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 work-up 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 to those who received therapy before transformation. With respect to the prognostic impact of antigenic markers, cases expressing CD20 exhibited higher overall survival compared to those CD20-negative, 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 non-transformed 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.

Adult T-cell leukemia/lymphoma (ATLL) is an aggressive lymphoma with a poor prognosis. The human T-lymphotropic virus 1 (HTLV-1) is associated with immunodeficiency and increased extranodal involvement in patients with diffuse large B-cell lymphoma (DLBCL). We report on a 47-year-old woman with spastic paraparesis and hepatitis B who was diagnosed with the acute form of ATLL. The clinical picture reveals peripheral generalized lymphadenopathy and splenomegaly. Findings on a hematologic exam indicated leukocytosis with lymphocytosis. A bone marrow biopsy/aspiration confirmed 50% T-cell lymphoid infiltration. Biochemistry results revealed hypercalcemia and a high lactate dehydrogenase value. Results of a CT scan indicated abdominal and thoracic adenopathy as well as moderate splenomegaly. A supraclavicular lymph node biopsy established a DLBCL diagnosis. The final diagnosis was composite lymphoma, DLBCL, and ATLL. The CHOP (cyclophosphamide, doxorubicin hydrochloride, vincristine sulfate [Oncovin], and prednisone) regimen was chosen due to the patient's ECOG performance status. Multiple infectious complications were diagnosed during chemotherapy-induced secondary aplasia. A complete remission, confirmed via PET-CT imaging, was obtained. After 1 month, a skin tumor on the upper right thigh was discovered and biopsied, and the histopathological exam and immunochemistry findings indicated Epstein-Barr virus-DLBCL lymphoma. The association of 2 aggressive lymphomas in a single HTLV-1 carrier is a rare report, and the evolution was severe, complicated by opportunistic infections, and unfavorable.

Autoimmune gastritis (AIG) is a chronic immune-mediated disease with potential for serious clinical consequences, yet early identification remains challenging. We aimed to assess whether deep oxyntic gland intraepithelial CD3+ T lymphocytosis may serve as a predictive histological marker of progression from potential -i.e., parietal cell antibody (PCA)-positive patients without baseline gastric atrophy- to overt AIG.

B-cell prolymphocytic leukemia (B-PLL) is a rare B-cell neoplasm that presents splenomegaly, lymphocytosis, minimal or absent lymphoadenopathy, at least 55% of prolymphocytes in peripheral blood and a variable clinical course. Complex/composite karyotype and recurrent structural variants (SVs), including TP53 aberrations (mutations/deletion) and MYC abnormalities (translocation or gain) are genetic features typically seen in B-PLL. We applied the genome-wide technology of optical genome mapping (OGM) in 3 cases with B-PLL, finding multiple genomic aberrations, including SVs, copy number variations (CNVs) and aneuploidies. MYC aberrations were not observed in our cases, whereas all B-PLL showed concomitant deletion 17p and TP53 mutations. TP53-disrupted B-PLL cells showed additional genomic alterations that affect genes implicated in extrinsic and intrinsic apoptotic pathways i.e., TNFRSF10, FAS, MDM2, BCL2, and BCL2L11 and genes involved in cell-cycle regulation i.e., IKBKB, CDK2, CDK4, and RB1, suggesting that a convergent multifactorial pathogenetic mechanism may be involved in B-PLL. Applying the OGM technology on cytogenetically complex rare hematological neoplasia may be useful to improve the genetic definition and differential diagnosis of B PLL/SBLPN and related splenic B cell neoplasms.

Atraumatic splenic rupture is an uncommon but life-threatening complication of Epstein-Barr virus (EBV) infection. While infectious mononucleosis classically presents with fever, pharyngitis, and lymphadenopathy, we recorded a spontaneous splenic rupture even in the absence of these symptoms. We report a case of a 26-year-old male presenting to the emergency department with syncope. A progressive clinical hemodynamic deterioration was detected, ending hemorrhagic shock. Imaging revealed an atraumatic grade V splenic injury and massive hemoperitoneum. Laboratory tests showed lymphocytosis, prompting EBV serology, which confirmed acute mononucleosis infection. Due to hemodynamic instability, the patient underwent splenectomy with uneventful recovery. This case highlights that EBV-related splenic rupture may represent the only manifestation of infection in otherwise asymptomatic individuals. Clinicians should maintain a high index of suspicion for EBV infection in patients presenting with unexplained atraumatic splenic rupture. Early diagnosis and timely management are crucial to reduce the risk of potentially life-threatening complications.

