A B S T R A C TPurpose: To explore the clinical, microbiological and immunological features of patients with fever and thrombocytopenia. Methods: Patients with unexplained fever and thrombocytopenia were enrolled. Viruses were detected using real-time PCR, and bacteria were measured by culturing methods. Serum cytokines, platelet antibody IgG (PA-IgG) and Helicobacter pylori (HP) were detected using ELISA. Results: Pathogens were detected in 74.68% of patients, which included single fungal/viral/bacterial infection and multiple infection. The pathogens could not be unidentified in 25.32% of cases. Cytokines including Interleukin (IL)-6, IL-10, interferon-γ(IFN-γ), platelet activating factor (PAF) and PA-IgG were significantly higher in patients as compared to healthy controls (P < .01 or P < .05). Principal component analyses extracted four groups of parameters that have a strong positive predicting value, revealing that disease status evaluation would be more accurate if we combined the platelet parameters and inflammatory biomarkers. While event-free survival (EFS) that indicates the time of platelet elevated after therapy was the highest in patients with single bacterial or fungal infection, EFS was affected by the levels of cytokines and PA-IgG. Conclusions: Differences in immune function may be the main factors affecting the prognosis of patients with fever and thrombocytopenia, while treatment based on precise etiological diagnosis is important for therapeutic efficacy.

Cytokine release syndrome (CRS), immune effector cell‐associated neurotoxicity syndrome (ICANS) and neutropenia are common toxicities associated with chimeric antigen receptor T (CAR‐T) cell therapy. The role of granulocyte colony stimulating factor (G‐CSF) in CAR‐T‐cell‐treated patients remains unclear. To explore the efficacy and safety of early G‐CSF administration in patients with relapsed/refractory B‐cell acute lymphoblastic leukemia (R/R B‐ALL) who were receiving autologous anti‐CD19 CAR‐T cells, we retrospectively collected and summarized clinical data to compare patients receiving G‐CSF within 14 days (early G‐CSF group) to patients receiving later or no G‐CSF (control group) after their CART infusion. The results showed that there was no significant difference in the incidence and duration of neutropenia between the early G‐CSF group and the control group (77% vs. 63%, p = 0.65; 8 vs. 4 days, p = 0.37, respectively). However, the incidence and duration of CRS were significantly higher in the early G‐CSF group than in the control group (81% vs. 38%, p = 0.03; 3 vs. 0 days, p = 0.004, respectively). Moreover, early G‐CSF application had no significant effect on the expansion and efficacy of CAR‐T cells. In conclusion, our study suggested that early G‐CSF administration did not reduce the incidence and duration of neutropenia but rather increased the incidence and duration of CRS.

Background: Hereditary elliptocytosis (HE) is a heterogeneous red blood cell membrane disorder characterized by the presence of elliptocytes on a peripheral blood smear. Clinical manifestations of HE vary widely from asymptomatic carriers to patients with severe transfusion-dependent anemia. Most patients are asymptomatic or have mild anemia, which hinders diagnosis. The proband in this case had mild anemia and jaundice over a period of 4 years, the etiology of which was unclear. Hence, he was admitted to our hospital for further diagnosis.Methods: Peripheral blood smears and routine blood tests were performed and biochemical parameters of the proband, and his family members were determined.To confirm the diagnosis, gene mutations were screened in the proband using nextgeneration sequencing (NGS) and verified by Sanger sequencing in other family members.Results: A novel mutation (c.1294delA, p.Ser432 fs) in exon 15 of the EPB41 gene was detected in the proband and his family members. This mutation results in a frameshift and a premature stop codon at position 455, encoding a truncated protein. The variant was likely pathogenic according to the criteria of the American College of Medical Genetics and Genomics. SWISS-MODEL protein structure prediction indicated partial loss of the spectrin and actin binding and C-terminal domains. Conclusion:A heterozygous mutation 1294delA in exon 15 of the EPB41 gene was identified using NGS and Sanger sequencing in members of a Chinese family. This identification expands the spectrum of EPB41 mutations and contributes to the genetic diagnosis of families with HE.

BackgroundLeukemoid reaction refers to reactive leukocytosis exceeding 50,000 cells/µl. Chronic neutrophilic leukemia is a rare clonal hematopoietic disorder characterized by sustained mature neutrophilia in the absence of monocytosis or basophilia. The differentiation between leukemoid reaction and chronic neutrophilic leukemia is problematic because both conditions share similar morphological features. Case presentationHere, we present an extremely rare case of a 62-year-old male patient who was initially diagnosed with chronic neutrophilic leukemia at another hospital. When the patient came to our hospital, no mutations in the CSF3R, SETBP1, ASXL1, TET2, SRSF2, SF3B1, ZRSR2 and U2AF1F genes were found by whole-exon sequencing. Further examination revealed the presence of immunoglobulin G kappa myeloma. Meanwhile, colonoscopy showed a mass in the colon, and biopsy confirmed the presence of colon adenocarcinoma. Therefore, we suggest that the increased white blood cell count in the patient was merely a neutrophilic leukemoid reaction caused by synchronous multiple myeloma and colon carcinoma.ConclusionThis is the first report of a case of coexisting multiple myeloma and colon carcinoma presenting with a neutrophilic leukemoid reaction. This case was presented to illustrate that the diagnosis of chronic neutrophilic leukemia must meet the strict WHO diagnostic criteria, especially if there is an underlying plasma cell disorder, and myeloid clonality must be demonstrated to make a distinction between chronic neutrophilic leukemia and leukemoid reaction. Meanwhile, this case provides us with a reference that further examination, especially pathological examination, should be performed on a patient diagnosed with multiple myeloma, who has extramedullary lesions, because other primary tumors may be also presenting the very similar symptoms. Pathological examination is helpful to differentiate the primary tumor from extramedullary invasion of multiple myeloma.