An Arterial‐Enhancing Liver Nodule With Washout in a Patient With Metabolic and Alcohol‐Associated Liver Disease

Abstract

A 74‐year‐old man with metabolic dysfunction and alcohol‐related liver disease (MetALD), with an alcohol intake of 280 g per week, was referred to our hepatology center for evaluation of a 5.3‐cm hepatic nodule detected on ultrasonography, which showed heterogeneous hypoechogenicity (Figure 1A). Serologic testing revealed positivity for hepatitis B core antibody with negative hepatitis B surface antigen and hepatitis C antibody. He had a family history of hepatitis B virus‐related liver cirrhosis in his mother. Liver function tests showed total bilirubin, 0.9 mg/dL; albumin 4.6 g/dL; aspartate aminotransferase, 167 U/L; alanine aminotransferase, 35 U/L; alkaline phosphatase, 58 U/L; and gamma glutamyl transferase, 129 U/L. Serum tumor markers, including alpha‐fetoprotein (3.69 ng/mL), carbohydrate antigen 19‐9 (20.1 ng/mL), and des‐γ‐carboxy prothrombin (23.13 mAU/mL), were within normal ranges. His FIB‐4 index was 9.08, and the nonalcoholic fatty liver disease fibrosis score was 3.33, suggesting advanced hepatic fibrosis or cirrhosis [1]. Upper endoscopy and colonoscopy showed no remarkable findings. To further characterize the hepatic lesion, dynamic contrast‐enhanced magnetic resonance imaging (MRI) using gadoxetate disodium was performed. A 5.3‐cm lesion in segment IV demonstrated arterial phase hyperenhancement (Figure 1B), followed by washout with partial capsular enhancement during the portal venous phase and hypointensity on the hepatobiliary phase (Figure 1C,D), consistent with LI‐RADS 5. In addition, the lesion exhibited diffusion restriction on diffusion‐weighted imaging (Figure 1E,F).

FIGURE 1.

Image findings on ultrasound and liver dynamic magnetic resonance imaging (MRI) with gadoxetate disodium. (A) Ultrasound imaging. Arterial phase (B), portal venous phase (PVP) (C), hepatobiliary phase (HBP), diffusion weighted image (DWI), and apparent diffusion coefficient (ADC) of the lesion on MRI.

1. What Is the Diagnosis of the Patient?

While hypervascular hepatic tumors with washout should be differentiated from hypervascular metastatic tumors, combined hepatocellular‐cholangiocarcinoma, hepatic adenoma, and sarcomatous tumors, based on the MRI findings fulfilling LI‐RADS 5 criteria and the presence of MetALD with advanced fibrosis or cirrhosis, HCC was initially suggested [2, 3, 4]. According to the updated Barcelona Clinic Liver Cancer (BCLC) guidelines (2026), the patient was classified as early stage (stage A) disease with preserved liver function; accordingly, surgical resection with laparoscopic left hemihepatectomy was performed for both diagnostic confirmation and curative intent [5]. Gross examination revealed a well‐demarcated, round tumor measuring 5.3 cm with a pinkish, firm cut surface (Figure 2A). Histopathological analysis demonstrated spindle‐shaped tumor cells with frequent mitoses (10 per 50 high‐power fields) (Figure 2B–D). Immunohistochemical staining showed strong positivity for c‐KIT (CD117) and CD34 (Figure 2E,F), confirming the diagnosis of a primary hepatic gastrointestinal stromal tumor (GIST). After resection, the patient received adjuvant imatinib therapy and has remained free of disease recurrence.

FIGURE 2.

Histopathology of the hepatic tumor. Gross specimen (A) and microscopic images with Hematoxylin and Eosin (H&E) (B‐D), C‐kit (E), and CD34 (F) staining.

GISTs are rare mesenchymal malignancies, typically arising from the gastrointestinal tract, with a median age at diagnosis of 60–65 years [6]. Primary hepatic GISTs are exceedingly rare, with only approximately 40 cases reported in the literature, and are thought to originate from interstitial Cajal‐like cells within the liver [7, 8]. They are also commonly associated with mutations in the KIT and PDGFRA genes [7, 8]. On imaging, hepatic GISTs often present as hypoattenuating lesions on computed tomography, while no characteristic MRI features have been definitively established [9]. However, hypointensity on the hepatobiliary phase and diffusion restriction may reflect the high cellularity of GISTs [6, 9]. Interestingly, in this case, the hepatic GIST exhibited typical HCC‐like imaging features in a patient with chronic liver disease, which made the preoperative diagnosis particularly challenging. As in our case, the standard treatment for localized GIST consists of surgical resection followed by 3 years of adjuvant imatinib therapy (400 mg once daily) in high‐risk cases [6, 7].

In conclusion, even in patients with chronic liver disease and typical radiological features of HCC, rare hepatic tumors such as primary hepatic GIST should be considered in the differential diagnosis.

Funding

This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (Ministry of Science and ICT, MSIT) (RS‐2024‐00451810) (S.K.L.). This research was also supported by a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (grant number: RS‐2025‐25459150).

Consent

Consent was obtained directly from the patient.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.