Abnormal Phospholipid Metabolism in Spur Cell Anemia: Decreased Fatty Acid Incorporation Into Phosphatidylethanolamine and Increased Incorporation Into Acylcarnitine in Spur Cell Anemia Erythrocytes

Abstract

Spur cell anemia is a hemolytic anemia seen in severe alcoholic cirrhosis that is characterized by unusual morphology and a decreased ratio of phospholipids to cholesterol in the erythrocyte membrane. We hypothesized that defective phospholipid repair may contribute to the red blood cell (RBC) phospholipid abnormalities of spur cell anemia. Therefore, we compared RBCs from normal control subjects with RBCs from spur cell anemia patients. The incorporation of [14C] arachidonic acid into the phospholipids and acylcarnitine (acyl-Cn) of spur cells and normal RBCs was analyzed by a direct-phase high performance liquid chromatography column to separate both the phospholipids and acyl-Cn. There was less uptake of the [14C] arachidonate into phosphatidylethanolamine of spur cell RBCs (12.9% +/- 1.0%) compared with normal RBCs (20.5% +/- 2.8%; P = .0245). However, more arachidonate was incorporated into the acyl-Cn of spur cells (spur cell acyl-Cn [24.5% +/- 2.9%] v normal control acyl-Cn [10.1% +/- 1.9%]; P = .0018). We conclude that phospholipid biosynthesis is inhibited and that acyl-Cn formation is spared in spur cell anemia RBCs. These metabolic changes may help account for the lipid abnormalities seen in spur cell anemia RBCs and contribute to the hemolytic process.