A man in his early 30s presented with fever, widespread pruritic rash and deranged liver function tests shortly after returning from a religious pilgrimage. Initial assessment focused on infectious and travel-related causes given recent international travel. Investigations revealed marked eosinophilia, lymphocytosis and a mixed hepatocellular-cholestatic liver injury. Extensive viral, parasitic and autoimmune testing was negative. Despite partial symptomatic improvement following cessation of recently initiated allopurinol, the patient developed progressive eosinophilia and new lymphadenopathy. Multidisciplinary review supported a diagnosis of drug reaction with eosinophilia and systemic symptoms (DRESS), with allopurinol identified as the most likely culprit. Oral corticosteroid therapy led to rapid clinical and biochemical improvement, with normalisation of eosinophil count and liver function prior to discharge. This case highlights the diagnostic challenge of drug hypersensitivity reactions in the context of recent travel and emphasises the importance of early medication review in patients presenting with fever, rash and organ dysfunction.

Yersiniosis is worldwide diffused and, among the different species, infection of Yersinia enterocolitica is responsible of the most cases both in humans and animals. Although it causes, often self-limiting, mild enteritis, severe manifestations could occur and can cause sepsis. The study reports a case of Y. enterocolitica infection in a juvenile female loggerhead sea turtle (Caretta caretta) recovered at the Regional Rescue Sea Turtle Centre in south Italy. The turtle was in poor body condition, dehydrated and emaciated. Complete blood count showed severe anaemia and lymphocytosis. Despite supportive therapies, the sea turtle died a few days after hospitalization. During necropsy, the dilatation of the colon, adhesions and liver lesions were detected as gross pathologic findings. Histologic assay was carried out for the liver showing granulomas with acellular central areas surrounded by fibrous capsules. Unfortunately, the cause of death is still unknown, but it could be hypothesized that the strain of Y. enterocolitica could have caused a colitis and hepatitis. This is the first report of Y. enterocolitica infection in a Caretta caretta, and it updates both the current literature on sea turtle diseases and protocols for their management and rehabilitation.

Mycosis fungoides (MF) is a rare extranodal T-cell lymphoma with primary cutaneous involvement. While it is the most common primary skin lymphoma, large-scale real-world data defining survival benchmarks and the prognostic significance of specific nodal sites remain limited. To address this, we conducted a retrospective cohort study using the TriNetX global health research network and identified 25 467 patients with MF. The 5- and 10-year OS for the overall cohort was 83.4% and 74.7%, respectively. Patients with disease limited to the skin had 5- and 10-year OS rates of 86.1% and 78.0%, respectively. Nodal involvement at diagnosis was associated with significantly inferior survival [adjusted HR (aHR) = 1.60; 95% CI: 1.50-1.71; p < 0.001], exhibiting 5- and 10-year OS rates of 74.5% and 63.6%, respectively. Among patients with single-site lymphadenopathy, survival outcomes varied substantially by anatomical site, revealing a potential prognostic hierarchy: patients with inguinal/lower limb involvement exhibited the most favorable outcomes (5-year OS 80.2%), while those with visceral lymphadenopathy had the poorest prognosis (5-year OS 62.9%). In multivariable analysis, elevated LDH (aHR 3.06), lymphocytosis (aHR 1.37), and eosinophilia (aHR 1.29) were strong independent predictors of mortality, among others. To summarize, this study of over 25 000 MF patients represents the largest real-world analysis to date. Data suggest a potential prognostic divergence based on the anatomical site of nodal involvement. Additionally, our findings reinforce the prognostic value of LDH, eosinophils, lymphocytes and the hypopigmented and poikilodermatous variants as independent predictors of mortality, supporting their integration into routine risk stratification.