Resolution of Nodular Regenerative Hyperplasia Following Heart Transplant

2021 
Introduction Liver abnormalities are common in patients with advanced heart failure. Chronically elevated right sided pressures and resulting hepatic congestion can cause progressive parenchymal changes including nodular regenerative hyperplasia (NRH) and fibrosis. Liver dysfunction and/or liver nodularity on imaging necessitates transjugular liver biopsy (TJLB) to assess for irreversible liver damage. Little is known about post-heart transplant (HT) liver architecture changes. We present a patient with nodular liver parenchyma due to NRH who experienced resolution of NRH after HT. Case Report A 43 year old man with non-ischemic cardiomyopathy, ejection fraction of 15%, and severely depressed right ventricular function was evaluated for HT. Liver function tests (LFT) were abnormal (AST 46, ALT 35, total bilirubin 1.6, alkaline phosphatase (AP) 141) and ultrasound revealed liver nodularity. Right heart catheterization (RHC) revealed elevated pressures (right atrium (RA) 18 mmHg, pulmonary artery (PA) 69/30 mmHg). TJLB had zone 3 sinusoidal dilation and congestion, stage 1 fibrosis, and NRH. 10 months post-HT, LFTs remained elevated (AST 41, ALT 71, total bilirubin 0.8, AP 121) while RHC showed improvement (RA 8 mmHg, PA 35/8 mmHg). Magnetic resonance elastography (MRE) was notable for hepatic stiffness (3 kPa) consistent with stage 1-2 fibrosis. Repeat TJLB showed minimal zone 3 fibrosis (stage 1) without NRH. 32 months post-HT, LFTs were improved (AST 42, ALT 49, total bilirubin 1.1, AP 65), repeat MRE showed slight reduction in stiffness (2.8 kPa), and RHC pressures were stable (RA 11 mmHg, PA 39/21 mmHg). Summary This case shows that congestive hepatopathy induced NRH may resolve after HT. NRH, characterized by focal liver regeneration without evidence of fibrosis, results from dysfunctional hepatic blood flow. Liver regions receiving normal or increased blood flow hypertrophy and form nodules while hypoperfused areas atrophy. Clinically, NRH can lead to portal hypertension and associated complications. TJLB in HT candidates allows closer examination of parenchymal injury. The goal of TJLB is to differentiate reversible liver injury from permanent damage, as the latter is a contraindication to HT. There is a paucity of information about post- HT parenchymal changes and prospective case series are needed to characterize hepatic recovery following HT.
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