Article Text
Abstract
Background Leukocytapheresis (LCAP) is a treatment using extracorporial circulation with a filter for the removal of white blood cells (WBCs) from the peripheral blood and has been reported to be an effective treatment for rheumatoid arthritis (RA). The effectiveness of LCAP in inflammatory disease is speculated through the removal of activated WBCs and platelets. However, the precise mechanism of LCAP treatment for the inflammatory diseases is still under investigation.
Objectives Because lactoferrin (LTF) and pentraxin 3 (PTX3) are stored in the granulocytes, we analyzed plasma LTF and PTX3 in patients with RA who were treated with LCAP.
Methods Plasma levels of LTF and PTX3 before and after LCAP treatment were measured by enzyme linked immunoassays in 7 patients with RA. Four of these patients reached moderate response by LCAP by EULAR criteria. Those levels before and after the LCAP columns in the circuits were also measured. Peripheral blood of 13 patients with RA was exposed to unwoven polyester fiber filters for LCAP in vitro and the changes of LTF and PTX3 were measured. In addition, the morphological changes of granulocytes was also observed.
Results Mean plasma levels of LTF and PTX3 after LCAP treatment (942.2ng/ml and 15.4ng/ml, respectively) were significantly higher than those before the treatment (134.2ng/ml and 1.9ng/ml, respectively) (p<0.01). Mean levels of LTF and PTX3 after the LCAP columns in the circuit were also markedly increased (1776.6 ng/ml and 11.2ng/ml, respectively). When the whole blood of 13 patients with RA was incubated with unwoven polyester fiber in vitro, the levels of LTF and PTX3 (2169.7 and 11.2ng/ml) were higher than those without incubation (174.9 and 1.9ng/ml) (p<0.01). Cytoplasmic vacuolation of granulocytes was observed in the incubated samples.
Conclusions Release of LTF and PTX3 from the WBCs captured in the LCAP columns was indicated in this study. Because LTF and PTX3 were suggested to have functions to modify the inflammation, the increased levels of these molecules after LCAP can be contributed to the therapeutic effect in RA.
Disclosure of Interest None Declared