hemoglobinuria/necroză

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Acute tubular necrosis in a patient with paroxysmal nocturnal hemoglobinuria.

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Acute renal failure (ARF) is a well-recognized complication of paroxysmal nocturnal hemoglobinuria (PNH). The predominant mechanism is intravascular hemolysis resulting in massive hemoglobinuria ARF. We report a case of acute tubular necrosis (ATN) developed in the absence of overwhelming evidence

Lip necrosis in a patient with paroxysmal nocturnal hemoglobinuria: Can it be triggered by COVID-19?

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Background: CIVID-19 due to SARS-CoV-2 was first described in the city of Wuhan in China and spread around the world turning into a pandemic. COVID-19 can affect different organ systems, including the oral mucosa.

Increased resistance of PIG-A- bone marrow progenitors to tumor necrosis factor a and interferon gamma: possible implications for the in vivo dominance of paroxysmal nocturnal hemoglobinuria clones.

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OBJECTIVE Paroxysmal nocturnal hemoglobinuria (PNH) is a clonal disorder due to a PIG-A gene mutation, resulting in deficient expression of GPI-anchored-proteins. Both immune-mediated suppression of hematopoiesis and cytokine alterations have been reported in aplastic anemia, a disease closely

Toxicity from a bite of the brown spider (Loxosceles reclusus). Skin necrosis, hemolytic anemia, and hemoglobinuria in a nine-year-old child.

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Zonal cutaneous ulceration and necrosis of the lower abdomen due to cutaneous thrombosis associated with paroxysmal nocturnal hemoglobinuria.

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Myofascial necrosis as a complication of central venous catheterization in a patient with paroxysmal nocturnal hemoglobinuria.

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Acute tubular necrosis in a patient with march hemoglobinuria.

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Extensive cutaneous ulcerations and necrosis associated with paroxysmal nocturnal hemoglobinuria.

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GPI-defective monocytes from paroxysmal nocturnal hemoglobinuria patients show impaired in vitro dendritic cell differentiation.

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Paroxysmal nocturnal hemoglobinuria (PNH) is a clonal, acquired hematopoietic disorder characterized by a phosphatidylinositol (PI) glycan-A gene mutation, which impairs the synthesis of the glycosyl-PI (GPI) anchor, thus causing the absence of all GPI-linked proteins on the membrane of the

[Acute renal failure in a patient with myelodysplastic syndrome and paroxysmal nocturnal hemoglobinuria phenotype].

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Hemoglobin and myoglobin heme pigments and iron have acute and chronic nephrotoxic effects, which are often associated with massive hemolysis and rhabdomyolysis. We report a patient with a myelodysplastic syndrome and paroxysmal nocturnal hemoglobinuria phenotype who developed an acute renal failure

A blue kidney--chronic renal failure as a consequence of siderosis in paroxysmal nocturnal hemoglobinuria?

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Acute renal failure is a known complication during hemolytic crisis in paroxysmal nocturnal hemoglobinuria (PNH). However, chronic renal failure is rare despite the well-known spectacular hemosiderosis of the kidneys due to chronic hemolysis. Here, we report about a 74-year-old man with PNH who

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

Catheter-directed thrombolysis and thrombectomy for the Budd-Chiari syndrome in paroxysmal nocturnal hemoglobinuria in three patients.

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Paroxysmal nocturnal hemoglobinuria (PNH) is a rare hematopoietic stem cell disorder characterized by hemolytic anemia, hemoglobinuria, bone marrow failure, and hypercoagulability. Thrombosis is the leading cause of mortality and occurs in one-half of PNH patients, with the hepatic veins being the

Splenectomy for massive splenic infarction unmasks paroxysmal nocturnal hemoglobinuria.

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Paroxysmal nocturnal hemoglobinuria (PNH) is a rare disorder characterized by pancytopenia, hemolysis, and thrombosis. Abdominal vein thrombosis is a life-threatening manifestation of this disease. We present a patient with complete spleen necrosis due to thrombosis of the splenic vessels. After

Transient severe pancytopenia due to elevated tumor necrosis factor-alpha in overwhelming infection.

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A 66-year-old woman complained of fever, sore throat, and neck pain due to pharyngitis and painful lymph node swelling. CBC revealed severe pancytopenia and markedly hypocellular marrow. The administration of antibiotics and granulocyte-colony stimulating factor (G-CSF) successfully ameliorated the

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