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Letters
November 16, 2005

Arginine Metabolism, Pulmonary Hypertension, and Sickle Cell Disease

Author Affiliations
 

Letters Section Editor: Robert M. Golub, MD, Senior Editor.

JAMA. 2005;294(19):2432-2434. doi:10.1001/jama.294.19.2432-c

To the Editor: In their study of arginine metabolism, Dr Morris and colleagues1 related lower plasma arginine concentrations to higher plasma arginase activity levels and higher plasma hemoglobin values in sickle cell disease (SCD). The authors hypothesize that increased plasma arginase activity may limit L-arginine bioavailability for vasoprotection in SCD. Their findings support the concept that L-arginine is a pivotal essential amino acid in sickle cell anemia and that deficiency of arginine-derived nitric oxide (NO) is in part responsible for insufficient vasoprotection and for hemolysis-associated morbidity in SCD.2,3 They confirm a previously reported in vitro correlation between reduced plasma L-arginine levels and both higher plasma hemoglobin levels and higher plasma arginase activity values in venous blood.2

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