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Correlation of Histopathologic Findings of Non-Graft Threatening Preservation/Reperfusion Injury in Time-Zero Liver Needle Biopsies With Short-Term Post-Transplantation Laboratory Alterations Publisher



Shahbazi N1 ; Haeri H1 ; Toosi MN2, 3 ; Jafarian A3, 4 ; Shahsiah R1, 3 ; Moghadam MT3 ; Poursaleh SS5 ; Azmoudehardalan F1, 3
Authors
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Authors Affiliations
  1. 1. Department of Pathology and Laboratory Medicine, Cancer Institute, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Department of Internal Medicine, Gastroenterology and Hepatology Division, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Liver Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Department of General Surgery, Hepatobiliary and Liver Transplantation Division, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
  5. 5. Iranian Tissue Bank and Research Center, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran

Source: Hepatitis Monthly Published:2015


Abstract

Background: Early post-transplantation alterations in liver tests are caused by a variety of etiologies including rejection, biliary or vascular complications, and preservation/reperfusion injury (PRI). Objectives: The aim of this study was to show the correlation between histopathologic changes of PRI and the alterations in liver tests in the early post-transplantation period. Materials and Methods: Between April 2013 and August 2014, histopathologic findings of protocol, time-zero, Tru-Cut, liver needle biopsies were evaluated in 94 cases of cadaveric liver transplantation. The histopathologic changes included ballooning degeneration, micro- and macro-vesicular steatosis, bilirubinostasis, apoptotic cells, bile plugs and neutrophilic infiltration. These histopathologic changes were compared with the early (15 days) post-transplantation liver laboratory findings. Results: Clinico-pathologic evaluation of all 94 cases was done by assessment of PRI findings in time-zero biopsies and possible causes of allograft injury were appraised. In 21 patients, a specific cause for allograft injury was found including rejection and/or surgical complications. In the remaining 73 cases, there was no specific cause for allograft injury and histopathologic findings of time-zero liver needle biopsies supported PRI. We classified liver laboratory tests alterations as: hepatocellular damage (elevation of transaminases and lactate dehydrogenase), cholestatic damage (elevation of alkaline phosphatase and total bilirubin) and mixed. Hepatocellular and cholestatic alterations in liver function tests were associated with the presence of marked apoptotic bodies and neutrophilic aggregates in time zero biopsies, respectively. On the other hand, macrovesicular steatosis was dominantly associated with mixed (hepatocellular and cholestatic) laboratory alterations of liver tests. Conclusions: Any discrepancy between histopathologic changes in time-zero biopsies and pattern of early liver laboratory alterations may be considered as a warning for causes other than PRI. © 2015 Kowsar Corp.