hemoglobinuria/seizures

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The impact of missense mutation in PIGA associated to paroxysmal nocturnal hemoglobinuria and multiple congenital anomalies-hypotonia-seizures syndrome 2: A computational study.

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Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired clonal blood disorder that manifests with hemolytic anemia, thrombosis, and peripheral blood cytopenias. The disease is caused by the deficiency of two glycosylphosphatidylinositols (GPI)-anchored proteins (CD55 and CD59) in the hemopoietic

An unusual cause of cerebral venous sinus thrombosis. Paroxysmal nocturnal hemoglobinuria.

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Cerebral venous sinus thrombosis caused by paroxysmal nocturnal hemoglobinuria is uncommon. Our case is a 44-year-old woman who presented with a 2 day history of headaches, nausea, and seizures followed by a Todd`s paresis; she had been diagnosed as paroxysmal nocturnal hemoglobinuria for 4 years. A

A likely pathogenic variant putatively affecting splicing of PIGA identified in a multiple congenital anomalies hypotonia-seizures syndrome 2 (MCAHS2) family pedigree via whole-exome sequencing.

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Glycosylphosphatidylinositol (GPI) anchoring is a special type of protein posttranslational modification, by which proteins with diverse function are attached to cell membrane through a covalent linkage between the protein and the glycolipid. Phosphatidylinositol glycan anchor biosynthesis class A

Recent advances in the diagnosis, monitoring, and management of patients with paroxysmal nocturnal hemoglobinuria.

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Until recently, there has been no specific therapy for PNH with clinical management mainly supportive in terms of cytopenias and control of thrombotic risk. Currently, the only curative procedure for PNH is bone marrow transplantation although for the majority of patients the associated risks are

Posterior reversible encephalopathy syndrome following paroxysmal nocturnal hemoglobinuria: a case report and literature review.

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Paroxysmal nocturnal hemoglobinuria (PNH) is a rare acquired disorder characterized by hemolytic anemia, marrow failure, and a high incidence of life-threatening venous thrombosis. It is subject to a considerable variety of complications like intestinal obstruction and visceral embolism. The current

The phenotype of a germline mutation in PIGA: the gene somatically mutated in paroxysmal nocturnal hemoglobinuria.

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Phosphatidylinositol glycan class A (PIGA) is involved in the first step of glycosylphosphatidylinositol (GPI) biosynthesis. Many proteins, including CD55 and CD59, are anchored to the cell by GPI. Loss of CD55 and CD59 on erythrocytes causes complement-mediated lysis in paroxysmal nocturnal

Paroxysmal nocturnal hemoglobinuria.

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Paroxysmal nocturnal hemoglobinuria (PNH) is a rare bone marrow failure disorder that manifests with hemolytic anemia, thrombosis, and peripheral blood cytopenias. The absence of two glycosylphosphatidylinositol (GPI)-anchored proteins, CD55 and CD59, leads to uncontrolled complement activation that

Generation of glycosylphosphatidylinositol anchor protein-deficient blood cells from human induced pluripotent stem cells.

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PIG-A is an X-linked gene required for the biosynthesis of glycosylphosphatidylinositol (GPI) anchors; thus, PIG-A mutant cells have a deficiency or absence of all GPI-anchored proteins (GPI-APs). Acquired mutations in hematopoietic stem cells result in the disease paroxysmal nocturnal

Histopathology of acute toxic responses in selected tissues from rats exposed by inhalation to methyl bromide.

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To determine and characterize the histological changes induced in selected tissues from the Fischer 344 rat by acute inhalation exposure to methyl bromide (MeBr), groups of 10 male rats (11-13 weeks old) were exposed to 0, 90, 175, 250, or 325 ppm MeBr 6 hr/day for 5 days. Animals were anesthetized

Antiphosphatidylserine Antibody as a Cause of Multiple Dural Venous Sinus Thromboses and ST-Elevation Myocardial Infarction.

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BACKGROUND Antiphospholipid syndrome (APS) is an autoimmune disease characterized by antibodies directed against phospholipids on plasma membranes. Through unclear mechanisms, APS confers hypercoagulability. APS may cause recurrent thromboses in the arterial and venous vasculature. We report a case

Imported severe falciparum malaria in Israel.

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Malaria remains an overwhelming problem in tropical developing countries, with 300 to 500 million new cases and 1.5 to 3.5 million deaths per year. Malaria is a potentially life-threatening disease for travelers to the tropics. Imported malaria is an important clinical problem in nonendemic areas of

Kerosene, Camphor, and Naphthalene Poisoning in Children.

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Kerosene poisoning is one of the most common accidental poisoning in children in developing countries due common use of kerosene in house-hold and unsafe storage practices. Aspiration pneumonitis is the most common manifestation of kerosene ingestion due to its low viscosity, high

Heinz body hemolytic anemia associated with high plasma zinc concentration in a dog.

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Acute zinc toxicosis from the ingestion of pennies was diagnosed in a dog with Heinz body hemolytic anemia (PCV = 14%), leukocytosis (51,000 cells/ml) with a left shift (3,060 band neutrophils; 37,740 segmented neutrophils) and monocytosis (4,080 cells/ml), azotemia (BUN = 60 mg/dl), bilirubinemia

The genotypic and phenotypic spectrum of PIGA deficiency.

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BACKGROUND Phosphatidylinositol glycan biosynthesis class A protein (PIGA) is one of the enzymes involved in the biosynthesis of glycosylphosphatidylinositol (GPI) anchor proteins, which function as enzymes, adhesion molecules, complement regulators and co-receptors in signal transduction pathways.

Severe falciparum malaria: an important cause of multiple organ failure in Indian intensive care unit patients.

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OBJECTIVE To study the incidence and severity of multiple organ dysfunction in severe falciparum malaria. METHODS Prospective, observational study. METHODS Intensive care unit of a tertiary care university hospital. METHODS Three hundred one consecutive patients with severe falciparum malaria

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