Prevalence of advanced fibrosis similar in lean, non-lean MASLD, linked to genetic risk
Click Here to Manage Email Alerts
Key takeaways:
- Prevalence of advanced fibrosis was similar between patients with lean and non-lean MASLD.
- Prevalence of PNPLA3 risk variants and HSD17B13 protective variants also was similar between groups.
WASHINGTON — The risk for advanced fibrosis was similar among patients with lean and non-lean metabolic dysfunction-associated steatotic liver disease and may be associated with genetic risk, according to data at Digestive Disease Week.
“There are conflicting studies on the severity of MASLD in patients with a normal BMI, termed lean MASLD, which is estimated to affect up to 10 million Americans,” Veeral H. Ajmera, MD, MAS, medical director of liver transplantation and associate professor of medicine at University of California, San Diego, told Healio. “We compared the burden of fibrosis in prospectively recruited patients with MASLD who were lean, overweight, obese or morbidly obese.”
In a cross-sectional study, Ajmera and colleagues identified 313 patients with MASLD from the UCSD MASLD Research Center (mean age, 58.3 years; 69.3% women; 42.8% Hispanic), of whom 45 had lean MASLD (BMI < 25 kg/m² or < 23 kg/m² in Asians) and were matched 1:2:2:2 based on age and sex to 90 overweight patients, 90 with obesity and 88 with morbid obesity.
All patients underwent MRI proton density fat fraction, magnetic resonance elastography (MRE), vibration-controlled transient elastography (VCTE) and controlled attenuation parameter. Additionally, researchers assessed the effect of a simple polygenic risk score (PRS) using established effect alleles in PNPLA3 and HSD17B13.
Studied outcomes included prevalence of advanced fibrosis, defined on liver biopsy or MRE of at least 3.63 kPa, as well as the prevalence of PNPLA3 risk variants and HSD17B13 protective variants in lean and non-lean MASLD.
According to results, there was no statistically significant difference in prevalence of advanced fibrosis between lean and non-lean MASLD (22% vs. 22%), with similar mean MRE reported between groups as well (2.96 kPa). There was, however, a nonsignificant trend toward lower MRE in overweight MASLD and higher MRE in morbidly obese MASLD.
“We found that lean MASLD patients had a similar amount of fibrosis as non-lean MASLD patients,” Ajmera said. “There was a nonsignificant trend toward more severe disease in those with morbid obesity.”
In addition, prevalence of cirrhosis was higher in lean MASLD (20% vs. 11%), although the trend was not significant.
Further, a dichotomized simple PRS correlated with advanced fibrosis and performed similarly among patients with lean and non-lean MASLD (26.7% vs. 26.1%).
Genetic risk evaluated at PNPLA3 and HSD17B13 did not differ significantly between lean and non-lean groups, Ajmera noted, although “the presence of PNPLA3 risk alleles was associated with fibrosis” and was similar in both lean and non-lean MASLD groups (26.3% vs. 24.8%).
“Lean MASLD is not a benign entity and shares a similar burden of fibrosis and genetic pathogenic drivers to non-lean MASLD,” Ajmera told Healio. “Lean MASLD patients warrant close clinical assessment and monitoring similar to non-lean MASLD patients.”
He continued, “Knowledge of genetic risk may help risk stratify patients with MASLD.”
Collapse
Ajmera VH, et al. Lean, overweight and obese MASLD patients have similar amounts of fibrosis that is associated with polygenic risk style. Presented at: Digestive Disease Week; May 18-21, 2024; Washington (hybrid).
Click Here to Manage Email Alerts