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Abstract
Background While hepatocellular carcinoma (HCC) may arise in other forms of chronic liver disease without cirrhosis, its occurrence seems to be more prevalent in non-alcoholic fatty liver disease (NAFLD). This poses a significant challenge, as clinical guidelines do not advocate for routine surveillance to detect early-stage HCC in patients lacking cirrhosis or advanced fibrosis. Our objective was to meticulously identify signs of dysplasia within the liver tissues of NAFLD patients who hadn’t yet developed cirrhosis. This dysplasia, if left undetected, possesses the potential to evolve into full-blown hepatocellular carcinoma (HCC), a severe and often fatal consequence.
Methods Sixty-four morbidly obese NAFLD patients were enrolled. Liver biopsies were obtained intraoperatively during bariatric surgery procedures. Formalin-fixed 4-µm thick sections stained with hematoxylin-eosin and Masson’s trichome. Biopsies were examined by two separate, blinded pathologists experienced in the field of liver histopathology. Biopsy findings were assessed for steatosis, ballooning, lobular inflammation & Fibrosis and dysplastic changes. NAFLD activity score (NAS) was derived from the scores for steatosis, lobular inflammation, and hepatocellular ballooning. Liver cell dysplasia was characterized by the presence of cellular and nuclear pleomorphism, Hyperchromasia, loss of polarity, Prominent nucleoli & increased nucleocytoplasmic ratio.
Results Most of our patients had metabolic syndrome (65%) (IDDF2024-ABS-0333 Figure 1). Low-grade dysplasia was detected in two patients out of 64 (4%) (IDDF2024-ABS-0333 Figure 2-3). NAS score of ≥ 5 (definite NASH ‘steatohepatitis’) was present in about 71.9% of cases. Whereas NAS ≤ 3 ‘not NASH ’ was 18.8%, Patients with NAS (3-5) are considered unconfirmed NASH were 9.4% (IDDF2024-ABS-0333 Figure 4). In both patients with low-grade dysplasia, Fibrosis was grade ‘1c’ & NAS score was ‘3’
Conclusions Dysplasia is prevalent in non-cirrhotic patients with NAFLD, which may progress to high-grade dysplasia and HCC. Minimizing the likelihood of HCC emergence among NAFLD patients must become a primary concern. Given that metabolic syndrome is not the only factor escalating NAFLD advancement but also a stand-alone contributor to HCC occurrence, prioritizing lifestyle interventions aimed at addressing these issues should lie at the core of preventive measures.
Prevalence of metabolic syndrome in the studied patients
Section within a liver tissue shows Mild dysplastic changes, atypia & hyperchromasia in liver section (Hematoxylin & Eosin X 400)
Another section in liver tissue showing mild dysplastic changes, atypia & hyperchromasia (H& EX 400)
Prevalence of steatohepatitis according to NAS score in liver biopsy
Definite NASH , liver tissue show mild steatosis (score 1) (blue arrow), marked baloning degeneration (black arrow) (score 2), marked infilammaton (red arrow) (score 3) and perisinasoidal , periportal and bridging fibrosis (F3) (black star) (Hematoxylin & Eosin X 200)