hemoglobinuria/inflammation

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Neutrophil activation and nucleosomes as markers of systemic inflammation in paroxysmal nocturnal hemoglobinuria: effects of eculizumab.

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BACKGROUND Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by complement-mediated hemolysis and a high risk of life-threatening venous and arterial thrombosis. Uncontrolled complement activation and the release of cell-free heme may result in systemic inflammation, neutrophil activation,

Migration to an inflammatory site in vivo of paroxysmal nocturnal hemoglobinuria lymphocytes.

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Thrombosis in patients with paroxysmal nocturnal hemoglobinuria.

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Paroxysmal nocturnal hemoglobinuria is a disorder associated with hemolysis, pancytopenia, and thrombosis due to the loss of the glycosylphosphatidylinositol (GPI) anchored complement regulatory proteins. The mechanism of thrombosis is multifactorial. Although intravascular hemolysis has been

Intestinal perforation in temporal arteritis, associated with paroxysmal nocturnal hemoglobinuria.

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Temporal arteritis (TA) is an adult-onset, focal granulomatous inflammatory disorder of the small and medium sized arteries. Intestinal perforation is a rare complication of TA. Regarding its etiology, steroid-induced or arteritis-induced ulceration have been proposed. We describe a patient who

Paroxysmal nocturnal hemoglobinuria (PNH) and primary p.Cys89Tyr mutation in CD59: Differences and similarities.

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CD59 encodes a 77 amino acid glycosylphosphatidylinositol (GPI)-anchored cell surface glycoprotein that inhibits the final step of membrane attack complex (MAC) formation. CD59 deficiency is a common finding in adult patients with paroxysmal nocturnal hemoglobinuria (PNH). In this condition, there

Mechanism of feedback regulation of neutrophil inflammation in Henoch-Schönlein purpura.

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The aim of this study is to investigate the role of complement-neutrophil feedback regulation of inflammatory response in Henoch-Schönlein purpura (HSP) through constructing an animal model of HSP. Twenty-four SPF grade Japanese large-eared white rabbits were randomly divided into normal group and

Atypical presentation of paroxysmal nocturnal hemoglobinuria treated by eculizumab: A case report.

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Paroxysmal nocturnal hemoglobinuria (PNH) is a nonmalignant acquired hematopoietic stem cell disease, which can be revealed by hemolytic anemia, thromboembolism, or bonemarrow failure. Thrombosis can occur at any site, but coronary thrombosis is extremely rare. Controlled trials have demonstrated

Engulfment of Hb-activated platelets differentiates monocytes into pro-inflammatory macrophages in PNH patients.

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The distinct response shown by different phenotypes of macrophages and monocytes under various clinical conditions has put the heterogeneity of these cells into focus of investigation for several diseases. Recently, we have described that after engulfing hemoglobin (Hb)-activated platelets,

Eculizumab Dosing Intervals Longer than 17 Days May Be Associated with Greater Risk of Breakthrough Hemolysis in Patients with Paroxysmal Nocturnal Hemoglobinuria.

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Eculizumab given bi-weekly is widely recommended for the treatment of paroxysmal nocturnal hemoglobinuria (PNH). We undertook a retrospective analysis on the medical records of 763 dosings of 14 PNH patients to investigate whether a threshold would exist in dosing intervals associated with

Paroxysmal Nocturnal Hemoglobinuria: Diagnostic Challenges in Pediatric Patient.

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Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, life-threatening hematologic stem cell disorder characterized by hemoglobinuria, thrombosis, and tendency for bone marrow failure. The rare incidence of PNH in children, its nonspecific clinical presentation, and occasional absence of

Hemolytic reaction in the washed salvaged blood of a patient with paroxysmal nocturnal hemoglobinuria.

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In patients with paroxysmal nocturnal hemoglobinuria (PNH), the membrane-attack complex (MAC) formed on red blood cells (RBCs) causes hemolysis due to the patient's own activated complement system by an infection, inflammation, or surgical stress. The efficacy of transfusion therapy

A Prospective Multicenter Study of Paroxysmal Nocturnal Hemoglobinuria Cells in Patients with Bone Marrow Failure.

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Background: Paroxysmal nocturnal hemoglobinuria (PNH), a rare clonal hematopoietic stem cell disorder, is characterized by chronic, uncontrolled complement activation leading to intravascular hemolysis and an inflammatory prothrombotic state. The EXPLORE study aimed to determine the prevalence of

Eculizumab therapy results in rapid and sustained decreases in markers of thrombin generation and inflammation in patients with PNH independent of its effects on hemolysis and microparticle formation.

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Paroxysmal Nocturnal Hemoglobinuria (PNH) is a clonal bone marrow disorder which results in the loss of glycosylphosphatidyl inositol (GPI) anchors from cell membranes. As a consequence, membrane inhibitors of complement are lost rendering the cells more susceptible to complement mediated

Development of pro-inflammatory phenotype in monocytes after engulfing Hb-activated platelets in hemolytic disorders.

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Monocytes and macrophage combat infections and maintain homeostatic balance by engulfing microbes and apoptotic cells, and releasing inflammatory cytokines. Studies have described that these cells develop anti-inflammatory properties upon recycling the free-hemoglobin (Hb) in hemolytic conditions.

Recurrent and progressive abdominal pain and enteritis in a Japanese patient with paroxysmal nocturnal hemoglobinuria.

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This case report describes a young male patient with recurrent abdominal pain persisting for more than 16 months. Clinical investigations showed signs of inflammation and pancytopenia. A diagnosis of paroxysmal nocturnal hemoglobinuria (PNH) was made 9 months after the onset of the abdominal pain,

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