Mediterranean Journal of Hematology and Infectious Diseases最新文献

Background: Hepatitis B virus (HBV) infection leads to liver fibrosis. Although liver biopsy remains the gold standard for diagnosis, its invasive nature limits routine application. Serum interleukin-34 (IL-34), which plays a role in macrophage activation and fibrogenesis, and shear wave elastography (SWE), a non-invasive method for measuring liver stiffness, represent potential diagnostic alternatives. This study compared the accuracy of IL-34 and SWE with liver biopsy findings in treatment-naive patients with chronic hepatitis B (CHB).

Material and methods: Between 2021 and 2022, 392 treatment-naive patients with CHB who were evaluated for liver biopsy were screened, and 105 eligible patients were prospectively enrolled in the study. Liver fibrosis was assessed by concurrently comparing SWE and IL-34 levels with histopathological biopsy findings.

Results: Of the 105 included patients (55% male; mean age 42.97 years), median IL-34 levels were significantly higher in those with fibrosis ≥2 than in patients with fibrosis 0-1 (10.70 vs. 6.20 pg/mL, p<0.001). ROC analysis identified optimal cut-off values of 8.1 pg/mL for IL-34 (AUC=0.955, sensitivity=88.2%, specificity=86.4%) and 8.18 kPa for SWE (AUC=0.939, sensitivity=100%, specificity=87.5%) for predicting significant fibrosis.

Conclusion: IL-34 and SWE exhibit high diagnostic performance as non-invasive methods for assessing liver fibrosis in CHB patients. The integration of these approaches into clinical practice may significantly reduce the need for biopsy and, due to their repeatability and lower cost, provide substantial advantages in patient management. This study is limited by its single-center design and the small number of cases with advanced fibrosis, which may affect its generalizability. Larger multicenter studies are warranted to validate these findings.

Plasma cell leukemia (PCL) is a rare and aggressive form of multiple myeloma (MM), characterized by the presence of malignant plasma cells in the peripheral blood. Until 2021, PCL was defined as plasmacytosis comprising at least 20% of the differential white blood cell count in peripheral blood. (CPCs). PCL was found in 2-4% of newly diagnosed MM cases. It can also develop from a preexisting, usually end-stage, MM, known as secondary PCL (sPCL), which exhibits distinct biological and clinical features. Both primary plasma cell leukemia (pPCL) and secondary plasma cell leukemia (sPCL) are very rare presentations of MM. According to the International Myeloma Working Group, plasma cell leukemia is generally diagnosed when the percentage of CPCs in peripheral blood exceeds 5%. PCL has a more aggressive clinical presentation than MM, involving more severe cytopenia, hypercalcemia, and renal failure. Higher tumor burden and proliferation activity in PCL are reflected by elevated levels of B2- B2-microglobulin and lactate dehydrogenase (LDH). Extramedullary localization at diagnosis is more common in pPCL and sPCL than in MM. Conversely, osteolytic lesions are less frequent in pPCL. The immunophenotype of PCL expresses the common MM markers, CD38 and CD138, but exhibits a more immature phenotype than MM. Molecularly, PCL lacks a specific marker but shows a markedly lower frequency of hyperploidy and significantly increased gains of chromosome 1 and translocations t(14;16) or t(14;20). Additionally, it has also been reported that the t(11;14) translocation occurs more frequently and is associated with a better prognosis. The recent therapy of PCL is similar to that of other high-grade myelomas, taking advantage of anti-proteasome, like bortezomib, an immunomodulator, like lenalidomide, and dexamethasone triplet + anti-CD38 antibody and/or cyclophosphamide, and hematopoietic stem cell transplantation. However, the results are not as good as in the other forms of myeloma.

Background: This study aimed to explore the role of SLC22A4 (encoding the organic cation transporter OCTN1) in acute myeloid leukaemia (AML) prognosis and therapy. Methods: RNA-sequencing data from 151 TCGA-AML samples and six Gene Expression Omnibus datasets (62 normal bone marrow and 520 AML samples) were analysed. Weighted gene co-expression network analysis identified immune-related gene modules. Differential expression analysis, survival analysis (Kaplan-Meier, Cox regression), methylation profiling, immune infiltration (xCell, EPIC), and drug sensitivity correlations were performed. Statistical methods included Wilcoxon rank-sum tests, ROC curves, and LASSO regression.

