The omentum is an important immune surveillance organ located in the abdominal cavity, especially noteworthy in diseases displaying tropism for the mononuclear phagocyte system, such as canine leishmaniosis (CanL). In this context, this study aimed to evaluate the immune-inflammatory response of the omentum in dogs naturally infected with Leishmania infantum through systemic inflammatory biomarkers and anatomopathological alterations. A total of 40 dogs were investigated, comprising 10 seronegative animals and 30 symptomatic seropositive dogs with CanL. Following clinical and laboratory evaluations, median celiotomy was performed and omental samples sent to histopathological analyses. Infected dogs displayed normocytic normochromic anemia, dysproteinemia, hypoalbuminemia, hyperglobulinemia, significant reductions in albumin-to-globulin ratios (AGR), and increased neutrophil-to-albumin ratios (NAR), with these as the main inflammatory biomarkers. Microscopically, chronic inflammatory infiltrates presenting a predominant lymphoplasmacytic pattern were observed, associated with hyperemia, fibrosis, and granulomas, in addition to the presence of amastigote Leishmania spp. forms within the macrophage cytoplasm. A strong association was observed between histological inflammation grade and inflammatory pattern, whereas erythrogram parameters showed progressive reductions with increasing inflammatory grades. The omentum is, thus, noted as actively participating in CanL immunopathogenesis, acting as a potential niche for parasite persistence and a complementary indicator of systemic disease severity, while AGR and NAR demonstrate potential diagnostic and prognostic value for the clinical monitoring of canine leishmaniosis.

Non-secretory multiple myeloma is an uncommon plasma cell neoplasm in which serum and urine electrophoresis and immunofixation fail to identify a measurable monoclonal component. This phenotype may delay diagnosis and make conventional biochemical monitoring difficult. We report three cases of clinically non-secretory multiple myeloma presenting with anemia and multifocal skeletal involvement despite negative monoclonal protein studies. Case 1 was a 33-year-old man with progressive fatigue, normocytic anemia, normal renal function and calcium levels, negative serum and urine monoclonal studies, and a normal serum free light chain ratio. Bone marrow aspiration showed 19% plasma cells, whereas bone marrow biopsy demonstrated extensive CD138-positive plasma cell infiltration; 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) revealed multifocal medullary lesions. Case 2 was a 63-year-old woman with low back pain and anemia, negative serum and urine immunofixation, and a normal serum free light chain ratio. Bone marrow aspiration showed 94% plasma cells, and 18F-FDG PET/CT demonstrated hypermetabolic skeletal lesions. She achieved partial remission after eight cycles of bortezomib, lenalidomide, and dexamethasone. Case 3 was a 68-year-old woman with fatigue, diffuse bone pain, anemia, negative serum and urine immunofixation, a normal serum free light chain ratio, 18% marrow plasma cells, and extensive PET/CT-positive skeletal disease. These cases emphasize that negative electrophoresis and immunofixation should not exclude multiple myeloma when the clinical, marrow, and imaging findings are suggestive. Bone marrow evaluation and whole-body imaging are central to diagnosis and follow-up in this rare entity.

VEXAS (Vacuoles, E1 enzyme, X-linked, Autoinflammatory, Somatic) syndrome is a recently established adult-onset autoinflammatory disorder caused by somatic mutations in the ubiquitin-activating enzyme 1 (UBA1) gene. The condition predominantly affects men in later stages of life and is characterised by recurrent systemic inflammation, fever, pulmonary involvement, dermatological manifestations, haematological abnormalities, and frequent corticosteroid dependence. Due to its heterogeneous clinical presentation, diagnosis can often be delayed, effectively resulting in significant morbidity and mortality. We report the case of a 78-year-old man who presented with recurrent episodes of high-grade fever, a widespread rash, pulmonary infiltrates, and repeated episodes initially diagnosed as periorbital cellulitis. Despite extensive investigations and multiple courses of antibiotics, no infective source was identified. The patient demonstrated recurrent inflammatory flares that responded to corticosteroids but relapsed during steroid tapering. Over the course of approximately one year, he developed progressive systemic inflammation, constitutional symptoms, pulmonary involvement, and normocytic normochromic anaemia. Following emerging recognition that macrocytosis may not be universally present in VEXAS syndrome, the diagnosis was considered and confirmed by bone marrow examination and genetic testing, demonstrating a pathogenic UBA1b mutation (p.Met41Val, c.121A>G). Unfortunately, the patient deteriorated rapidly and died before the diagnostic results became available. This case highlights the diagnostic challenges associated with VEXAS syndrome, particularly in patients lacking classical haematological features such as macrocytosis. Increased awareness of the expanding phenotypic spectrum of VEXAS syndrome is essential to facilitate earlier diagnosis and timely multidisciplinary management.

