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Nishimura, Jun-ichi; Yamamoto, Masaki; Hayashi, Shin; Ohyashiki, Kazuma; Ando, Kiyoshi; Brodsky, Andres L; Noji, Hideyoshi; Kitamura, Kunio; Eto, Tetsuya; Takahashi, Toru; Masuko, Masayoshi; Matsumoto, Takuro; Wano, Yuji; Shichishima, Tsutomu; Shibayama, Hirohiko; Hase, Masakazu; Li, Lan; Johnson, Krista; Lazarowski, Alberto; Tamburini, Paul; Inazawa, Johji; Kinoshita, Taroh; Kanakura, Yuzuru
New England journal of medicine/The New England journal of medicine, 02/2014, Letnik: 370, Številka: 7Journal Article
Patients with paroxysmal nocturnal hemoglobinuria who had a poor response to eculizumab therapy were found to have a genetic polymorphism in C5 that prevents binding by the antibody. Paroxysmal nocturnal hemoglobinuria (PNH) arises as a consequence of clonal expansion of hematopoietic stem cells that have acquired a somatic mutation in the gene encoding phosphatidylinositol glycan anchor biosynthesis class A ( PIGA ). 1 – 3 The resulting hematopoietic cells are deficient in glycosylphosphatidylinositol-anchored proteins, including the complement regulatory proteins CD55 and CD59; this accounts for the intravascular hemolysis that is the primary clinical manifestation of PNH. 4 – 6 PNH frequently develops in association with disorders involving bone marrow failure, particularly aplastic anemia. Thrombosis is a major cause of PNH-associated morbidity and mortality, particularly among white patients. 7 – 9 Eculizumab (Soliris, Alexion Pharmaceuticals) . . .
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Dostop do baze podatkov JCR je dovoljen samo uporabnikom iz Slovenije. Vaš trenutni IP-naslov ni na seznamu dovoljenih za dostop, zato je potrebna avtentikacija z ustreznim računom AAI.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Povezave do osebnih bibliografij avtorjev | Povezave do podatkov o raziskovalcih v sistemu SICRIS |
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Vir: Osebne bibliografije
in: SICRIS
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