DLBCL.

Conclusion: EBV-positive DLBCL is a rare group of highly aggressive lymphomas with predominantly ABC subtypes, with a high overall morbidity and mortality. The expression of EBER and the ECOG score were associated with DLBCL prognosis.

Objective: Three methods were used to identify ABO blood group of discrepancies samples to determine the appropriate combination of identification methods and genetic mechanism.

Methods: ABO blood group discrepancies samples were collected and identified with serological methods and molecular biological methods. The phenotype was determined with micro-column gel card and tube method. Molecular biological methods included the polymerase chain reaction with sequence-specific primers (PCR-SSP) for genotype determination, and genetic basis was determined by Sanger sequencing.

Results: Among 28 samples, 15 ABO alleles were identified, including 5 A alleles, 5 B alleles, 2 O alleles, 1 B(A) allele and 2 CisAB alleles. The PCR-SSP genotyping results were inconsistent with sequencing genotyping results in 5 cases. Three novel base sequences were discovered by sequencing.

Conclusion: Combined serological methods and sequencing is helpful for precise ABO grouping, the combination can discover the subtype phenotype and genetic mechanism.

Anaplastic large cell lymphoma (ALCL) is a rare CD30-positive T-cell non-Hodgkin lymphoma, primarily classified into two subtypes: ALK-positive ( ALK ⁺) and ALK-negative ( ALK ^-). ALK ⁺ ALCL is commonly seen in younger patients and characterized by rapid progression, with the majority of patients achieving complete remission after chemotherapy. In contrast, ALK ^-ALCL generally affects older patients, presenting with similar clinical features but a poorer prognosis. Genetic rearrangements, such as DUSP22 and TP63, have a significant impact on patient survival. The current treatment regimen primarily involves CHOP, but its efficacy is limited, especially in relapsed cases. Consequently, there is an urgent need to improve frontline and salvage treatment options. Future research should focus on the integration of targeted therapies with molecular mechanisms to enhance therapeutic outcomes and survival rates. Understanding the subtypes and molecular characteristics of ALCL is essential for optimizing therapeutic strategies. Therefore, this review summarizes recent research advances on ALK ^+/- ALCL to provide insights for optimizing treatment approaches.

Objective: To investigate the influencing factors of apheresis platelet aggregation.

Methods: Data from platelet collections by using the Amicus blood cell separator between August 2024 and December 2024 were analyzed. The occurrence of platelet aggregation and its contributing factors were analyzed.

Results: The overall platelet aggregation rate was 16.4%. Aggregation rates in male and female donors were 15.9% and 26.1% , respectively, with no statistically significant difference. Donors with platelet aggregation showed significantly lower HB, HCT, and MCV values but higher Pre-PLT and PCT levels compared to non-aggregated donors. Binary logistic regression analysis revealed that the cause of apheresis platelet aggregation was associated with a history of aggregation and unrelated to other factors. Using aggregation status as the state variable (aggregation=1, non-aggregation=0), the areas under the curve (AUC) for aggregation history, Pre-PLT, and PCT-AUC were 0.784, 0.633, and 0.617, respectively.

Conclusion: Blood donors who have experienced aggregation are more likely to experience aggregation again. In addition, Special attention should be given to donors with elevated Pre-PLT/PCT levels to avoid the occurrence of serious aggregation, and routine practices should mark donors with platelet aggregation history.

Objective: To perform genotyping on a specimen serologically identified as a D variant, and conduct a family survey and analysis.

Methods: Serological methods were used to confirm RhD and detect RhD antigen epitopes in the proband and his family members' specimens. PCR-SSP method was applied to analyze RHD gene zygosity and perform preliminary RHD genotyping. Sanger sequencing and single-molecule real-time sequencing were used to perform sequencing analysis of RHD gene exons 1-10 and whole-genome sequencing for the proband and his family members' specimens. The tertiary structure models of the protein before and after mutation were constructed using AlphaFold 3 software to analyze the changes in interactions between the mutated amino acid and surrounding residues. Additionally, online tools were employed to predict the impact of the amino acid substitution due to the mutations on RhD protein function.

