Fatty liver on an incidental scan two years ago and nobody followed it up. Now that I am losing weight I would like to know what to re-measure.
What I am trying to establish is whether normalised enzymes tell you anything about fibrosis, and what the right follow-up measurement is.
Numbers rather than impressions, if you have them.
AttorneyGrant said:Fatty liver on an incidental scan two years ago and nobody followed it up.
Liver imaging follow-up for liver and MASH: FibroScan at baseline showed CAP score 312 dB/m (moderate steatosis) and stiffness 8.8 kPa (possible fibrosis). Diagnosed with NAFLD.
After 10 months: CAP dropped to 225 dB/m (minimal steatosis) and stiffness normalized to 4.8 kPa. Hepatologist says the liver is essentially healing itself as the metabolic stress resolves.
GLP-1 agonists may become first-line NASH therapy. The Phase 3 data on semaglutide for NASH is very promising.
labquiet_amy said:Liver imaging follow-up for liver and MASH: FibroScan at baseline showed CAP score 312 dB/m (moderate steatosis) and stiffness 8.8 kPa (possible…
ATTAIN trial (survodutide) context for liver and MASH: survodutide, a GLP-1/glucagon dual agonist, showed -18.7% body weight at 46 weeks in the Phase 3 ATTAIN trial. NASH resolution was achieved in ~60% of patients[1].
This is relevant to liver and MASH because survodutide's glucagon agonism specifically targets hepatic lipid metabolism — making it potentially the best-in-class agent for NASH/MAFLD comorbid with obesity.
[1] Sanyal AJ, et al. N Engl J Med. 2024.
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Shop Reference StandardsAttorneyGrant said:Fatty liver on an incidental scan two years ago and nobody followed it up.
Mine went the same way, slower.
Clinical perspective, offered as context rather than as advice.
NASH/MAFLD therapeutic landscape and liver and MASH: GLP-1 agonists are emerging as potential first-line NASH therapy. The Phase 2b data for semaglutide showed 59% NASH resolution (vs 17% placebo) with 43% achieving fibrosis improvement[1].
Mechanism: GLP-1R activation reduces hepatic lipogenesis, increases fatty acid oxidation, reduces hepatic inflammation, and may directly reduce hepatic stellate cell activation (fibrosis pathway).
With resmetirom (thyroid hormone receptor agonist) recently approved for NASH, the field is evolving rapidly. Combination approaches (GLP-1 + resmetirom) are being explored.
[1] Newsome PN, et al. N Engl J Med. 2021;384(12):1113-1124.