DAY 3: Delayed Recognition Leads to Worse Outcomes in Lean Patients with Steatotic Liver Disease

Retrospective data presented at the 2026 Annual Scientific Meeting of the American College of Gastroenterology (ACG 2026) reinforced previous observations that non-obesity-related steatotic liver disease may carry a significant risk of worse hepatic outcomes despite a lower body mass index (BMI) and a reduced burden of metabolic comorbidities. 

Lean metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a distinct phenotype, characterized by hepatic steatosis with cardiometabolic risk despite a normal BMI (defined as a BMI < 25 kg/m²). Recent research has suggested that, even in the absence of obesity, individuals with lean MASLD frequently experience equivalent or higher all-cause and liver-related mortality compared with people with higher BMIs [Chowdhary R et al. Hepatol Res 2026;56:1026-1046]. 

Researchers at the University of Arkansas for Medical Sciences in Little Rock, Arkansas designed a retrospective cohort study of adults with hepatic steatosis and at least one non-BMI-related cardiometabolic risk factor to compare long-term liver outcomes and mortality associated with lean and non-lean MASLD. The investigators used data collected from 47,383 lean and 676,750 non-lean adults with MASLD based in the United States, who were followed up for up to 10 years. Before propensity matching, lean patients were older, more often female, and more often Asian, and carried a lower metabolic burden, reflected in lower rates of type 2 diabetes, hypertension, hyperlipidemia, and metformin use. The final analysis included 47,230 propensity-matched pairs of lean (BMI < 25 kg/m²) and non-lean (BMI ≥25 kg/m²) patients with MASLD. 

Despite the lower metabolic burden, lean patients with MASLD had a 70% higher risk of all-cause mortality and a 34% higher risk of hepatic decompensation compared with their non-lean counterparts. On the other hand, individuals with the lean MASLD phenotype were less likely to develop hepatocellular carcinoma or compensated cirrhosis and less likely to need a liver transplant compared with non-lean individuals.
 
“Lean MASLD is not benign,” lead author Shambhavi Anshumali, MD, an internal medicine resident at the University of Arkansas for Medical Sciences, said during a poster session. “It carries a higher mortality and more decompensation than non-lean MASLD. The combination of fewer cirrhosis and cancer diagnoses with more decompensation suggests delayed recognition. Without an elevated BMI to prompt screening, lean MASLD may first present already decompensated. Lean patients deserve closer surveillance, regardless of BMI.” Cardiometabolic risk factors should prompt screening for MASLD. Moreover, longitudinal data and tracking specific causes of death are critical for mapping the trajectories of progressive liver disease in the lean population, Anshumali added. 

A separate retrospective analysis presented at ACG 2026 showed that lean patients with metabolic dysfunction-associated steatohepatitis (MASH) had worse hepatic outcomes than those living with MASH and obesity (BMI ≥ 30 kg/m²). The propensity-matched, global cohort included 28,578 individuals with lean MASH and an equal number of people with MASH and obesity. Patients with viral hepatitis, alcohol-related liver disease, autoimmune hepatitis, hereditary liver diseases, liver transplantation, pre-existing cirrhosis, or baseline hepatocellular carcinoma were excluded. 

Despite the lower BMI, lean MASH significantly increased risk for cirrhosis, hepatic decompensation, hepatocellular carcinoma, and mortality compared with obesity-associated MASH. Individuals with lean MASH also had higher rates of portal hypertension, ascites, variceal bleeding, and hepatic encephalopathy. 

The authors concluded that lean MASH may represent a biologically distinct and potentially more aggressive disease phenotype that warrants closer surveillance and risk assessment. “Lean MASH is not simply less fat, less disease,” presenting author Elizabeth Beyene, MD, an internal medicine resident at Howard University College of Medicine, remarked. “Despite a normal BMI, patients may have visceral adiposity, insulin resistance, altered lipid metabolism, and ectopic hepatic fat accumulation, promoting hepatocyte injury and inflammation.” The author noted that genetic and metabolic risk factors may be drivers of progressive liver disease even in the absence of obesity. 
Expanding screening and surveillance of steatotic liver disease beyond BMI could improve identification of lean patients who are at risk of disease progression, given that screening models based on BMI alone may underestimate metabolic and hepatic risks in this population.