Results: The serological testing of the proband's mother revealed an RhD-negative blood type with the antigen profile CCee, RHD exon sequencing identified a heterozygous genotype: RHD*01N.03/RHD*01N.01. Both the proband and his father exhibited serological D variants with the antigen profile CcEe, and preliminary PCR-SSP analysis indicated RhD heterozygosity. Sanger sequencing of exons 1-10 of the RHD gene and whole-genome sequencing of the proband and his father revealed a c.179T>C mutation in exon 2 and a c.1154-31T>C mutation in exon 9. AlphaFold 3 modeling predicted that the loss of hydrophobic contact between the Ile-60 and Val-56 residues leads to reduced protein stability. Among the three software tools used for predicting protein function damage, two suggested that this mutation might be deleterious to the function of the RhD protein.

Conclusion: The proband has a heterozygous genotype of RHD*01N.01/RHD*(c.179T>C, c.1154-31T>C). The p.Ile60Thr mutation leads to changes in intramolecular forces between amino acid residues, thereby causing partial changes in the structure and function of the mutated protein.

Objective: To evaluate the feasibility of in-class transition（iCT） first-line bortezomib intolerance to carfilzomib in the treatment of patients with multiple myeloma（MM）.

Methods: It was retrospectively collected that the clinical data of MM patients who transitioned to carfilzomib due to intolerance, such as ≥grade 1 painful peripheral neuropathy （PN）, during the treatment with first-line bortezomib-based triple regimens in the First Affiliated Hospital of Soochow University and Soochow Hopes Hematology Hospital from March 2023 to January 2025, and their safety and efficacy were analyzed.

Results: A total of 23 MM patients were included. The cohort had a median age of 63 （46-75） years. The median treatment cycle of bortezomib before iCT was 4 （1-6）. Among the causes of intolerance, there were 22 cases of PN and 1 case of diarrhea. With a median follow-up of 10（2-23） months, at 1 month, 2 months and 4 months, 1/22, 3/22, and 12/20 of patients reduced by one grade in PN after transition. At 4 months after transition, all patients' peripheral neuropathic pain symptoms had disappeared. After 2 months of transition, there was a significant decrease in overall neuropathy limitations scale (ONLS) and total neuropathy score (TNS) scores compared to baseline （P <0.001）. After carfilzomib treatment, the decrease in grade≥3 neutropenia from 21.7% to 17.4%（P=0.021）.The additional non-hematological toxicity was transient, with grade 1-2 hypertension（47.8%） and QTcF prolongation（13.0%）. In terms of efficacy analysis, the conversion rate of ≥CR increased from 30.4% to 69.5% （P=0.047）, and the sCR rate and mininal residual disease (MRD) negative conversion rate both increased from 30.4% to 65.2% （P=0.026）.

Conclusion: The transition of first-line bortezomib intolerance to carfilzomib can significantly improve symptoms such as PN and deepen remission.

Objective: To analyze the influence of massive transfusion on blood test indexes in children, and to explore the risk factors of survival outcome in order to prevent complications and improve survival rate of children.

Methods: One hundred and sixteen children with massive transfusion during operation from January to April 2024 were selected, according to the multiples of the amount of intraoperative blood transfusion and their own blood volume, they were divided into three groups: 1-2 times transfusion volume group (71 cases), >2,≤3 times transfusion volume group (35 cases), >3 times transfusion volume group (10 cases). The difference of blood test indexes before and after massive transfusion in children was analyzed, and the correlation between those differential indicators and transfusion times, and the high risk factors affecting children's survival outcome were predicted.

