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Peak Serum AST Is a Better Predictor of Acute Liver Graft Injury after Liver Transplantation When Adjusted for Donor/Recipient BSA Size Mismatch (ASTi)

DOI: 10.1155/2014/351984

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Abstract:

Background. Despite the marked advances in the perioperative management of the liver transplant recipient, an assessment of clinically significant graft injury following preservation and reperfusion remains difficult. In this study, we hypothesized that size-adjusted AST could better approximate real AST values and consequently provide a better reflection of the extent of graft damage, with better sensitivity and specificity than current criteria. Methods. We reviewed data on 930 orthotopic liver transplant recipients. Size-adjusted AST (ASTi) was calculated by dividing peak AST by our previously reported index for donor-recipient size mismatch, the BSAi. The predictive value of ASTi of primary nonfunction (PNF) and graft survival was assessed by receiver operating characteristic curve, logistic regression, Kaplan-Meier survival, and Cox proportional hazard model. Results. Size-adjusted peak AST (ASTi) was significantly associated with subsequent occurrence of PNF and graft failure. In our study cohort, the prediction of PNF by the combination of ASTi and PT-INR had a higher sensitivity and specificity compared to current UNOS criteria. Conclusions. We conclude that size-adjusted AST (ASTi) is a simple, reproducible, and sensitive marker of clinically significant graft damage. 1. Introduction Despite the marked advances in the perioperative management of the liver transplant recipient, an assessment of clinically significant graft injury following preservation and reperfusion remains difficult [1]. The lack of a sensitive clinical marker of acute liver injury has a profound impact on clinical practice and the success of translational research in liver transplantation. Such a clinical marker could aid the management of graft dysfunction in early identification of recipients who will require retransplantation. Currently, posttransplant peak aspartate aminotransferase (AST) is a widely accepted clinical marker for graft damage in liver transplant practice [2–6]. In fact, the United Network for Organ Sharing (UNOS) suggests relisting criteria for the recipients with primary graft dysfunction (PNF) on the basis of the post-transplant peak AST [7]. AST is an enzyme that is involved in amino acid metabolism, primarily existing in hepatocytes. During transplantation graft hepatocytes are inevitably injured, and intracellular enzymes are subsequently released into the systemic circulation of the recipient. We theorized that the recipient AST serum concentration is a function of the total amount of AST released by the graft liver diluted by the total circulating

References

[1]  R. R. Razonable, J. Y. Findlay, A. O'Riordan et al., “Critical care issues in patients after liver transplantation,” Liver Transplantation, vol. 17, no. 5, pp. 511–527, 2011.
[2]  E. Ardite, C. Ramos, A. Rimola, L. Grande, and J. C. Fernández-Checa, “Hepatocellular oxidative stress and initial graft injury in human liver transplantation,” Journal of Hepatology, vol. 31, no. 5, pp. 921–927, 1999.
[3]  F. X. González, A. Rimola, L. Grande et al., “Predictive factors of early postoperative graft function in human liver transplantation,” Hepatology, vol. 20, no. 3, pp. 565–573, 1994.
[4]  E. Mor, W. Tillery, H. Solomon, G. Netto, I. Watemberg, and G. B. Klintmalm, “The predictive value of hepatocyte glycogen content on liver allograft biopsy. Correlation with early graft function,” Transplantation, vol. 59, no. 1, pp. 141–143, 1995.
[5]  R. J. Ploeg, A. M. D'Alessandro, S. J. Knechtle et al., “Risk factors for primary dysfunction after liver transplantation—a multivariate analysis,” Transplantation, vol. 55, no. 4, pp. 807–813, 1993.
[6]  S. M. Strasberg, T. K. Howard, E. P. Molmenti, and M. Hertl, “Selecting the donor liver: risk factors for poor function after orthotopic liver transplantation,” Hepatology, vol. 20, no. 4 I, pp. 829–838, 1994.
[7]  Organ Distribution: Allocation of Livers, 2011, http://optn.transplant.hrsa.gov/PoliciesandBylaws2/policies/pdfs/policy_8.pdf.
[8]  K. Fukazawa, S. Nishida, A. Volsky, A. G. Tzakis, and E. A. Pretto Jr., “Body surface area index predicts outcome in orthotopic liver transplantation,” Journal of Hepato-Biliary-Pancreatic Sciences, vol. 18, no. 2, pp. 216–225, 2011.
[9]  K. Fukazawa, Y. Yamada, S. Nishida, T. Hibi, K. L. Arheart, and E. A. Pretto Jr., “Determination of the safe range of graft size mismatch using body surface area index in deceased liver transplantation,” Transplant International, vol. 26, no. 7, pp. 724–733, 2013.
[10]  S. Feng, N. P. Goodrich, J. L. Bragg-Gresham et al., “Characteristics associated with liver graft failure: the concept of a donor risk index,” American Journal of Transplantation, vol. 6, no. 4, pp. 783–790, 2006.
[11]  K. M. Olthoff, L. Kulik, B. Samstein et al., “Validation of a current definition of early allograft dysfunction in liver transplant recipients and analysis of risk factors,” Liver Transplantation, vol. 16, no. 8, pp. 943–949, 2010.
[12]  S. Roedder, M. Vitalone, P. Khatri, and M. M. Sarwal, “Biomarkers in solid organ transplantation: establishing personalized transplantation medicine,” Genome Medicine, vol. 3, no. 6, article 37, 2011.
[13]  National Institute of Allergy and Infectious Diseases (NIAID), Clinical Trials in Organ Transplantation 3. Effects of Donor and Recipient Genetic Expression on Heart, Lung, Liver, or Kidney Transplant Survival, 2012, http://clinicaltrials.gov/ct2/show/NCT00531921.
[14]  R. Taub, “Liver regeneration: from myth to mechanism,” Nature Reviews Molecular Cell Biology, vol. 5, no. 10, pp. 836–847, 2004.
[15]  K. M. Olthoff, “Hepatic regeneration in living donor liver transplantation,” Liver Transplantation, vol. 9, no. 10, pp. S35–S41, 2003.
[16]  J. W. Grisham, “A morphologic study of deoxyribonucleic acid synthesis and cell proliferation in regenerating rat liver; autoradiography with thymidine-H3,” Cancer Research, vol. 22, pp. 842–849, 1962.
[17]  I. R. Kamel, N. Erbay, G. Warmbrand, J. B. Kruskal, E. A. Pomfret, and V. Raptopoulos, “Liver regeneration after living adult right lobe transplantation,” Abdominal Imaging, vol. 28, no. 1, pp. 53–57, 2003.
[18]  A. Marcos, R. A. Fisher, J. M. Ham et al., “Liver regeneration and function in donor and recipient after right lobe adult to adult living donor liver transplantation,” Transplantation, vol. 69, no. 7, pp. 1375–1379, 2000.
[19]  K. Urata, S. Kawasaki, H. Matsunami et al., “Calculation of child and adult standard liver volume for liver transplantation,” Hepatology, vol. 21, no. 5, pp. 1317–1321, 1995.

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