Burr cells, hemolytic anemia and cirrhosis

A prolonged hemolytic disorder characterized by sustained burr poikilocytosis, reticulocytosis, thrombocytopenia and high serum levels of unconjugated bilirubin is described in ten patients, of whom nine had alcoholic cirrhosis and one cardiac cirrhosis. Six patients with the disorder died within five months of its recognition. As a readily identifiable and constant feature of the syndrome, the detection of burr cells in the blood film of a patient with cirrhosis serves to indicate the presence of the disorder. Patients with liver disease had an increased incidence in wet preparations of another variety of morphologically abnormal erythrocytes resembling acanthocytes (acanthroid). Of forty-seven of 103 patients with severe alcoholic liver injury, acanthroid cells comprised more than 10 per cent of the cells in wet preparations. In wet preparations of red blood cells from fifty-six additional patients with alcoholic liver injury and fifteen patients with nonalcoholic liver disease, less than 10 per cent of the cells were acanthroid. In alcoholic patients having only acanthroid cells, a decrease in the percentage of acanthroid cells appeared to be related temporally to improvement in hepatic function. In vitro, the serum of patients with burr or acanthroid cells induced acanthroid transformation of normal erythrocytes. Conversely, normal serum restored acanthroid, but not burr cells, to a normal morphologic appearance. A serum factor related in some way to serum albumin appeared to be associated with acanthroid transformation. An additional factor acting in vivo is posulated to be necessary for the formation of burr cells.