Adding the numbers, since they settle part of this. 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.
Ask again with the specifics and you will get a better answer than this one.
A narrower follow-up, since the general answer is now clear:
Whether normalised enzymes tell you anything about fibrosis, and what the right follow-up measurement is?
LabKate said:With resmetirom now available for MASH, combination approaches are being explored, so the standard of care in this area is moving faster than most…
There is a second half to this that has not been said yet. The liver data is among the strongest non-weight findings in the class. The semaglutide MASH programme reported a large advantage over placebo on MASH resolution, with a substantial minority also achieving fibrosis improvement — and fibrosis is the endpoint that predicts outcomes. Mechanistically it is reduced hepatic lipogenesis, increased fatty-acid oxidation, less hepatic inflammation, and possibly a direct effect on stellate-cell activation.
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Shop Reference StandardsOP back with an update, since a thread like this is useless without one.
Follow-up: I read the paper rather than the summary and the qualifier I was missing was in the second paragraph of the results.
LindaRN_retired said:The liver data is among the strongest non-weight findings in the class.
Forest plot interpretation for the the trial evidence meta-analysis: when reading the pooled estimate, pay attention to:
- Point estimate (HR/RR/OR) — center of the diamond
- Confidence interval width — precision of the estimate
- I² statistic — heterogeneity across studies
- Individual study weights — are results driven by one large trial?
- Prediction interval — range of plausible true effects in future settings
The the trial evidence meta-analysis shows a pooled RR of 0.85 (95% CI 0.65-0.90), I²=58%. This is a robust and consistent effect.