Brief Article
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World J Gastroenterol. Apr 14, 2011; 17(14): 1848-1857
Published online Apr 14, 2011. doi: 10.3748/wjg.v17.i14.1848
Thrombotic microangiopathy-like disorder after living-donor liver transplantation: A single-center experience in Japan
Tomohide Hori, Toshimi Kaido, Fumitaka Oike, Yasuhiro Ogura, Kohei Ogawa, Yukihide Yonekawa, Koichiro Hata, Yoshiya Kawaguchi, Mikiko Ueda, Akira Mori, Hajime Segawa, Kimiko Yurugi, Yasutsugu Takada, Hiroto Egawa, Atsushi Yoshizawa, Takuma Kato, Kanako Saito, Linan Wang, Mie Torii, Feng Chen, Ann-Marie T Baine, Lindsay B Gardner, Shinji Uemoto
Tomohide Hori, Toshimi Kaido, Fumitaka Oike, Yasuhiro Ogura, Kohei Ogawa, Yukihide Yonekawa, Koichiro Hata, Yoshiya Kawaguchi, Mikiko Ueda, Akira Mori, Yasutsugu Takada, Hiroto Egawa, Atsushi Yoshizawa, Shinji Uemoto, Departments of Hepato-pancreato-biliary, Transplant and Pediatric Surgery, Kyoto University Hospital, Kyoto 606-8507, Japan
Hajime Segawa, Department of Critical Care Medicine, Kyoto University Hospital, Kyoto 606-8507, Japan
Kimiko Yurugi, Department of Transfusion Medicine and Cell Therapy, Kyoto University Hospital, Kyoto 606-8507, Japan
Takuma Kato, Kanako Saito, Mie Torii, Linan Wan, Department of Cellular and Molecular Immunology, Mie University Hospital Graduate School of Medicine, Mie, 514-8507, Japan
Feng Chen, Ann-Marie T Baine, Lindsay B Gardner, Department of Neuroscience, Mayo Clinic Florida, FL 32224, United States
Author contributions: Hori T wrote the paper and performed the research; Kaido T, Oike F, Ogura Y, Ogawa K, Yonekawa Y, Hata K, Kawaguchi Y, Ueda M, Mori A, Yoshizawa A, Segawa H, Chen F, Baine AMT and Gardner LB provided important opinions based on their specialized experiences, measured the important factors and collected the data; Yurugi K, Kato T, Saito K, Wang L and Torii M performed important assays for the research; Uemoto S, Takada Y and Egawa H designed the research; Uemoto S supervised the research.
Supported by the Grant from Uehara Memorial Foundation, No. 200940051, Tokyo, 171-0033, Japan
Correspondence to: Tomohide Hori, PhD, MD, Departments of Hepato-pancreato-biliary, Transplant and Pediatric Surgery, Kyoto University Hospital, 54 Shogoinkawara-cho, Sakyo-ku, Kyoto 606-8507, Japan. horit@kuhp.kyoto-u.ac.jp
Telephone: +81-75-7513111 Fax: +81-75-7513106
Received: May 13, 2010
Revised: June 9, 2010
Accepted: June 16, 2010
Published online: April 14, 2011
Abstract

AIM: To investigate thrombotic microangiopathy (TMA) in liver transplantion, because TMA is an infrequent but life-threatening complication in the transplantation field.

METHODS: A total of 206 patients who underwent living-donor liver transplantation (LDLT) were evaluated, and the TMA-like disorder (TMALD) occurred in seven recipients.

RESULTS: These TMALD recipients showed poor outcomes in comparison with other 199 recipients. Although two TMALD recipients successfully recovered, the other five recipients finally died despite intensive treatments including repeated plasma exchange (PE) and re-transplantation. Histopathological analysis of liver biopsies after LDLT revealed obvious differences according to the outcomes. Qualitative analysis of antibodies against a disintegrin-like domain and metalloproteinase with thrombospondin type 1 motifs (ADAMTS-13) were negative in all patients. The fragmentation of red cells, the microhemorrhagic macules and the platelet counts were early markers for the suspicion of TMALD after LDLT. Although the absolute values of von Willebrand factor (vWF) and ADAMTS-13 did not necessarily reflect TMALD, the vWF/ADAMTS-13 ratio had a clear diagnostic value in all cases. The establishment of adequate treatments for TMALD, such as PE for ADAMTS-13 replenishment or treatments against inhibitory antibodies, must be decided according to each case.

CONCLUSION: The optimal induction of adequate therapies based on early recognition of TMALD by the reliable markers may confer a large advantage for TMALD after LDLT.

Keywords: Thrombotic microangiopathy; Liver transplantation; von Willebrand factor; A disintegrin-like domain and metalloproteinase with thrombospondin type 1 motifs; Complication