A 54-year-old female, who was diagnosed with alcoholic liver disease 8 years ago due to liver dysfunction and abdominal distension was advised to quit alcohol consumption. Two years prior, she experienced worsening joint pain and visited a local clinic. During this visit, liver dysfunction, decreased platelet count, and complement deficiency were observed, prompting a referral to our hospital for a comprehensive evaluation. Upon evaluation at our hospital, the patient exhibited liver dysfunction, decreased platelet count, and elevated indirect bilirubin levels. Further diagnostic workup revealed evidence of hemolysis, including low haptoglobin and elevated reticulocyte count, confirming a diagnosis of hemolytic anemia in addition to hypersplenism. During her hospitalization, her liver function showed improvement. Her drinking history was approximately 14 standard drinks per day in her late thirties. The laboratory data are summarized in Table 1. Detailed examinations, including contrast-enhanced dynamic computed tomography (CT) and gadolinium-ethoxybenzyl-diethylenetriamine-pentaacetic acid-enhanced MRI (Gd-EOB-DTPA-enhanced MRI) were performed to evaluate liver function disorders. Plain CT revealed a diffuse, ill-defined hypodense area within the liver parenchyma, and contrast-enhanced CT revealed non-uniform hypodense areas around the Glisson’s sheath and hepatic veins (Fig. 1a, b). On MRI, the liver parenchyma exhibited non-uniform signal intensity on fat-suppression T2-weighted image (FST2WI), with a prominent low-signal area around the hepatic veins (Fig. 1c). In the hepatobiliary phase (HBP), the liver parenchyma showed a low signal intensity in the same region and R2* mapping indicated elevated values, suggesting iron deposition (Fig. 1d). Fat Fraction mapping revealed a mildly high signal area around the hepatic veins, indicating mild fat deposition. Transjugular liver biopsy (TJLB) was performed to investigate the cause of the hepatic disorder. Histologically, the lobular architecture of the liver was disrupted, and significant fibrosis was observed around the portal areas in a perilobular pattern and around the hepatocytes, often associated with bridging fibrosis. Approximately 10% of the liver parenchyma exhibited fat deposition and features such as ballooning hepatocytes, nuclear glycogen, and focal necrosis were scattered throughout. This condition was considered consistent with alcoholic steatohepatitis and pre-cirrhotic liver changes. Iron staining revealed moderate deposition of positive granules within hepatocytes.

Image and histological findings of case 1. (a) Plain CT: Diffuse ill-defined low-density areas were observed. (b) Equilibrium Phase with Contrast: Heterogeneous low-attenuation areas were noted around the Glisson’s sheath and hepatic veins.　(c) FST2WI: Prominent low-signal areas were observed around the hepatic veins (arrows).　(d) R2*map: High values were detected around the hepatic veins (arrowheads), suggesting iron deposition in the hepatic parenchyma

A 45-year-old female with daily alcohol consumption was diagnosed 8 years ago with depression, alcoholism, and alcoholic cirrhosis after presenting with hallucinations. Over time, her liver function worsened. One year ago, she developed progressive anemia, elevated indirect bilirubin, and low haptoglobin, along with an increase in reticulocytes. After further evaluation by the hematology department, she was diagnosed with spur cell hemolytic anemia associated with alcoholic cirrhosis, and transfusion therapy was initiated. As her liver function worsened, she was referred to our hospital for a brain-dead liver transplant. Pre-transplant contrast-enhanced CT and MRI were conducted. A suitable donor was found during hospitalization, and the transplant was performed. The laboratory data are in Table 1. She had a drinking history of about seven standard drinks per day. Plain CT revealed heterogeneous hypodense areas in the hepatic parenchyma. Contrast-enhanced dynamic CT in the arterial phase revealed a heterogeneous pattern of hypodense areas within the liver parenchyma, whereas in the equilibrium phase, the liver parenchyma showed uniform enhancement. On MRI, the dynamic study findings were showing nonuniform enhancement within the liver parenchyma and prominent areas of poor enhancement around the veins. In the HBP, the same area showed a low signal intensity. The liver parenchyma around the hepatic veins showed signal reduction extending from out-of-phase to in-phase T1-weighted images (T1WI) because of echo time (TE) prolongation, and R2* mapping indicated elevated values, suggesting iron deposition. The same area exhibited low signal intensity on FST2WI (Fig. 2a-f). Pathological findings of the excised liver for brain-dead liver transplantation showed that, grossly, the liver surface had mild irregularities, with a cut surface displaying a yellow to reddish-brown hue and reddish-brown areas prominent around the hepatic veins. Histologically, small regenerative nodules surrounded by fibrous septa were diffusely observed, showing the image of liver cirrhosis. Prominent regenerative nodules with hemosiderin deposition were also observed. The findings were consistent with cirrhosis caused by alcoholic liver disease. Iron staining revealed that the reddish-brown pigment stained blue, indicating a state of hemosiderosis. The reddish-brown areas suspected of iron deposition were grossly prominent around the large hepatic veins, and a significant iron deposition pattern was observed in the same region (Fig. 3).

Image findings of case 2. (a) Contrast T1WI (arterial phase): Heterogeneous enhancement was observed.　(b) EOB HBP: Prominent low-signal areas were observed around the hepatic vein. (c) FST2WI: The same area exhibited a low signal, suggesting iron deposition. (d) T1WI Out of Phase and (e) T1WI In Phase: The liver parenchyma around the hepatic veins showed signal reduction extending from out of phase to in phase T1WI because of TE prolongation. (f) R2*map: High values were detected around the hepatic vein

Pathological findings of case 2. (a) Macroscopically, the liver surface exhibited mild irregularities, and the cut surfaces displayed a range of colors from yellow to reddish-brown tones. Prominent reddish-brown areas were observed around the hepatic veins (indicated by arrowheads).　(b) Comparing the gross findings with the iron staining images, the reddish-brown areas that raised suspicion of iron deposition were more prominent around the large hepatic veins (arrowheads) compared to the areas around the portal vein (arrows)