Aplastic anemia (AA) and paroxysmal nocturnal hemoglobinuria (PNH) are closely related bone marrow (BM) failure syndromes linked by shared immunological mechanisms. The frequent emergence of PNH-type blood cells during AA, together with the co-occurrence of the disorders and their overlapping therapeutic responses, supports the concept that they represent a spectrum of immune-mediated hematopoietic injury rather than distinct disease entities.AA is a prototypical immune-mediated BM failure characterized by cytotoxic T-cell-driven suppression of hematopoietic stem and progenitor cells. Within this immune-hostile environment, glycosylphosphatidylinositol (GPI)-anchor-deficient PNH clones commonly emerge and persist, a phenomenon best explained by immune selection rather than intrinsic proliferative advantage. Although most PNH clones detected in AA remain small and clinically silent, their presence reflects ongoing or past immune pressure within the BM microenvironment.Advances in high-sensitivity flow cytometry have revealed that minor PNH populations are frequent in AA, indicating that immune-driven clonal selection occurs at an early stage of hematopoiesis. Longitudinal studies further demonstrate that clonal dynamics parallel changes in immune activity, supporting their relevance for risk-adapted monitoring.In this review, we highlight immune-mediated BM failure as the common soil from which PNH clones arise and discuss implications for diagnosis, monitoring, and phenotype-driven management.

A 34-year-old previously healthy woman presented with right-sided, pleuritic chest pain three weeks after a viral respiratory infection. Labs revealed hemoglobin of 10.2 g/dL (nadir 7.0), platelets of 109 × 109/L, LDH of 1129 U/L (Ref: 122-222 U/L), undetectable haptoglobin, indirect hyperbilirubinemia, and elevated reticulocytes. Troponins were elevated. CRP was 184 mg/L (Ref: ≤ 5 mg/L). Peripheral smear was without schistocytes. Direct antiglobulin testing was negative. Urinalysis showed microscopic hematuria and positive hemosiderin. Echocardiogram revealed normal left ventricular (LV) function with left lateral wall hypokinesis and a 2.5 × 3 cm LV thrombus. Cardiac MRI was concerning for myopericarditis and new right ventricular (RV) thrombus, later verified by biopsy. There was also an infarction of the RV endomyocardium. Anticoagulation was initiated. Bone marrow biopsy showed erythroid hyperplasia without clonal myeloid features. Flow cytometry showed 57% CD59 deficient red blood cells, 88% CD157 deficient monocytes, and 91% CD157 deficient neutrophils, consistent with a new diagnosis of paroxysmal nocturnal hemoglobinuria (PNH). She was urgently vaccinated against encapsulated organisms, treated with eculizumab, and given antibacterial prophylaxis. Follow-up imaging showed near resolution of thrombi; hemoglobin and hemolysis markers normalized. PNH is a clonal hematopoietic disorder causing complement-mediated hemolysis and thrombosis. While thrombosis typically affects atypical venous sites, intracardiac thrombi are rare. PNH was the patient's only identified prothrombotic factor. This is the first reported case of intracardiac thrombosis in a previously healthy patient with new-onset PNH. Early recognition and complement inhibition are critical to reduce hemolysis, thrombosis, and mortality in PNH.

Patients with paroxysmal nocturnal hemoglobinuria (PNH) on anti-C5 often experience extravascular hemolysis with anemia. Iptacopan, the first oral proximal complement inhibitor targeting factor B, has shown efficacy and safety in PNH patients. APPULSE-PNH (NCT05630001), a phase 3b, single‑arm, open-label trial, enrolled adult patients with PNH and hemoglobin ≥10 g/dL on stable anti-C5 for ≥6 months. Patients switched to iptacopan monotherapy (200 mg twice daily; 24 weeks). Primary endpoint: mean hemoglobin change from baseline across four visits (Days 126-168). At baseline, 57.7% of patients had elevated absolute reticulocyte counts (ARCs; above ULN = 123 × 109/L) and 50% had C3 deposition on red blood cells (RBCs) >10%, indicative of extravascular hemolysis. There was a statistically significant increase in hemoglobin during the trial; adjusted mean change from baseline (95% CI) was +2.0 g/dL (1.7-2.3) overall, and in patients with baseline hemoglobin <12 g/dL and ≥12 g/dL, +2.4 (2.0-2.7) and +1.4 (1.0-1.8), respectively. Patients maintained transfusion independence, 92.7% with hemoglobin ≥12 g/dL. Adjusted mean change from baseline (95% CI) in lactate dehydrogenase and ARC were -1.3% (-6.6 to 4.3) and -89.2 × 109/L (-95.5 to -82.9), respectively. Mean (SD) proportion of C3d+ PNH RBCs, assessed by flow cytometry, decreased from 11.0% (8.6) to 0.2% (0.7) at Day 168. No patients had breakthrough hemolysis or major adverse vascular events. FACIT-Fatigue and treatment satisfaction scores improved by Days 84 and 168. Safety showed consistency with previous iptacopan PNH trials. Iptacopan improved hematologic outcomes in PNH patients with hemoglobin ≥10 g/dL on anti-C5, maintaining control of intravascular hemolysis and resolving extravascular hemolysis.

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.

Paroxysmal nocturnal hemoglobinuria (PNH) is a clonal hematopoietic stem cell disease characterized by hemolytic anemia, bone marrow failure, and thrombosis. Some PNH patients carrying the C5 mutation (Arg885) show poor response to eculizumab and ravulizumab.

This report presents the case of a 60-year-old woman who was admitted with symptoms of fatigue and poor appetite. Laboratory investigations revealed severe acute kidney injury (AKI), indicated by a serum creatinine level of 2,065 μmol/L, necessitating the initiation of emergency hemodialysis. The patient also exhibited hemolytic anemia (hemoglobin, 69 g/L), thrombocytopenia (platelet nadir, 45 × 10[9]/L), venous thrombosis, a positive direct antiglobulin test (DAT), and a low absolute reticulocyte count. Conventional flow cytometry (red blood cells and neutrophils CD55/CD59) did not detect a paroxysmal nocturnal hemoglobinuria (PNH) clone. Renal biopsy revealed hemoglobin cast nephropathy and intrarenal venous thrombosis. Subsequent bone marrow evaluation, high-sensitivity flow cytometry (FLAER method), and supportive PIGA sequencing findings established the diagnosis of PNH. Treatment with eculizumab led to hematologic remission and progressive renal recovery. This case underscores the importance of considering PNH in patients with severe AKI and hemolysis, even when initial conventional flow cytometry is negative.

Bovine hemoplasmas, including Mycoplasma wenyonii (M. wenyonii) and Candidatus Mycoplasma haemobos (C. M. haemobos), are vector-borne pathogens that can cause significant clinical diseases in cattle. This case report from Türkiye describes the clinical findings, hematological analysis, and serum biochemistry results of a cow presenting with hemoglobinuria caused by C. M. haemobos. Blood samples from the infected animal were analyzed using hematological, biochemical, microscopic, and molecular methods. Multiplex polymerase chain reaction assay confirmed the infection, and microscopic analysis revealed a parasitemia rate of 6.99%. Clinical signs included hemoglobinuria, icterus, and anemia. The treatment included fluid therapy, antibiotic (oxytetracycline), and antianemic drugs. The cattle died 1 month post-treatment, reportedly due to a lower respiratory tract infection. This case report describes the diagnostic methods, clinical findings, and laboratory results. A widescale molecular survey of C. M. haemobos in cattle is warranted, with investigation of its pathogenicity and pathogenies.