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Serum elastase and antithrombin‐3 in patients with acute graft‐vs.‐host disease after bone marrow transplantation
Author(s) -
Toda Akinari,
Takatsuka Hiroyuki,
Nakajima Tosiyuki,
Nomura Kaori,
Wakae Takeshi,
Itoi Hisayuki,
Okada Masaya,
Misawa Mahito,
Hara Hiroshi
Publication year - 2005
Publication title -
clinical transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 76
eISSN - 1399-0012
pISSN - 0902-0063
DOI - 10.1111/j.1399-0012.2005.00355.x
Subject(s) - medicine , transplantation , elastase , hematopoietic stem cell transplantation , graft versus host disease , immunology , bone marrow , gastroenterology , enzyme , biology , biochemistry
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.