Transient improvement of polymorphonuclear leukocyte function by splenectomy in beta-thalassemia.

Host defense mechanisms in transfusion-dependent non-splenectomized patients with beta-thalassemia were studied. Polymorphonuclear leukocytes (PMNLs) of non-splenectomized patients responded poorly to zymosan generated chemotactic factors. Chemotactic indices were 22.1 microns +/- 2.8 (mean +/- S.D.) using zymosan activated serum (ZAS) as the attractant in comparison to 20.4 microns +/- 2.6 when fresh untreated serum was used. In contrast, chemotactic indices of normal PMNLs increased from 21.1 microns to 33.6 microns +/- 3.1 in response to ZAS. Normal PMNL responses to a mixture of normal ZAS and thalassemic serum were inhibited; the mean chemotactic index was 18.1 microns +/- 5.1 with use of ZAS alone. Splenectomy temporarily reverses these alterations. Adherence to nylon wool of PMNLs suspended in fresh thalassemic serum prior to splenectomy was 3.1% +/- 1.1 (mean +/- S.D.); 20 days after splenectomy adherence increased to 14.0% +/- 2.8 (P = 0.0001) and remained at this level for 90 days. At 120 and 150 days after splenectomy adherence decreased to 1.5% +/- 0.8 and 1.0% +/- 0.85 respectively. Splenectomy also transiently abrogated the failure of zymosan to generate chemotactic factors in thalassemic serum.