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hemoglobinuria/kanama

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Sayfa 1 itibaren 119 Sonuçlar

Cerebral venous thrombosis presenting with intracerebral hemorrhage in a patient with paroxysmal nocturnal hemoglobinuria.

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Cerebral venous thrombosis (CVT) is an uncommon cause of stroke. Paroxysmal nocturnal hemoglobinuria (PNH) is a rare type of hemolytic anemia, frequently associated with thrombophilia. PNH may rarely present with CVT. Approximately, one-third of the patients with CVT develop cerebral hemorrhage.
Paroxysmal nocturnal hemoglobinuria (PNH) is a rare disorder characterized by intravascular hemolysis, hemoglobinuria, and thrombosis. Thrombotic attacks are life threatening and are responsible for nearly 50% of PNH-related deaths. Compared with thrombotic events, bleeding related to

[Between thrombosis and bleeding - a case of paroxysmal nocturnal hemoglobinuria].

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A 67-year-old lady was admitted with a myocardial infarction. Coronarography revealed thrombotic material within coronary arteries. The underlying disease was paroxysmal nocturnal hemoglobinuria (PNH), a stem cell defect characterized by episodes of complement-induced hemolysis and thromboembolic
OBJECTIVE To report a patient with paroxysmal nocturnal hemoglobinuria who complained of transient obscurations of vision and exhibited bilateral papilledema with retinal hemorrhages. METHODS Case report. Computed tomography did not demonstrate any abnormality but magnetic resonance imaging

Hemoglobinuria after massive intraperitoneal hemorrhage.

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Hemorrhagic bullae in an anemic women. Paroxysmal nocturnal hemoglobinuria (PNH).

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[Determination of blood loss by protein-, erythrocyt- and hemoglobinuria indices].

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Delayed hemolytic transfusion reaction and paroxysmal cold hemoglobinuria: an unusual association.

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An 80-year-old female presented with melena and anemia due to bleeding from a benign gastric ulcer. Her blood group was O, D+. The serum contained anti-B and a weak anti-A (titer 2 at 18 degrees C). She was inadvertently transfused with approximately 3.5 units of group A red blood cells with no

[Experiences in clinical diagnosis of paroxysmal nocturnal hemoglobinuria (PNH)].

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Two hundred and three cases of PNH diagnosed (according to the National Unified Diagnosed Criteria, 1987) and treated from 1949 to 1992 in Peking Union Medical Hospital were analyzed retrospectively in an attempt to investigate the factors leading to delayed diagnosis. The presenting manifestation

Paroxysmal nocturnal hemoglobinuria in childhood: an uncommon presentation.

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An eight year old boy presented with severe anemia and bleeding spots. Complete blood count showed pancytopenia. There was mild reticulocytosis. Bone marrow was hypocellular with normoblastic erythroid hyperplasia. Ham's test (acidified serum test) was positive which confirmed the diagnosis of

[Bleeding time and volume in vitro by THROMBOSTAT].

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We tested an in vitro system simulating bleeding time reported by Kratzer et al. Primary hemostasis was studied perfusing an artificial vessel with citrated blood under a constant pressure of 40 mmHg, measuring the blood volume perfused (bleeding volume) and the time until blood flow stopped

Marrow transplantation for paroxysmal nocturnal hemoglobinuria.

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Between 1971 and 1990, nine patients ranging in age from 14-38 years received marrow transplants for paroxysmal nocturnal hemoglobinuria (PNH). Six were transplanted for aplastic complications of PNH. Four of these were from HLA-identical siblings, and the patients were conditioned with

Paroxysmal nocturnal hemoglobinuria in pregnancy.

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Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired hemolytic anemia in which a defect of glycophosphatidylinositol (GPI)-anchored proteins in the cell membrane of bone marrow stem cells leads to increased sensitivity of the red cells to complement, causing intravascular hemolysis and

Portal hypertension resulted from paroxysmal nocturnal hemoglobinuria: a case report and review of literature.

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Paroxysmal nocturnal hemoglobinuria is a rare intravascular hemolytic anemia, and thrombosis is the leading cause of mortality rate. The hepatic veins is the common site where Budd-Chiari syndrome usually occurs. We confronted a patient who simultaneously happened to have portal vein and superior

Chromosomic findings in patients with paroxysmal nocturnal hemoglobinuria.

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The chromosomes of 14 patients (9 males, 5 females) suffering from paroxysmal nocturnal hemoglobinuria in Merida, Mexico between April 1989 and July 1992 were analyzed. Four of the patients were children (range, 3-15 years old) and 9 were adults (range, 19-62 years old). None of the patients had any
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