Revisiting the hyperhemolysis paradigm

In this issue of Blood, 2 articles test fundamental hypotheses relating intravascular hemolysis to sickle cell disease (SCD) pathogenesis. Detterich et al confirm a role for hemolysis and cell-free plasma hemoglobin (Hb) in pulmonary and systemic endothelial dysfunction in humans. Almeida et al show...

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Bibliographic Details
Published inBlood Vol. 126; no. 6; pp. 695 - 696
Main Author Gladwin, Mark T.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 06.08.2015
Subjects
Anemia, Sickle Cell - physiopathology
Animals
Blood Transfusion
Brachial Artery - physiopathology
Cyclic N-Oxides - pharmacology
Female
Free Radical Scavengers - pharmacology
Hemoglobins - metabolism
Humans
Hydroxyurea - pharmacology
Hypertension, Pulmonary - physiopathology
Imidazoles - pharmacology
Leukocytes - drug effects
Lung - physiopathology
Male
Nitric Oxide - metabolism
Tricuspid Valve Insufficiency - physiopathology
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Summary:In this issue of Blood, 2 articles test fundamental hypotheses relating intravascular hemolysis to sickle cell disease (SCD) pathogenesis. Detterich et al confirm a role for hemolysis and cell-free plasma hemoglobin (Hb) in pulmonary and systemic endothelial dysfunction in humans. Almeida et al show in mice that hemolysis induces inflammation that is caused by nitric oxide (NO) scavenging and ameliorated by NO donors and the NO-donor properties of hydroxyurea (HU).
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
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ObjectType-Commentary-1
ISSN:0006-4971
1528-0020
DOI:10.1182/blood-2015-06-649491