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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

Oral L-citrulline decreases venous plasma peroxidase activity levels, measured at a near-physiologic pH of 6.9, and decreases plasma hemoglobin levels in children with SCD.⁴ Deoxyhemoglobin scavenges NO avidly, limiting its . . . [Full Text of this Article]

William H. Waugh, MD
egwhwaugh@webtv.net
Department of Physiology
Brody School of Medicine
East Carolina University
Greenville, NC

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