The recent ACG guideline says that test-of-cure is required in all patients after treatment. Urea breath test or fecal antigen, at least 4 weeks post-completion, PPIs held for 2 weeks prior.

As a GI doctor, I believe in this recommendation. But in my experience, test-of-cure is one of those things that falls apart at the follow-up stage. Patient might be feeling fine, symptoms might be resolved, they don't come back. Or the ordering physician assumes someone else will arrange it. Or the patient gets the test but still has PPI on board because nobody told them to stop it, and you get a false negative.

I have started giving patients a written instruction sheet at the time of prescription: Please Finish antibiotics, wait 4 weeks, stop PPI 2 weeks before the breath test, then call me.

But I am yet to find a system-level solution for this,

Genuinely asking because I might be misreading the room here.

The NCD-RisC paper is technically using "plateau" correctly. It says that prevalence stopped accelerating in the US, UK, Canada around the early 2000s.

Ref: NCD Risk Factor Collaboration (NCD-RisC). Obesity rise plateaus in developed nations and accelerates in developing nations. Nature (2026).

The US plateaued at 23% childhood obesity in boys. France plateaued at 3-4%. Both get labelled plateaued. That's not the same phenomenon according to me. That's two completely different baselines that both stopped moving. A plateau at 40% isn't a plateau.

And in GI specifically, a plateau in prevalence doesn't do anything for the downstream queue. The 20-year lag between obesity onset and MASLD cirrhosis, Barrett's progression, colorectal cancer - that cohort that plateaued in 2005 is who I'm scoping right now.

The LMIC framing bothers me more though. Several of those trajectories aren't "catching up to Western levels". Maybe I'm reading too much into language. But words matter when they reach health ministers and hospital planners.

Is anyone else noticed this framing in how the paper's being discussed?

Genuinely asking because I might be misreading the room here.

The NCD-RisC paper is technically using "plateau" correctly. It says that prevalence stopped accelerating in the US, UK, Canada around the early 2000s.

Ref: NCD Risk Factor Collaboration (NCD-RisC). Obesity rise plateaus in developed nations and accelerates in developing nations. Nature (2026).

The US plateaued at 23% childhood obesity in boys. France plateaued at 3-4%. Both get labelled plateaued. That's not the same phenomenon according to me. That's two completely different baselines that both stopped moving. A plateau at 40% isn't a plateau.

And in GI specifically, a plateau in prevalence doesn't do anything for the downstream queue. The 20-year lag between obesity onset and MASLD cirrhosis, Barrett's progression, colorectal cancer - that cohort that plateaued in 2005 is who I'm scoping right now.

The LMIC framing bothers me more though. Several of those trajectories aren't "catching up to Western levels". Maybe I'm reading too much into language. But words matter when they reach health ministers and hospital planners.

Is anyone else noticed this framing in how the paper's being discussed?

Genuinely asking because I might be misreading the room here.

The NCD-RisC paper is technically using "plateau" correctly. It says that prevalence stopped accelerating in the US, UK, Canada around the early 2000s.

Ref: NCD Risk Factor Collaboration (NCD-RisC). Obesity rise plateaus in developed nations and accelerates in developing nations. Nature (2026).

The US plateaued at 23% childhood obesity in boys. France plateaued at 3-4%. Both get labelled plateaued. That's not the same phenomenon according to me. That's two completely different baselines that both stopped moving. A plateau at 40% isn't a plateau.

And in GI specifically, a plateau in prevalence doesn't do anything for the downstream queue. The 20-year lag between obesity onset and MASLD cirrhosis, Barrett's progression, colorectal cancer - that cohort that plateaued in 2005 is who I'm scoping right now.

The LMIC framing bothers me more though. Several of those trajectories aren't "catching up to Western levels". Maybe I'm reading too much into language. But words matter when they reach health ministers and hospital planners.

Is anyone else noticed this framing in how the paper's being discussed?

I went through the discussions that happened in DDW 2026 in Chicago. And the highlight that I loved the most is that -> EUS is no longer an advanced skill. It's becoming the baseline.

It wasn't in just one session. It was every session.

The other thing that struck me the most was that - the economics track was unusually direct. Demonstrating EUS value to payers (diagnostic yield, downstream decision impact, procedure pairing efficiency) is now being framed as a survival skill for GI programs, not an administrative afterthought.

There was also strong signal on ESG finally being positioned less as "bariatric lite" and more as a legitimate first intervention in appropriate obesity patients, with 18-24 month weight loss data.

And quietly, the target trial emulation data on early ERCP in elderly choledocholithiasis. The reflex to scope everyone urgently is being challenged with actual numbers now.

A lot came out of DDW. But if you can only act on one thing right now is that if your the GI program doesn't have a structured EUS training, you're already behind.

As a GI practitioner, are you communicating this in your clinics/labs??

I have been seeing SDD dismissed in ICU rounds with "but resistance".

See! I get it, the concern makes biological sense. But every time I go back to the actual trial data, I can't find solid evidence that it's happening at the unit level.

