IngentaConnect Serum elastase and antithrombin-3 in patients with acute graft-vs...

Authors: Toda, Akinari; Takatsuka, Hiroyuki; Nakajima, Tosiyuki; Nomura, Kaori; Wakae, Takeshi; Itoi, Hisayuki; Okada, Masaya; Misawa, Mahito; Hara, Hiroshi

Source: Clinical Transplantation, Volume 19, Number 4, August 2005 , pp. 466-469(4)

Publisher: Blackwell Publishing

Abstract:

Toda A, Takatsuka H, Nakajima T, Nomura K, Wakae T, Itoi H, Okada M, Misawa M, Hara H. Serum elastase and antithrombin-3 in patients with acute graft-vs.-host disease after bone marrow transplantation.

Clin Transplant 2005: 19: 466–469. © Blackwell Munksgaard, 2005 Abstract:

The mechanism by which inflammatory cytokines are involved in acute graft-vs.-host disease (GVHD) after hematopoietic stem cell transplantation has only been studied recently. We focused on the changes of serum elastase and antithrombin-3 (AT-3) from before pre-treatment until the leukocyte recovery period after transplantation. We examined the correlation between these two parameters and the grade of acute GVHD, as well as the mechanism of onset. We measured the serum elastase and AT-3 levels before pre-treatment and during the leukocyte recovery period in 49 consecutive patients receiving bone marrow transplantation. The severity of acute GVHD was divided into five grades (0–4). No significant differences of pre-transplantation elastase levels were observed among the GVHD grades, but the elastase level during the leukocyte recovery period showed a significant correlation with the grade of GVHD (p < 0.01). A significant inverse correlation was also observed (p < 0.05) between the pre-transplantation level of AT-3 and the grade of GVHD, as well as a significant correlation at the time of leukocyte recovery (p < 0.0001). Furthermore, a significant correlation (p < 0.0001) was observed between the elastase and AT-3 levels during the leukocyte recovery period. These results suggest that elastase levels during the leukocyte recovery period are related to the grade of acute GVHD and the mechanism appears to include vascular endothelial injury mediated via AT-3.

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