The clinical sequelae of intravascular hemolysis and extracellular plasma hemoglobin: a novel mechanism of human disease.

By R. Rother, L. Bell, P. Hillmen, M. Gladwin. Journal of the American Medical Association (JAMA), 2005

1,607 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

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, background): “Intravascular hemolysis disrupts this protective compartmentalization, and allows pathologic biochemical reactions to occur.(34) At least two such reactions are known.”
Dysregulated arginine metabolism, hemolysis-associated pulmonary hypertension, and mortality in sickle cell disease. (2005, background): “Pulmonary hypertension also develops in most other hereditary and chronic hemolytic anemias, including thalassemia,(32) hereditary spherocytosis,(33) paroxysmal nocturnal hemoglobinuria,(34) and other hemolytic disorders,(35-38) supporting the existence of a clinical syndrome of hemolysis-associated”
Multicenter phase 3 study of the complement inhibitor eculizumab for the treatment of patients with paroxysmal nocturnal hemoglobinuria. (2008, background): “There were a total of 44 serious adverse events (SAEs) during 52 weeks of eculizumab treatment in SHEPHERD, of which 7 were considered to be possibly related to study drug including pyrexia (2), headache (1), abdominal distension (1), viral infection (1), anxiety (1), and renal impairment (1).”