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Plasma protein C is a useful clinical marker for hepatic veno‐occlusive disease (VOD) in stem cell transplantation
Author(s) -
Iguchi Akihiro,
Kobayashi Ryoji,
Kaneda Makoto,
Kobayashi Kunihiko
Publication year - 2010
Publication title -
pediatric blood and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.116
H-Index - 105
eISSN - 1545-5017
pISSN - 1545-5009
DOI - 10.1002/pbc.22314
Subject(s) - melphalan , medicine , hepatic veno occlusive disease , etoposide , transplantation , blood proteins , gastroenterology , hematopoietic stem cell transplantation , oncology , chemotherapy
Abstract Background Hepatic veno‐occlusive disease (VOD) is one of the most serious complications in stem cell transplantation (SCT). Although plasma protein C activity decreases in VOD after SCT, the timeframe of plasma protein C activity decreases during SCT is not known. Procedure We examined levels of plasma protein C serially during the course of SCT to determine the critical level and risk factors for VOD. Results Of 151 children who received SCT, 12 of them (7.9%) developed VOD. The mean minimum protein C activity in patients with VOD was significantly lower compared to that in patients without VOD ( P < 0.0001). Receiver operating characteristic curve analysis revealed that the critical plasma protein C activity (cut‐off point) for VOD was identified to be 34.5% with high sensitivity (100%) and specificity (83.3%), and the reduction of plasma protein C below the cut‐off level (day +6.50 ± 2.43) was observed mostly prior to the onset of VOD (day +7.33 ± 2.64). The patients receiving melphalan in conditioning were found to be at high risk for VOD ( P = 0.003). Among the melphalan containing regimens, melphalan + carboplatin + etoposide was a significant risk factor for depression of plasma protein C ( P = 0.037). Conclusion Plasma protein C level was a useful parameter of VOD after SCT, and activity below 34.5% was critical for VOD. The use of melphalan in conditioning causes a high risk for VOD. Pediatr Blood Cancer 2010;54:437–443. © 2009 Wiley‐Liss, Inc.