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 after is whether normalised enzymes tell you anything about fibrosis, and what the right follow-up measurement is.
I have searched first, so if this is covered somewhere point me at it and I will read it.
tampaLisa73 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 331 dB/m (moderate steatosis) and stiffness 9.8 kPa (possible fibrosis). Diagnosed with NAFLD.
After 11 months: CAP dropped to 234 dB/m (minimal steatosis) and stiffness normalized to 5.2 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.
LabKate said:Liver imaging follow-up for liver and MASH: FibroScan at baseline showed CAP score 331 dB/m (moderate steatosis) and stiffness 9.8 kPa (possible…
Liver enzyme update related to liver and MASH: I had mildly elevated ALT/AST at baseline (likely NAFLD). After 7 months on GLP-1 therapy:
| Marker | Baseline | Current | Normal Range |
|---|---|---|---|
| ALT | 71 | 23 | 7-56 U/L |
| AST | 59 | 27 | 10-40 U/L |
| GGT | 66 | 35 | 9-48 U/L |
| ALP | 106 | 73 | 44-147 U/L |
FibroScan also improved — liver stiffness from 9.5 kPa to 6.2 kPa. The evidence for GLP-1 agonists in NAFLD/NASH is very promising.
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Browse GL BiochemtampaLisa73 said:Fatty liver on an incidental scan two years ago and nobody followed it up.
Same pattern here, and in the same order.
Adding the clinical framing, because it changes how the question reads.
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.