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.
The question I want answered is whether normalised enzymes tell you anything about fibrosis, and what the right follow-up measurement is.
Tell me what I have not thought of.
TrialNerd_Beth said:Fatty liver on an incidental scan two years ago and nobody followed it up.
Liver ultrasound comparison for liver and MASH: my hepatologist ordered serial ultrasounds to track NAFLD regression.
Baseline: "Moderate hepatic steatosis, liver span 17.2cm, echogenic texture consistent with fat infiltration"
Month 8: "Mild steatosis, liver span 15.8cm, improved echogenicity"
Month 14: "Minimal to no steatosis, normal liver span 14.5cm, normal echotexture"
My liver literally shrank and de-fattened. The ultrasound tech said she's seen this pattern increasingly in GLP-1 patients and it's remarkable how consistently the fatty liver resolves.
Dr.AddMedPHL said:Liver ultrasound comparison for liver and MASH: my hepatologist ordered serial ultrasounds to track NAFLD regression.
Liver imaging follow-up for liver and MASH: FibroScan at baseline showed CAP score 326 dB/m (moderate steatosis) and stiffness 10.8 kPa (possible fibrosis). Diagnosed with NAFLD.
After 12 months: CAP dropped to 239 dB/m (minimal steatosis) and stiffness normalized to 6.199999999999999 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.
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Browse GL BiochemTrialNerd_Beth said:Fatty liver on an incidental scan two years ago and nobody followed it up.
Same experience, arrived at from the opposite direction.
From the other side of the consultation, briefly.
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.