Pulmonary hypertension as a risk factor for death in patients with sickle cell disease.
By P. Hassoun, J. Krishnan. New England Journal of Medicine, 2004
793 citations recorded by the source corpus.
Subfields: Genetics, Nephrology
View Paper: https://www.semanticscholar.org/paper/d173dea949698f70da36ae131c9cca17ef474bf9
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Citations in the corpus
- Lactate dehydrogenase as a biomarker of hemolysis-associated nitric oxide resistance, priapism, leg ulceration, pulmonary hypertension, and death in patients with sickle cell disease. (2005, methodology): “To further evaluate the relationship of LDH to severity of pulmonary hypertension, we compared the LDH values for 3 groups of patients: (1) no pulmonary hypertension, defined as TRV less than 2.”
- Dysregulated arginine metabolism, hemolysis-associated pulmonary hypertension, and mortality in sickle cell disease. (2005, methodology): “0 m/s corresponds to moderate to severe pulmonary hypertension.(29) Pulmonary hypertension was prospectively defined as a tricuspid regurgitant jet velocity of at least 2.”
- The clinical sequelae of intravascular hemolysis and extracellular plasma hemoglobin: a novel mechanism of human disease. (2005, background): “Markers of hemolysis, including anemia, bilirubin, lactate dehydrogenase (LDH), and aspartate aminotransferase (but not liver-specific alanine aminotransferase), were associated with pulmonary hypertension.(22) In addition to limiting nitric oxide bioavailability via hemoglobin-based nitric oxide sc”
- Pediatric Pulmonary Hypertension: Guidelines From the American Heart Association and American Thoracic Society (2015, background): “common in adults with SCD and is strongly associated with increased mortality.(601) According to cardiac catheterization”