Circulating extracellular vesicles and cytokines in congenital and acquired hemolytic anemias

Barcellini, Wilma; Zaninoni, Anna; Giannotta, Juri Alessandro; Merati, Giuliana; Capecchi, Marco; Fattizzo, Bruno; Trombetta, Elena; Artoni, Andrea

doi:10.1002/ajh.26108

Cited by 4 publications

(3 citation statements)

References 8 publications

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“…Thus, it may be hypothesized that augmented red cell mass and nitric oxide depletion during intravascular hemolysis both contribute to the thrombotic process. Additionally, a recent study demonstrated an increased level of erythrocyte derived microparticles in hyper‐hemolytic AIHA, particularly after splenectomy 19 . Such microparticles are enriched in procoagulant mediators and phosphatidyl serine and may further favor thrombotic episodes 20 .…”

Section: Discussionmentioning

confidence: 99%

“…Death AIHA-related, N (%) ticles in hyper-hemolytic AIHA, particularly after splenectomy. 19 Such microparticles are enriched in procoagulant mediators and phosphatidyl serine and may further favor thrombotic episodes. 20 Although splenectomy is a recognized risk factor for thrombosis in various conditions, [21][22][23][24][25] here we found only a slightly higher frequency of thrombosis in splenectomized patients.…”

Section: Complications and Outcomementioning

confidence: 99%

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Intravascular hemolysis and multitreatment predict thrombosis in patients with autoimmune hemolytic anemia

Fattizzo

Bortolotti

Giannotta

et al. 2022

Journal of Thrombosis and Haemostasis

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Background Thrombosis may complicate autoimmune hemolytic anemia (AIHA), but its predictors are still lacking, and no clear‐cut indications for anticoagulant prophylaxis are available. Objectives To characterize frequency and severity of thromboses in AIHA patients and identify risk factors for thrombosis that may advise primary anticoagulant prophylaxis. Patients/Methods A total of 287 consecutive AIHA patients diagnosed and followed from 1978 at a tertiary Italian center were retrospectively studied; 174 of them were prospectively evaluated from January 2020 until December 2021. AIHA relapse, thrombosis occurrence, and primary anticoagulant prophylaxis were evaluated. Results Thirty‐three AIHA patients (11.4%) experienced thrombosis, 70% of whom hospitalized. The cumulative thrombosis incidence was higher in patients with lactate dehydrogenase (LDH) ≥ 1.5 (hazard ratio [HR] 3.22), in those experiencing infections (HR 3.57), receiving transfusions (HR 3.06), rituximab (HR 3.3), or cyclophosphamide (HR 2.67). By multivariable analysis, LDH, transfusions, rituximab, and cyclophosphamide treatment emerged as independent factors associated with thrombosis. Among 174 patients prospectively followed in the past 2 years, we observed 70 acute hemolytic episodes in 45 patients; 33/45 displayed LDH ≥1.5 × upper limit of normal, and 17 received anticoagulant prophylaxis with low molecular weight heparin for a median of 70 days (30–300). In those receiving prophylaxis no thrombotic complications occurred, whereas five thrombotic episodes were registered in the remaining 16 cases. Conclusions Thrombosis was observed in about 11% of AIHA patients, mainly grade 3, and associated with intravascular hemolysis, need of transfusions, multitreatment, and infections, advising primary anticoagulant prophylaxis in these settings.

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Section: Discussionmentioning

confidence: 99%

Section: Complications and Outcomementioning

confidence: 99%

Intravascular hemolysis and multitreatment predict thrombosis in patients with autoimmune hemolytic anemia

Fattizzo

Bortolotti

Giannotta

et al. 2022

Journal of Thrombosis and Haemostasis

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“…Importantly, RBCEV have been demonstrated to very efficiently transfer mRNA into target cells [ 73 ]. Elevated levels of RBCEV have been also found in CAD patients; moreover, it correlated with the severity of anemia and hemolytic features [ 74 ].…”

Section: Discussionmentioning

confidence: 99%

Gene expression analysis revealed downregulation of complement receptor 1 in clonal B cells in cold agglutinin disease

Małecka,

Østlie,

Trøen

et al. 2023

Clinical and Experimental Immunology

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Cold Agglutinin Disease (CAD) is a rare B-cell lymphoproliferative disorder of the bone marrow, manifested by autoimmune hemolytic anemia caused by binding of monoclonal IgM autoantibodies to the I antigen. Underlying genetic changes have previously been reported, but their impact on gene expression profile has been unknown. Here, we define differentially expressed genes in CAD B cells. To unravel downstream alteration in cellular pathways, gene expression by RNA sequencing was undertaken. Clonal B-cell samples from twelve CAD patients and IgM-expressing memory B cells from four healthy individuals were analyzed. Differential expression analysis and filtering resulted in 93 genes with significant differential expression. Top upregulated genes included SLC4A1, SPTA1, YBX3, TESC, HBD, AHSP, TRAF1, HBA2, RHAG, CA1, SPTB, IL10, UBASH3B, ALAS2, HBA1, CRYM, RGCC, KANK2 and IGHV4-34. They were upregulated at least 8-fold, while complement receptor 1 (CR1/CD35) was downregulated 11-fold in clonal CAD B cells compared to control B cells. Flow cytometry analyses further confirmed reduced CR1 (CD35) protein expression by clonal CAD IgM+ B cells compared to IgM+ memory B cells in controls. CR1 (CD35) is an important negative regulator of B-cell activation and differentiation. Therefore, reduced CR1 (CD35) expression may increase activation, proliferation, and antibody production in CAD-associated clonal B cells.

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It takes two to thrombosis: Hemolysis and complement

Delvasto-Núñez

Jongerius

2021

Blood Reviews

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Circulating extracellular vesicles and cytokines in congenital and acquired hemolytic anemias

Cited by 4 publications

References 8 publications

Intravascular hemolysis and multitreatment predict thrombosis in patients with autoimmune hemolytic anemia

Intravascular hemolysis and multitreatment predict thrombosis in patients with autoimmune hemolytic anemia

Gene expression analysis revealed downregulation of complement receptor 1 in clonal B cells in cold agglutinin disease

It takes two to thrombosis: Hemolysis and complement

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