Epstein-Barr virus infection usually presents as infectious mononucleosis with fever, pharyngitis, and lymphadenopathy, while cholestatic jaundice is a rare manifestation. We report a 36-year-old man who presented with progressive jaundice, pruritus, and dark-coloured urine with deranged liver function tests showing a cholestatic pattern. Evaluation revealed atypical lymphocytosis and positive EBV IgM serology after exclusion of biliary obstruction and other common causes of hepatitis. The patient improved with supportive treatment alone. This case highlights the importance of considering EBV infection in the differential diagnosis of cholestatic jaundice.

A 1.5-year-old female Spitz dog was presented with a sudden onset of inappetence, weakness, anemia, and hemoglobinuria persisting for two days. The dog had a prior history of tick infestation. A thorough physical examination revealed pyrexia, lymphadenopathy, pale conjunctival and gingival mucous membranes, and a normal capillary refill time. Microscopic analysis of a Giemsa-stained peripheral blood smear identified the presence of Babesia gibsoni, which was further confirmed through PCR. Hematological analysis revealed severe anemia, neutropenia, eosinophilia, lymphocytosis, and thrombocytopenia. Serum biochemistry indicated significant hypoglycemia, hypoproteinemia, and hypoalbuminemia. Serum oxidant-antioxidant parameters revealed a marked increase in the level of oxidant and a decreased level of antioxidants. Genetic characterization based on the 18S rRNA gene fragment demonstrated complete sequence identity with B. gibsoni strains from Asia, Europe, and North America. Phylogenetic analysis revealed that the isolate (PQ143276) was most closely related to B. gibsoni strains from Sri Lanka and Spain, following a distinct geographical pattern. The therapy included a combination of oral metronidazole, doxycycline, and clindamycin which resulted in a favourable response. The dog regained appetite and vigor by the 10th day post-treatment. To the best of the authors' knowledge, this is one of the few documented reports from Tripura that provides a comprehensive analysis of genetic characterization, phylogenetics, hemato-biochemical findings, and serum oxidant-antioxidant status of the infection, while also contributing to the understanding of its evolutionary relationships within the Babesia genus.

Background: Leukemic non-nodal variant mantle cell lymphoma (nnMCL) is an uncommon subtype of mantle cell lymphoma that lacks lymphadenopathy and generally follows an indolent clinical course. Adverse genetic alterations such as TP53 inactivation and del(13q) may have prognostic significance. Clinical findings such as splenomegaly may serve as a clue to the diagnosis and should prompt further evaluation. Case Presentation: We describe a 91-year-old woman who presented with a one-month history of anemia (hemoglobin 12.3 g/dL), mild thrombocytopenia (platelets 136 × 10[9]/L), isolated splenomegaly and no palpable lymphadenopathy. Despite a normal total white blood cell count, intermittent relative lymphocytosis with atypical lymphocytes (4%) and smudge cells was detected on the complete blood count. Peripheral blood flow cytometry demonstrated a monoclonal kappa-restricted B-cell population negative for CD5 and CD10, comprising approximately 20% of lymphocytes. Conventional karyotyping and fluorescent in situ hybridization (FISH) analysis identified del(13q), del(17p)/TP53, and IGH-CCND1 rearrangement in 8-19.5% of peripheral blood leukocytes. A month after the initial assessment, the patient presented following a fall. CT imaging of the abdomen revealed marked splenomegaly, a large subcapsular/perisplenic hematoma, and moderate-to-large hemoperitoneum. Emergent laparotomy showed an enlarged spleen (1490 g, 23 × 16 × 7.5 cm) with laceration. Histologic evaluation showed atypical lymphoid cells positive for CD20 and cyclin D1, with strong p53 expression, negative for CD5 and SOX11, and a low Ki-67 index. Similar involvement was identified in the small bowel and appendix. Targeted sequencing of splenic tissue, performed as part of a retrospective molecular characterization, identified a pathogenic TP53 variant (p.His179Gln). Conclusions: This case provides a rare opportunity to evaluate splenic and small intestinal involvement by nnMCL at both the gross and histologic levels. It highlights the importance of integrating clinical findings with flow cytometry, imaging, cytogenetic, and molecular data in establishing the diagnosis. Even when peripheral blood findings suggest a low disease burden, imaging may better define the extent of disease and support appropriate clinical assessment, particularly in elderly patients at risk for complications related to splenomegaly.

