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.
With resmetirom now available for MASH, combination approaches are being explored, so the standard of care in this area is moving faster than most threads assume.
What I am after is whether normalised enzymes tell you anything about fibrosis, and what the right follow-up measurement is.
I would rather have one careful answer than five confident ones.
KevinCompounds 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.
julia.endo said:Liver ultrasound comparison for liver and MASH: my hepatologist ordered serial ultrasounds to track NAFLD regression.
Liver enzyme update related to liver and MASH: I had mildly elevated ALT/AST at baseline (likely NAFLD). After 9 months on GLP-1 therapy:
| Marker | Baseline | Current | Normal Range |
|---|---|---|---|
| ALT | 60 | 27 | 7-56 U/L |
| AST | 63 | 23 | 10-40 U/L |
| GGT | 80 | 31 | 9-48 U/L |
| ALP | 110 | 72 | 44-147 U/L |
FibroScan also improved — liver stiffness from 8.5 kPa to 6.2 kPa. The evidence for GLP-1 agonists in NAFLD/NASH is very promising.
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Shop Reference StandardsKevinCompounds said:Fatty liver on an incidental scan two years ago and nobody followed it up.
Can confirm. Same sequence, different timescale. I had assumed I was the exception until I read this.
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.