S5966 Unexpectedly Young Case of HCC

Introduction: Hepatocellular carcinoma (HCC) is the most common primary liver malignancy, typically affecting individuals over age 50 with underlying cirrhosis. Major risk factors include viral hepatitis (hepatitis B and C), alcoholic liver disease, and non-alcoholic fatty liver disease.1 In younger patients, HCC is rare but increasingly linked with obesity and hepatocyte lipid remodeling.2 Pediatric liver cancers typically arise in healthy liver, except in cases like hereditary tyrosinemia and genetic hemochromatosis.2 Hepatitis B (HBV) related HCC often presents at a younger age, though presentation without fibrosis is atypical. This case highlights HCC in a 26-year-old man with no prior liver disease but newly diagnosed HBV. Case Description/Methods: A 26-year-old Latino male presented with epigastric and right upper quadrant (RUQ) abdominal pain. He denied liver disease, alcohol, or drug use. Initial labs showed cholestatic liver injury: aspartate aminotransferase 221 U/L, alanine aminotransferase 261 U/L, alkaline phosphatase 160 U/L, and TBili 1.2 mg/dL. Tumor markers revealed AFP >200,000 ng/mL, PSA 4.41 ng/mL, and normal CEA and CA 19-9 levels. A RUQ ultrasound showed bilateral heterogeneous hyperechoic liver lesions, the largest measuring 11.5 × 10.0 × 7.6 cm. Magnetic resonance imaging confirmed multifocal liver masses with arterial enhancement and delayed washout, suggesting HCC. No cirrhosis or steatosis was noted. Computed tomography (CT) thorax revealed bilateral noncalcified pulmonary nodules. Bone scan and CT head were negative. Colonoscopy was normal; liver biopsy confirmed HCC. Hepatitis serologies showed reactive HBsAg with low-level viremia (HBV DNA 109 IU/mL); HBeAg and anti-HBe were unavailable. HCV and HIV were negative. Labs showed Hgb decline (17.3 to 13.7 g/dL), thrombocytosis (Plt 413), and elevated LDH. Autoimmune and metabolic liver workup was unremarkable. The patient remained stable with no signs of decompensation. He was discharged for outpatient hepatology and oncology follow-up. Discussion: This case illustrates the diagnostic challenges of HCC in young adults without classic risk factors. Despite no cirrhosis, imaging and AFP levels supported the diagnosis. HBV-related HCC may occur in non-cirrhotic livers due to its viral genome integration. Clinicians should suspect HCC in HBV-positive patients, regardless of viral load or fibrosis. Early recognition is crucial for timely interventions, including curative and life-prolonging therapies. References 1. Akinyemiju T, et al. Liver Cancer. StatPearls Publishing; 2023. 2. Kattapuram TM, et al. Pediatric Liver Tumors. StatPearls Publishing; 2023.

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Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001151324.04828.11
Primary Topic
Liver Disease Diagnosis and Treatment
Type
article
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article

S5966 Unexpectedly Young Case of HCC

Masuma Syed, Eric Ngo, Vishvinder Sharma
The American Journal of Gastroenterology
Liver Disease Diagnosis and Treatment
article

S5966 Unexpectedly Young Case of HCC

Masuma Syed, Eric Ngo, Vishvinder Sharma
article en

Abstract

Introduction: Hepatocellular carcinoma (HCC) is the most common primary liver malignancy, typically affecting individuals over age 50 with underlying cirrhosis. Major risk factors include viral hepatitis (hepatitis B and C), alcoholic liver disease, and non-alcoholic fatty liver disease.1 In younger patients, HCC is rare but increasingly linked with obesity and hepatocyte lipid remodeling.2 Pediatric liver cancers typically arise in healthy liver, except in cases like hereditary tyrosinemia and genetic hemochromatosis.2 Hepatitis B (HBV) related HCC often presents at a younger age, though presentation without fibrosis is atypical. This case highlights HCC in a 26-year-old man with no prior liver disease but newly diagnosed HBV. Case Description/Methods: A 26-year-old Latino male presented with epigastric and right upper quadrant (RUQ) abdominal pain. He denied liver disease, alcohol, or drug use. Initial labs showed cholestatic liver injury: aspartate aminotransferase 221 U/L, alanine aminotransferase 261 U/L, alkaline phosphatase 160 U/L, and TBili 1.2 mg/dL. Tumor markers revealed AFP >200,000 ng/mL, PSA 4.41 ng/mL, and normal CEA and CA 19-9 levels. A RUQ ultrasound showed bilateral heterogeneous hyperechoic liver lesions, the largest measuring 11.5 × 10.0 × 7.6 cm. Magnetic resonance imaging confirmed multifocal liver masses with arterial enhancement and delayed washout, suggesting HCC. No cirrhosis or steatosis was noted. Computed tomography (CT) thorax revealed bilateral noncalcified pulmonary nodules. Bone scan and CT head were negative. Colonoscopy was normal; liver biopsy confirmed HCC. Hepatitis serologies showed reactive HBsAg with low-level viremia (HBV DNA 109 IU/mL); HBeAg and anti-HBe were unavailable. HCV and HIV were negative. Labs showed Hgb decline (17.3 to 13.7 g/dL), thrombocytosis (Plt 413), and elevated LDH. Autoimmune and metabolic liver workup was unremarkable. The patient remained stable with no signs of decompensation. He was discharged for outpatient hepatology and oncology follow-up. Discussion: This case illustrates the diagnostic challenges of HCC in young adults without classic risk factors. Despite no cirrhosis, imaging and AFP levels supported the diagnosis. HBV-related HCC may occur in non-cirrhotic livers due to its viral genome integration. Clinicians should suspect HCC in HBV-positive patients, regardless of viral load or fibrosis. Early recognition is crucial for timely interventions, including curative and life-prolonging therapies. References 1. Akinyemiju T, et al. Liver Cancer. StatPearls Publishing; 2023. 2. Kattapuram TM, et al. Pediatric Liver Tumors. StatPearls Publishing; 2023.

The American Journal of GastroenterologyVol. 120(10S2)
Openalex Percentile: Top 49%
Liver Disease Diagnosis and Treatment
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