Results: SLC22A4 expression was significantly decreased in AML compared with normal samples. The high-expression group was associated with a better prognosis than the low-expression group. Gene set enrichment analysis revealed enrichment in metabolic transport, immune, and tumour-related pathways. SLC22A4 expression was negatively correlated with immune cells, and methylation of SLC22A4 was significantly negatively correlated with expression. Moreover, it was predicted that 5 miRNAs could regulate SLC22A4 expression. Drug-sensitivity analysis showed positive correlations with cyclobenzaprine, hydrochloride, SGX-523, and simvastatin, and negative correlations with fluorouracil, abexinostat, EMD-534085, hypothemycin, tamoxifen, and sunitinib.

Conclusion: SLC22A4 may be useful as a potent molecular-targeted agent in AML.

Iron is required for several vital biological processes in all human cells. In mammals, a considerable number of proteins are involved in iron metabolism and utilize iron in many essential cellular processes, such as oxygen transport, mitochondrial respiration, gene regulation, and DNA synthesis or repair. Iron metabolism is a complex system finely regulated at both systemic and cellular levels. It involves the development of specialized mechanisms for iron absorption, transport, recycling, storage, and export, and protection against toxic compounds that can be generated during iron redox cycling in the presence of oxygen. The erythropoietic compartment consumes the majority of iron to support the high demand for hemoglobin synthesis. A tightly regulated system enables efficient iron uptake by erythroid cells and its subsequent processing for the synthesis of large amounts of heme, which is then incorporated into hemoglobin. A bidirectional regulatory system between erythropoiesis and iron metabolism ensures precise coordination between the two processes. This regulation is often disrupted in various anemic conditions.

Pidotimod, a synthetic dipeptide, has been utilized for over three decades as an immunomodulatory agent to prevent recurrent respiratory infections, particularly in immunocompromised populations such as children and the elderly. Originally developed for its ability to enhance innate and adaptive immune responses, pidotimod is now being revisited in light of new clinical insights and emerging therapeutic needs. Recent studies have expanded its potential beyond traditional indications, with evidence supporting its role in patients with chronic respiratory diseases, such as chronic obstructive pulmonary disease (COPD), allergic rhinitis, and even viral infections, including SARS-CoV-2. Pidotimod exerts its effects by stimulating dendritic cells, enhancing toll-like receptor (TLR) expression, and promoting cytokine production, including IL-2 and IFN-γ, thereby supporting both cellular and humoral immunity. This broad-spectrum immune modulation makes pidotimod a promising adjunct in managing immune-mediated diseases and infections in both immunocompetent and immunocompromised individuals. In this review, we examine pidotimod's pharmacodynamics, summarize clinical evidence from recent studies, and explore its evolving role in modern therapeutic strategies for infectious diseases. Given its safety profile and oral administration, pidotimod holds significant promise not only for preventing infections but also as part of a broader immunomodulatory approach in complex disease management.

Background: Efficient management of sepsis requires precise antibiotic therapy. This study examines the efficacy of guiding such therapy using Procalcitonin (PCT), C-Reactive Protein (CRP), and albumin levels.

Methods: A total of 127 adult sepsis patients were assigned to either standard care or a biomarker-guided group where antibiotic use was adjusted based on biomarker levels.

Results: The biomarker-guided approach significantly reduced the duration of antibiotic therapy (9.0 vs. 10.5 days, P=0.04) and expedited antibiotic de-escalation. Hospital costs were lower in the biomarker-guided group (20,000 vs. 24,000 CNY, P=0.04), though reductions in secondary infections did not reach statistical significance. There was no significant difference in 28-day mortality rates.

Conclusion: Biomarker-guided antibiotic therapy can enhance the efficiency of treatment in sepsis, reducing both duration and cost without impacting patient safety. These findings suggest the potential benefits of incorporating biomarkers into standard sepsis management protocols.