The Mechanism of Neutropenia in Felty's Syndrome
P. C. Vincent, John A. Levi, Ann Macqueen
Abstract
P. C. Vincent, John A. Levi, Ann Macqueen
Abstract
Summary. Neutrophil kinetics were studied in 17 patients with Felty's syndrome using an in vitro diisopropylfluorophosphate‐32P technique. Excessive margination of neutrophils was present in all patients, and was solely responsible for the neutro‐penia in 12. Five patients had a total blood neutrophil pool which was so low that they would have been neutropenic even with a normal ratio of marginated to circulating cells; in these the production rate was subnormal. In no case was neutropenia due to shortened nueutrophil survival. There was no correlation between either the degree of marrow cellularity, or serum lysozyme levels, and the measured neutrophil production rate. Two patients studied before and after splenectomy showed improvement in kinetic abnormalities following operation. We conclude that the principal mechanism responsible for the neutropenia in Felty's syndronie is excessive margination of cells. In about one third of patients neutrophil production is subnormal in addition, but excessive neutrophil destruction is an uncommon finding. Conventional laboratory investigations are of little or no help in defining the mechanism in an individual patient. The value of splenectomy still has to be established, although short‐term improvement in kinetic parameters may occur.
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Summary. Neutrophil kinetics were studied in 17 patients with Felty's syndrome using an in vitro diisopropylfluorophosphate‐32P technique. Excessive margination of neutrophils was present in all patients, and was solely responsible for the neutro‐penia in 12. Five patients had a total blood neutrophil pool which was so low that they would have been neutropenic even with a normal ratio of marginated to circulating cells; in these the production rate was subnormal. In no case was neutropenia due to shortened nueutrophil survival. There was no correlation between either the degree of marrow cellularity, or serum lysozyme levels, and the measured neutrophil production rate. Two patients studied before and after splenectomy showed improvement in kinetic abnormalities following operation. We conclude that the principal mechanism responsible for the neutropenia in Felty's syndronie is excessive margination of cells. In about one third of patients neutrophil production is subnormal in addition, but excessive neutrophil destruction is an uncommon finding. Conventional laboratory investigations are of little or no help in defining the mechanism in an individual patient. The value of splenectomy still has to be established, although short‐term improvement in kinetic parameters may occur.
Key concepts: Felty's syndrome, Neutropenia, Splenectomy, Medicine, Absolute neutrophil count, Immunology, Gastroenterology, Internal medicine