Pure red cell aplasia is a rare hematologic disorder characterized by severe normocytic anemia, reticulocytopenia, and absence of erythroid precursors. Since the COVID-19 pandemic, pure red cell aplasia has emerged as an uncommon post-infectious complication, likely driven by immune dysregulation. A 72-year-old man developed transfusion-dependent anemia several weeks after a mild COVID-19 infection. Laboratory evaluation revealed normocytic anemia (hemoglobin of 7.0 g/dL) with profound reticulocytopenia, and bone marrow biopsy showed markedly reduced erythropoiesis with preserved granulopoiesis and megakaryopoiesis. Secondary causes, including nutritional deficiencies, hemolysis, autoimmune disease, parvovirus B19, and hematologic malignancy, were excluded. The patient failed to respond to intravenous immunoglobulin, corticosteroids, and cyclosporine, achieving only a transient partial remission. Rituximab therapy was subsequently initiated and resulted in complete hematologic recovery and sustained remission at 1 year. COVID-19-associated pure red cell aplasia is a rare but clinically important complication. Clinicians should consider it in patients with severe post-COVID anemia, and rituximab may be effective in cases refractory to standard immunosuppressive therapy.

Background Anemia is a common and often underrecognized comorbidity in patients with hypothyroidism. Its etiology is multifactorial and is influenced by thyroid hormone deficiency, nutritional status, and concomitant chronic conditions. Understanding the prevalence, hematological patterns, and predictors of anemia in patients with hypothyroidism is necessary to improve clinical outcomes. This study aimed to assess the prevalence of anemia, describe its types and features, examine its association with thyroid hormone status, and identify the independent predictors of anemia in patients with hypothyroidism. Materials and methods A retrospective study was conducted in 444 patients diagnosed with hypothyroidism. Demographic, clinical, and laboratory data were extracted from the electronic medical records. Hematological indices were compared between the anemic and non‑anemic groups using independent t-tests and chi-square tests. Multivariate logistic regression was performed to identify the independent predictors of anemia after adjusting for age, sex, diabetes, and hypertension. Results Anemia was present in 112 (25.2%) patients. In anemic patients, the most common type was normocytic anemia, occurring in 64 (57.1%), followed by microcytic anemia in 46 (41.1%) and macrocytic anemia in two (1.8%). Patients with anemia had significantly higher platelet counts than those without anemia (p < 0.001). Markers of thyroid function (TSH, T3, and T4) did not differ significantly between the groups (p > 0.05). Multivariate analysis revealed that female sex (adjusted odds ratio (AOR) = 3.210, 95% confidence interval (CI): 1.323-7.789, p = 0.010) and the presence of chronic diseases (AOR = 3.458, 95% CI: 1.829-6.536, p < 0.001) were independent predictors of anemia. Conclusions One in four patients with hypothyroidism had anemia, and the most common type was normocytic anemia. No significant differences in thyroid hormone levels were observed between anemic and non-anemic patients. Female sex and chronic diseases were significant risk factors for anemia, emphasizing the importance of targeted screening and comprehensive evaluation of these subgroups. Early diagnosis and treatment of anemia may improve overall clinical outcomes in patients with hypothyroidism.

Thrombotic thrombocytopenic purpura (TTP) is a rare, life-threatening thrombotic microangiopathy caused by severe ADAMTS13 deficiency, usually due to autoantibody-mediated inhibition. Its presentation is heterogeneous and often lacks the classic pentad, leading to diagnostic delays. Neurological symptoms may predominate, masking the underlying hematologic emergency. In our case, a 37-year-old previously healthy woman presented with acute headache, speech disturbance, and altered mental status. Despite normal neuroimaging, laboratory tests revealed severe thrombocytopenia and normocytic anemia. Lack of response to erythrocyte and platelet transfusions prompted further evaluation, revealing microangiopathic hemolytic anemia with elevated lactate dehydrogenase, undetectable haptoglobin, indirect hyperbilirubinemia, reticulocytosis, and normal coagulation parameters. A PLASMIC score of 6/7 indicated a high probability of severe ADAMTS13 deficiency. Treatment with high-dose corticosteroids was initiated immediately, followed by plasma exchange and rituximab. ADAMTS13 activity confirmed severe deficiency at 0.3%, supporting the diagnosis of acquired TTP in the clinical context. The patient achieved rapid remission and complete neurological recovery. This case highlights the importance of early recognition of microangiopathic hemolysis and prompt treatment without waiting for confirmatory ADAMTS13 results to reduce morbidity and mortality.