Aggressive natural killer (NK) -cell leukemia (ANKL) is a rare hematological malignancy characterized by the abnormal proliferation of NK cells. It progresses rapidly and has a high mortality rate. This article reports the diagnosis and treatment of a rare case of a patient with ANKL and concurrent CD5(+)CD10(-) monoclonal B-cell lymphocytosis and hemophagocytic lymphohistiocytosis (HLH), and the relevant literature was reviewed. The patient was a 73-year-old male who presented with fever and lymphadenopathy in multiple areas without any obvious cause for over 1 month. Laboratory examinations, including bone marrow cell morphology and biopsy, revealed two distinct populations of abnormal cells. Flow cytometry, immunohistochemical staining, and gene testing confirmed the diagnoses of ANKL and CD5(+)CD10(-) monoclonal B-cell lymphocytosis, with concurrent HLH. The patient was initially treated with etoposide and dexamethasone. After receiving three courses of chemotherapy based on pegaspargase and other combination regimens, the patient's condition deteriorated. Resuscitation treatment was ineffective; the patient died due to multiple organ failure.

Cold agglutinin disease (CAD) is an uncommon hemolytic anemia by complement-fixing IgM autoantibodies and is frequently associated with a distinct clonal B-cell lymphoproliferative disorder (CAD-LPD). We report a woman in her 50's with progressive fatigue who presented with hemolytic anemia and an IgM-κ paraprotein. Bone marrow examination revealed a small clonal B-cell population (5.8%) with a CLL-like immunophenotype. Despite the absence of peripheral lymphocytosis or established treatment indications for chronic lymphocytic leukemia (CLL), B-cell-directed therapy, including ibrutinib and venetoclax plus rituximab, was administered over the course of approximately one year based on the initial diagnostic impression, but failed to control hemolysis. Targeted next-generation sequencing identified a KMT2D frameshift mutation, supporting a diagnosis of CAD-LPD rather than monoclonal B-cell lymphocytosis. Subsequent treatment with the C1s inhibitor sutimlimab resulted in sustained resolution of hemolysis. This case highlights diagnostic pitfalls in CAD and underscores the value of molecular profiling in guiding appropriate therapy.

Quercetin is widely used in dietary supplements, yet its sub-acute organ safety profile in healthy organisms remains incompletely characterized. This study evaluated dose-dependent effects of intraperitoneal quercetin administration in healthy female Wistar rats (n = 6/group) receiving normal saline (control) or quercetin (5, 10, 20, or 30 mg/kg) every 72 h for 21 days. Endpoints included body and organ weights, serum biochemistry, hematology, systemic and tissue oxidative stress markers, and semi-quantitative multi-organ histopathology. Quercetin at ≥ 20 mg/kg significantly reduced percent weight gain (Dunn's test vs. control: p = 0.041 and p = 0.008, respectively) and increased liver, kidney, and spleen relative weight, with concurrent leukocytosis and lymphocytosis. Despite these changes, all serum hepatic, renal, and systemic oxidative stress markers were preserved across groups (Kruskal-Wallis, all p > 0.05). In contrast, liver and kidney tissue at ≥ 20 mg/kg showed elevated glutathione, superoxide dismutase, and catalase alongside reduced malondialdehyde. Histopathology revealed dose-related structural alterations in kidney, liver, and spleen at doses ≥ 20 mg/kg; cardiac changes were mild-to-moderate only at 30 mg/kg. Serum biomarkers consistently indicated preserved organ function despite concurrent tissue-level injury, demonstrating that conventional markers underestimate early structural damage. The co-occurrence of tissue antioxidant upregulation with histological lesions reflects a compensatory stress response consistent with hormesis. These findings underscore the value of integrating histopathological endpoints into preclinical safety evaluation of quercetin.

Richter transformation diffuse large B-cell lymphoma type (DLBCL-RT) is a biologically complex process that requires a comprehensive workup for an accurate diagnosis. Detailed information regarding DLBCL-RT immunophenotype is limited. We used multiparametric flow cytometry and immunohistochemistry to assess the phenotypic profile of 63 patients diagnosed with DLBCL-RT. Cases partially retained the immunophenotype of the previous chronic lymphocytic leukemia (CLL), although modulation of markers, such as CD43, CD5, CD200, CD23, and CD38, was common. Moreover, the phenotype of DLBCL-RT differed according to prior exposure or not to CLL therapy, with treatment-naïve patients showing more immunophenotypic variations against prior CLL compared with those who received therapy before transformation. With respect to the prognostic impact of antigenic markers, cases expressing CD20 exhibited higher overall survival compared with CD20-negative cases, whereas CD43 expression was associated with worse prognosis. DLBCL-RT cases exhibited several antigenic differences in CLL-associated markers compared with an independent cohort of nontransformed DLBCL without concurrent CLL-like monoclonal B-cell lymphocytosis (MBL) (n = 28). In contrast, a separate cohort of patients with de novo DLBCL and concomitant CLL-like MBL (n = 25) exhibited biological similarities to DLBCL-RT, including comparable phenotypic profiles and a high rate of clonal relatedness between MBL and DLBCL. We conclude that DLBCL-RT is associated with a CLL-like immunophenotype influenced by pre-existing CLL characteristics, and we propose that, in some cases, de novo DLBCL with concomitant MBL may be considered as RT.