Results: There were significant differences in blood indexes including hcrp, PT, APTT, TT, FIB, ALT and Ca²⁺.before and after massive transfusion. There were positive correlation between hcrp, PT, APTT, TT, ALT and transfusion times (r=0.053，P=0.040；r=0.118,P=0.020；r=0.186，P=0.045；r=0.046，P=0.034；r=0.075，P=0.042), and negative correlation between FIB, Ca²⁺ and transfusion times(r=-0.096，P=0.031；r=-0.097，P=0.029). hcrp, PT, APTT, TT, ALT were positively correlated with the blood components ratio(r=0.060，P=0.003；r＝0.049，P=0.049；r＝0.149，P=0.046；r＝0.045，P=0.047；r＝0.095，P=0.024), while FIB, Ca²⁺ were negatively correlated with the blood components ratio r＝-0.033，P=0.047；r＝-0.002，P=0.046). Multivariate analysis showed that weight (<2.1 kg), blood loss (>355 ml), operative time (>102.5 min), red blood cell infusion (>2.75 U), plasma infusion (>125 ml), cryoprecipitate infusion (>3 U), PT(>31.8 s), APTT(>78 s), TT(>29.4 s), FIB(<0.85 g/L) were independent risk factors for children's survival outcome.

Conclusion: Massive blood transfusion in children is associated with postoperative complications such as coagulation disorders, liver damage and electrolyte disturbance, the changes of blood transfusion volume and the blood component ratio can affect the severity of symptoms. Low weight, much intraoperative blood loss, long operative time, excessive transfusion volume and coagulation dysfunction can predict high risk of death in children.

Donor-recipient sex significantly influences the outcomes of allogeneic hematopoietic stem cell transplantation (allo-HSCT). Traditionally, female-to-male (F→M) transplants were associated with a higher risk of chronic graft-versus-host disease (cGVHD) and poorer prognosis. However, recent large cohort studies have reported inconsistent results. Partial reports indicated that the sex of the recipient has more predictive value for long-term survival, while sex mismatch shows limited impact on overall survival (OS). Advances in haploidentical HSCT (haplo-HSCT) and immunosuppressive regimens have reduced sex-related GVHD incidence. Meanwhile, the graft-versus-tumor (GVT) effect has gained recognition for its role in relapse prevention. Balancing GVHD risk and GVT effect benefit has become central to transplant strategy. This review integrates relevant literature to examine the biological mechanisms underlying sex differences, their impact on prognosis, and recent advances in intervention strategies.

Objective: To investigate the regulatory effect and molecular mechanism of lncRNA MALAT1 mediated by myeloma-derived exosomes on angiogenesis through in vitro and in vivo experiments.

Methods: Using the GSE72213 database, we screened for differentially expressed genes in multiple myeloma patients compared to the control group, identifying MALAT1 as a candidate molecule. The subcellular localization of MALAT1 in bone marrow samples was determined by RNA fluorescence in situ hybridization, and patients were classified into high-risk and low-risk groups based on MALAT1 expression levels, and the survival differences between two groups were observed. Immunohi- stochemical staining combined with microscopic counting was used to assess the correlation between MALAT1 and VEGFA, MVD. A subcutaneous tumor model was established by injecting U266 cell exosomes. The effects of lnc MALAT1 on angiogenesis mediated by exosomes were evaluated through measuring tumor size, using the hematoxylin-eosin staining method, and performing IHC staining for VEGFA, CD31, and Ki67. In HUVEC cells, the effects of U266 exosomes after MALAT1 knockout on angiogenesis were investigated using tube formation assays and measuring MALAT1 and VEGFA levels. To further explore potential regulatory mechanisms, TargetScan and miRanda were used to predict downstream miRNAs of MALAT1 and their target mRNAs, and a ceRNA network was constructed using Cytoscape v3.10.2.

Results: Bioinformatics analysis indicated that MALAT1 was highly expressed in patients with MM. Clinical studies showned that high-risk patients had a significantly shorter survival period. There was a significant positive correlation between MALAT1 levels and the expressions of VEGFA and MVD, and high MALAT1 levels were closely associated with a poor prognosis in patients with MM. Both in vitro and in vivo experiments confirmed that exosomes derived from myeloma cells can promote angiogenesis, and knocking out MALAT1 can reverse this effect. MALAT1 may reduce the inhibitory effect of hsa-miR-140-5p on VEGFA by competitively binding to it, forming a regulatory axis involving MALAT1/miR-140-5p/VEGFA, thereby promoting the proliferation and migration of vascular endothelial cells.

Conclusion: Our results suggest that exosome lnc MALAT1 promotes angiogenesis in MM by regulating VEGFA, and may serve as a biomarker for MM prognosis evaluation and a potential target for anti-angiogenic therapy.