An 84-year-old man with rheumatoid arthritis undergoing treatment with methotrexate presented with fever, general fatigue, and appetite loss. He had a 3-month history of unexplained normocytic anaemia with reticulocytopenia. Bone marrow examination revealed erythroid hypoplasia with giant pro-erythroblasts, leading to a diagnosis of parvovirus B19 infection. In this case, intravenous immunoglobulin therapy improved the patient's anaemia and systemic symptoms. Six months after the treatment, parvovirus B19 DNA remained detectable using polymerase chain reaction; however, the viral load had markedly decreased, indicating a favourable virological response. Twenty cases of parvovirus B19 infection in older adults (aged ≥65 years) were identified in the literature. Immunocompromised older patients frequently develop persistent parvovirus B19 infections that require treatment with intravenous immunoglobulin therapy, whereas persistent infections are not observed in immunocompetent older individuals. Therefore, this case suggests that clinicians should be aware of persistent parvovirus B19 infection in older immunosuppressed patients who develop unexplained anaemia with reticulocytopenia. Moreover, intravenous immunoglobulin therapy may be considered as an effective therapeutic option for persistent parvovirus B19 infection in immunocompromised patients.

Lymphoplasmacytic lymphoma (LPL) and multiple myeloma (MM) are distinct B-cell neoplasms whose synchronous occurrence is extremely rare. We report a case of a 68-year-old man presenting with fatigue and bone pain. Laboratory studies showed hyperglobulinemia (71.1 g/L), severe normocytic anemia (hemoglobin 44 g/L, MCV 79.5 fL), and thrombocytopenia. Serum immunofixation revealed dual IgG-kappa and IgM-kappa monoclonal proteins. Imaging showed diffuse osteolytic lesions in the skull and spine. Bone marrow flow cytometry identified two immunophenotypically distinct populations: CD19+/CD20+/CD5-/CD10- B-cells (34.1%) and CD138+/CD38+/cytoplasmic kappa+ plasma cells (4.5%). Next-generation sequencing on unsorted whole bone marrow detected MYD88 c.779T>C (p.Leu260Pro, canonical L265P) with a variant allele frequency (VAF) of 40.00% and CXCR4 c.1013C>G (p.Ser338*) nonsense mutation with VAF 15.53%, confirming LPL. Although the clonal plasma cell percentage was below the traditional 10% threshold, the presence of unequivocal osteolytic lesions and severe anemia (CRAB criteria) supported a diagnosis of active MM. The patient was treated with zanubrutinib, bortezomib, and dexamethasone, achieving a partial response. This case strongly suggests that LPL and MM can coexist, but definitive proof of biclonality would require sorted-cell molecular studies. We highlight the diagnostic challenges and the importance of integrating clinical, immunophenotypic, and molecular data.

Gastric antral vascular ectasia (GAVE) is an under-recognised cause of chronic gastrointestinal blood loss and iron-deficiency anaemia, caused by dilated antral vessels that cause chronic gastrointestinal bleeding, gradually depleting iron stores and leading to reduced haemoglobin levels. Its presentation is often subtle and may occur without overt gastrointestinal bleeding. We report an 82-year-old patient admitted following an unwitnessed fall, associated with postural hypotension and normocytic anaemia (Hb 90 g/L). Oesophagogastroduodenoscopy (OGD) demonstrated linear GAVE in the gastric antrum without active bleeding. The patient also sustained a fragility pelvic fracture. Intravenous iron therapy was administered to correct severe iron deficiency, resulting in improved haemoglobin levels and resolution of underlying clinical symptoms. This case highlights an important and often under-recognised presentation of GAVE, in which anaemia manifests predominantly through falls or orthostatic features rather than gastrointestinal symptoms. Early recognition of this pattern is crucial, as targeted treatment may reduce the risk of recurrent falls, fractures, and subsequent functional decline in older adults.