Introduction Alcoholic liver disease (ALD) remains one of the commonest indications for liver transplantation in Europe. The histological features of ALD vary, depending on extent and stage of injury, No features are reliably pathognomonic of ALD. We describe the histological spectrum of explants of well characterised cohort of patients undergoing transplantation for ALD.
Methods Consecutive explants (n = 84) of patients transplanted for ALD in our institution between 2002 and 2011 were selected for retrospective histological assessment. Explants were scored blinded by two pathologists using a predetermined pro-forma. Histological assessment including the presence and degree of cirrhosis, steatosis, inflammation, inclusions, siderosis and neoplastic changes were scored semi-quantitatively.
Results Median age was 54 and the majority (70%) were male. All patients had a long history of alcohol excess but reported abstinence for at least 6 months by transplantation. The aetiology was ALD (n = 80) and mixed ALD/HCV (n = 4). The majority (n = 83) had a mixed or macronodular cirrhosis with evidence of re-modelling in a significant number; one had pre-septal cirrhosis. Alpha-1 antitrypsin inclusion bodies were seen in 9 (10.7%); only 4 of these had serum A1AT levels below normal. Parenchymal siderosis was present in 39 (46.4%); in 19 (22.6%) this was grade 3–4. Amongst these, only single mutations of the HFE gene were identified. Induced cell change was seen in 67 (79.8%) and 47 (56%) had the “abstinent cell” phenotype. While 46 (54.8%) had Mallory-denk bodies (MDB), 22 (26.1% of total) patients had both “abstinent cells” and MDB. Ballooning (n = 45, 53.6%) and steatosis (n = 31, 36.9%) were also seen. HCC was present in 14 (16.7%), with dysplastic nodules in 15 (17.9%), small-cell change in 20 (23.8%) and large-cell change 50 (59.5%). Phlebosclerosis and parenchymal extinction were universal findings.
Conclusion We describe a wide spectrum of histological features in a large cohort transplanted for end-stage ALD. We demonstrate that despite abstinence, over half have residual MDB and ballooning. Conversely, over half had the recently described “abstinent cell” phenotype. Therefore, the presence of MDB should not be used as evidence of continued alcohol consumption; the presence of induced or abstinent cells correlates more strongly with reported abstinence.
Disclosure of Interest None Declared
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