Background: Patients with hematological malignancies have an increased risk of arterial thrombotic events (ATEs) after diagnosis, compared to matched controls without cancer. However, data about incidence and risk factors for ATE development in patients with acute myeloid leukemia (AML) are missing. Aim: The objectives of this study were to determine the incidence of ATE in non-promyelocytic-AML patients and to define the potential risk factors for ATE development. Methods: We conducted a retrospective cohort study of adult patients with newly diagnosed AML. The primary outcome was the occurrence of confirmed ATE, defined as myocardial infarction, stroke or critical limb ischemia. Results: Out of 626 eligible AML patients, 18 (2.9%) patients developed ATE in the median time of 3 (range: 0.23–6) months. Half of these patients died due to ATE complications. Five parameters were predictors of ATE: BMI > 30 (p = 0.000, odds ratio [OR] 20.488, 95% CI: 6.581–63.780), prior history of TE (p = 0.041, OR 4.233, 95% CI: 1.329–13.486), presence of comorbidities (p = 0.027, OR 5.318, 95% CI: 1.212–23.342), presence of cardiovascular comorbidities (p < 0.0001, OR 8.0168, 95% CI: 2.948–21.800) and cytogenetic risk score (p = 0.002, OR 2.113, 95% CI: 1.092–5.007). Conclusions: Our study showed that patients with AML are at increased risk of ATE. The risk was increased in patients with cardiovascular comorbidities, previous thrombosis, adverse cytogenetic risk as well as BMI > 30.

Autoimmune hemolytic anemia (AIHA) is a rare, very heterogeneous, and sometimes life-threatening acquired hematologic disease characterized by increased red blood cell (RBC) destruction by autoantibodies (autoAbs), either with or without complement involvement. Recent studies have shown that the involvement of T- and B-cell dysregulation and an imbalance of T-helper 2 (Th2) and Th17 phenotypes play major roles in the pathogenesis of AIHA. AIHA can be primary (idiopathic) but is more often secondary, triggered by infections or drug use or as a part of other diseases. As the location of origin of autoAbs and the location of autoAb-mediated RBC clearance, as well as the location of extramedullary hematopoiesis, the spleen is crucially involved in all the steps of AIHA pathobiology. Splenectomy, which was the established second-line therapeutic option in corticosteroid-resistant AIHA patients for decades, has become less common due to increasing knowledge of immunopathogenesis and the introduction of targeted therapy. This article provides a comprehensive overview of current knowledge regarding the place of the spleen in the immunological background of AIHA and the rapidly growing spectrum of novel therapeutic approaches. Furthermore, this review emphasizes the still-existing expediency of laparoscopic splenectomy with appropriate perioperative thromboprophylaxis and the prevention of infection as a safe and reliable therapeutic option in the context of the limited availability of rituximab and other novel therapies.

Introduction: Coronavirus disease 2019 (COVID-19) vaccines are considered to be safe. Only few cases of vaccine-induced immune thrombocytopenia or immune hemolysis have been reported so far. Evans syndrome (ES) is a very rare syndrome characterized mainly by warm autoimmune hemolytic anemia (wAIHA) and immune thrombocytopenia (ITP). Case presentation: We present a case of a 47‐year‐old male with a history of wAIHA, diagnosed in 1995 and successfully treated with glucocorticoids, with sustained remission. ITP was diagnosed in May 2016. Due to refractoriness to glucocorticoids, intravenous immunoglobulins (IVIGs), azathioprine and vinblastine, he was splenectomised in April 2017, resulting in complete remission. In May 2021, eight days after the second dose of BNT162b2 (Pfizer-BioNTech) COVID-19 vaccine, he experienced mucocutaneous bleeding. Blood tests showed platelet count (PC) of 8×109/L, while his hemoglobin (Hb) was normal (153 g/L). He was treated with prednisone and azathioprine, without response. On day 28 after vaccine administration, weakness, jaundice and dark brown urine occurred. His laboratory tests: PC 27×109/L, Hb 45 g/L, reticulocytes 10.4%, total bilirubin 106.6 μmol/L, direct bilirubin 19.8 μmol/L, lactate dehydrogenase 633 U/L, haptoglobin ˂0.08 g/L, and positive Coombs test were consistent with ES relapse. After treatment with glucocorticoids, azathioprine and IVIGs, his blood count finally improved (PC 490×109/L, Hb 109 g/L) and remained stable on day 40 of hospitalization. Conclusions: Although it is unclear whether the relationship between COVID-19 vaccination and relapse of ES in our patient is coincidental or causal, it highlights the need for monitoring of serious outcomes following vaccination.

Standard ELN risk stratification for thrombosis and overall survival (OS) in patients with polycythemia vera (PV) is based on advanced age and history of thrombosis. Recently, the triple A (AAA) risk model was developed for OS prediction in patients with essential thrombocythemia, which, besides rising age, incorporates high (≥8x10⁹/L) absolute neutrophil and low(<1.7 × 10⁹/L) lymphocyte counts. The presented multicenter international study on a large cohort of PV patients validated the findings from prior reports and demonstrated excellent prognostic properties of the triple A model with respect to both thrombosis and survival in PV. Moreover, it revealed that the addition of patient comorbidities (assessed through the Charlson comorbidity index (CCI)) to ELN and triple A score may not help to further refine the survival prognostication of these patients. Therefore, the triple A score with its simplicity seems to offer excellent balance during the initial risk assessment in PV, implicating its global applicability.