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thrombocytopenia/carbohydrate
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Carbohydrate-deficient glycoprotein syndrome type 1 with profound thrombocytopenia and normal phosphomannomutase and phosphomannose isomerase activities.
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We report siblings with a variant of carbohydrate-deficient glycoprotein syndrome, type 1 (CDGS1), characterized by normal phosphomannomutase and phosphomannose isomerase activities, severe thrombocytopenia, and respiratory compromise. Each infant died after a course of intensive care, suggesting
Characterization of the structural requirements for a carbohydrate based anticoagulant with a reduced risk of inducing the immunological type of heparin-associated thrombocytopenia.
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HAT is the most frequent drug induced immune-thrombocytopenia. We recently identified multimolecular PF4/heparin complexes as the major antigen. In order to evaluate the structural requirements for formation of the antigenic complex, we chemically synthesized 13 glucan sulfates and used 5 heparin
Absence of cross-reactivity of SR90107A/ORG31540 pentasaccharide with antibodies to heparin-PF4 complexes developed in heparin-induced thrombocytopenia.
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New carbohydrate-based anticoagulants devoid of the side effects of unfractionated heparin are currently under development and show a major potential for patients with heparin-induced thrombocytopenia (HIT) who still require efficient antithrombotic therapy. As HIT is usually associated with
Studies on a patient with thrombocytopenia, giant platelets and a platelet membrane glycoprotein Ib with reduced amount of sialic acid.
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A 70-year-old patient with a life-long bleeding tendency, giant platelets and thrombocytopenia (10-40 x 10(9) platelets/l) has been studied. This is a condition often associated with lack of platelet membrane glycoprotein Ib (GP Ib). Electron microscopy of fixed platelets incubated with monoclonal
Glucosamine sulfate does not crossreact with the antibodies of patients with heparin-induced thrombocytopenia.
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OBJECTIVE
To assess the crossreactivity of glucosamine sulfate, used for treatment of degenerative joint disease with antibodies induced in heparin-induced thrombocytopenia (HIT).
BACKGROUND
HIT is a severe adverse effect of heparin therapy induced by an immunological mechanism. The antibodies in
Alloantibody against new platelet alloantigen (Lap(a)) on glycoprotein IIb is responsible for a case of fetal and neonatal alloimmune thrombocytopenia.
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BACKGROUND
Fetal and neonatal alloimmune thrombocytopenia (FNAIT) is caused by the destruction of platelets (PLTs) in the fetus or newborn by maternal PLT antibodies that crossed the placenta during pregnancy.
METHODS
In this study, we aim to elucidate the properties of a new PLT alloantigen
The levels of glycosphingolipids, ceramides, sialic acid and glycogen are changed in plasma membranes of rat platelets harvested during recovery from immune-mediated thrombocytopenia.
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Plasma membranes of rat platelets produced at normal platelet counts and during early recovery from immune-mediated thrombocytopenia were examined for the contents of carbohydrates, lipids and glycosphingolipids. Glucosylceramide, two monosialo-gangliosides and one disialo-ganglioside were found to
Amiprilose hydrochloride for rheumatoid arthritis.
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OBJECTIVE
To assess the safety and efficacy of amiprilose hydrochloride (HCl), a novel synthetic carbohydrate with anti-inflammatory and immunomodulatory properties, in patients with rheumatoid arthritis.
METHODS
Prospective, multicenter, randomized, parallel group, double-blind placebo-controlled
Amino acid 489 is encoded by a mutational "hot spot" on the beta 3 integrin chain: the CA/TU human platelet alloantigen system.
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A new platelet alloantigen, termed CA, has recently been implicated in a case of neonatal alloimmune thrombocytopenia (NATP) in a Filipino family in Canada. Maternal anti-CA serum reacted with glycoprotein (GP) IIIa and maintained its reactivity after removal of high mannose carbohydrate residues
Hematologic Findings of Inherited Metabolic Disease: They are More Than Expected.
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Inherited metabolic diseases are pathologic conditions that generally develop as a result of impairment of the production or breakdown of protein, carbohydrate, and fatty acids. Early determination of hematological findings has a positive effect on the prognosis of metabolic diseases. Three hundred
Low-dose rituximab in the treatment of acquired haemophilia.
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OBJECTIVE
Acquired haemophilia is a rare hemorrhagic disease caused by inhibitory autoantibodies against coagulation factor VIII. Rituximab has become a popular choice for immunosuppressive therapy in acquired haemophilia, almost with the same schedule of 375 mg/m(2) per week for 4-6 doses. While
[Hypophosphatemia and refeeding syndrome: a severe and underdiagnosed adverse effect].
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A 68-year-old woman was hospitalised because of generalised weakness and development of confusional state, related to severe hyponatremia, probably due to an eating disorder with malnutrition. During the first days of hospitalisation the patient eats surprising large amounts of food. The worsening
Primary porcine Kupffer cell phagocytosis of human platelets involves the CD18 receptor.
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BACKGROUND
Hepatic failure has been treated successfully with clinical extracorporeal perfusions of porcine livers. However, dog-to-pig and pig-to-baboon liver xenotransplant models have resulted in severe bleeding secondary to liver xenograft-induced thrombocytopenia. Kupffer cells (KC) are
Pre-clinical pharmacological profile of the novel glycoconjugate Org 36764 with both factor Xa and thrombin (IIa) inhibitory activities.
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Org 36764, is an antithrombin III (AT) and thrombin binding carbohydrate, which accelerates the inactivation of both factor Xa and thrombin by AT. It displays in buffer an anti-Xa and anti-thrombin activity of 415 and 2 U/mg, respectively, compared to 172 and 114 U/mg, respectively, for
Amino acid sequence of a platelet-binding human anti-DNA monoclonal autoantibody.
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The complete amino acid sequences of the variable regions of the heavy and light chains of a human IgM monoclonal platelet-binding autoantibody have been determined. This antibody, HF2-1/17, produced by a human x human hybridoma prepared from lymphocytes of a patient with systemic lupus
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