What even is MASH? My doc mentioned it and I panicked — anyone have experience?

CarlaRPh_TPA said:

ALT was mildly raised at baseline, normalised at month five, and I now have no idea whether anything happened to the fibrosis that actually matters.

Liver imaging follow-up for liver and MASH: FibroScan at baseline showed CAP score 338 dB/m (moderate steatosis) and stiffness 10.8 kPa (possible fibrosis). Diagnosed with NAFLD.

After 12 months: CAP dropped to 231 dB/m (minimal steatosis) and stiffness normalized to 5.9 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.

SarahChen_PharmD said:

Liver imaging follow-up for liver and MASH: FibroScan at baseline showed CAP score 338 dB/m (moderate steatosis) and stiffness 10.8 kPa (possible…

Liver enzyme update related to liver and MASH: I had mildly elevated ALT/AST at baseline (likely NAFLD). After 6 months on GLP-1 therapy:

FibroScan also improved — liver stiffness from 8.5 kPa to 5.2 kPa. The evidence for GLP-1 agonists in NAFLD/NASH is very promising.

CarlaRPh_TPA said:

ALT was mildly raised at baseline, normalised at month five, and I now have no idea whether anything happened to the fibrosis that actually matters.

Same experience, arrived at from the opposite direction. Posting only so the count is not one.

From the other side of the consultation, briefly.

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.