GenomicsKate ↑ said:

Fatty liver on an incidental scan two years ago and nobody followed it up.

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.

TrialTracker_MD ↑ said:

Liver enzyme update related to liver and MASH: I had mildly elevated ALT/AST at baseline (likely NAFLD).

Coming at TrialTracker_MD’s question from a different direction. Worth answering the question that was asked rather than the one behind it. The narrow version usually has an answer; the broad version usually does not, and answering the broad one is how a thread stops being useful.

A narrower follow-up, since the general answer is now clear:

How would you tell the difference between that and the alternative explanation?

OP back with an update, since a thread like this is useless without one.

Reporting back with a partial result, because a partial result is still better than silence. Two of the three things suggested helped; I cannot separate them and I am not going to pretend otherwise.