Hyperlipidemia in acute hemolysis

Summary

In 27 (78%) of 36 patients with massive hemolysis (defined as a fall in hematocrit of more than 12% within 12 h due to intravascular red cell destruction), hypertriglyceridemia (plasma triglycerides > 175 mg/dl) was present or appeared within two days after the hemolytic crisis. Eighteen subjects with triglycerides exceeding 300 mg/dl (peak 516 ± 39 mg/dl) were further analyzed. The development of hyperlipidemia was independent of the etiology of hemolysis (microangiopathic hemolytic disease 7, toxicemia 3, parainfectious complications 3, autoimmune hemolysis 2, glucose-6-phosphate dehydrogenase deficiency 2). Factors known to increase plasma triglycerides, such as shock, infections, or pancreatitis, were present in only a few cases. Hemolysis-associated complications were activation of intravascular coagulation (16), coma (13), acute renal failure (13), and respiratory insufficiency (5), organ dysfunctions indicating diffuse microvascular injury. Plasma triglycerides fell within a few days if the cause of red cell destruction was eliminated. In 5 of the 8 patients presenting with triglycerides below 175 mg/dl, severe hepatic dysfunction was present. We conclude that hemolysis causes transient hyperlipidemia, either directly by red cell destruction or indirectly by inducing intravascular coagulation, and possibly due to both increased triglyceride synthesis and decreased catabolism.