I was reading this article on NEJM, The RGNOSIS trial compared SDD, SOD, and chlorhexidine across 13 Dutch ICUs. No significant increase in resistant Gram-negative carriage during SDD periods. And chlorhexidine actually performed worse on outcomes.

Meanwhile the updated Bayesian meta-analysis (30+ RCTs, 24,000+ patients) puts the posterior probability of ICU mortality benefit from SDD above 95%. That's almost as strong as RCT evidence gets in critical care.

The way I'm reading it now is!

• Low-to-moderate resistance settings (<20% ESBL) → SDD should work, resistance concern not borne out in trial durations
• High carbapenem-resistance settings → picture is murkier, SOD alone may be the pragmatic call
• Chlorhexidine → worse outcomes, arguably less justification than SDD

Am I reading this wrong, or is the resistance concern doing more work than the data supports?

Let me know if you want article links.

Something that confused me for a while in medicine postings is that - HE patient comes in confused, ammonia is high, and lactulose gets started.

But nobody is talking about how Ammonia doesn't grade the patient. West Haven can do that, and it's purely clinical.

• Grade 1: oriented but slightly off, altered sleep
• Grade 2: disoriented to time, asterixis on examination
• Grade 3: somnolent, arousable but can't follow commands
• Grade 4: coma

A Grade 3 patient can have a "not that high" ammonia. A compensated cirrhotic can have a sky-high ammonia and look fine. The number is not the diagnosis.

The bigger point I am trying to make is that lactulose doesn't end the case. Finding the precipitant does.

Cirrhotic patients with SBP are often afebrile. No fever, no obvious peritonism. The only way to catch it is diagnostic paracentesis.

The full checklist in my opinion should be THIS: GI bleed → infection (SBP, UTI, pneumonia) → electrolytes (low sodium, low potassium) → renal function → medications (benzodiazepines, opioids) → diuretic overdose.

For those in medicine or GI postings RIGHT NOW, is this being taught clearly at your centre, or is it mostly "start lactulose and check ammonia" on the ward?

Something that confused me for a while in medicine postings is that - HE patient comes in confused, ammonia is high, and lactulose gets started.

But nobody is talking about how Ammonia doesn't grade the patient. West Haven can do that, and it's purely clinical.

• Grade 1: oriented but slightly off, altered sleep
• Grade 2: disoriented to time, asterixis on examination
• Grade 3: somnolent, arousable but can't follow commands
• Grade 4: coma

A Grade 3 patient can have a "not that high" ammonia. A compensated cirrhotic can have a sky-high ammonia and look fine. The number is not the diagnosis.

The bigger point I am trying to make is that lactulose doesn't end the case. Finding the precipitant does.

Cirrhotic patients with SBP are often afebrile. No fever, no obvious peritonism. The only way to catch it is diagnostic paracentesis.

The full checklist in my opinion should be THIS: GI bleed → infection (SBP, UTI, pneumonia) → electrolytes (low sodium, low potassium) → renal function → medications (benzodiazepines, opioids) → diuretic overdose.

For those in medicine or GI postings RIGHT NOW, is this being taught clearly at your centre, or is it mostly "start lactulose and check ammonia" on the ward?

Something that confused me for a while in medicine postings is that - HE patient comes in confused, ammonia is high, and lactulose gets started.

But nobody is talking about how Ammonia doesn't grade the patient. West Haven can do that, and it's purely clinical.

• Grade 1: oriented but slightly off, altered sleep
• Grade 2: disoriented to time, asterixis on examination
• Grade 3: somnolent, arousable but can't follow commands
• Grade 4: coma

A Grade 3 patient can have a "not that high" ammonia. A compensated cirrhotic can have a sky-high ammonia and look fine. The number is not the diagnosis.

The bigger point I am trying to make is that lactulose doesn't end the case. Finding the precipitant does.

Cirrhotic patients with SBP are often afebrile. No fever, no obvious peritonism. The only way to catch it is diagnostic paracentesis.

The full checklist in my opinion should be THIS: GI bleed → infection (SBP, UTI, pneumonia) → electrolytes (low sodium, low potassium) → renal function → medications (benzodiazepines, opioids) → diuretic overdose.

For those in medicine or GI postings RIGHT NOW, is this being taught clearly at your centre, or is it mostly "start lactulose and check ammonia" on the ward?

I've been thinking about this more than I should.

I have been practicing in India for 20 years now! Most of us were trained on PPI + clarithromycin + amoxicillin as the default first move. It's still what gets prescribed in a huge chunk of Indian centres. But the resistance data is pretty hard to ignore at this point.

National clarithromycin resistance is sitting around 35–45%, and in some southern cities it's pushing 60-96% depending on whose data you trust.

The Maastricht VI threshold for abandoning empiric clarithromycin is 15%. We crossed that nationally years ago.

I am worried now! If you prescribe CLR triple empirically in Hyderabad or Chennai right now, you're statistically more likely to fail than succeed.

The ACG 2024 guideline made bismuth quadruple therapy its only strong first-line recommendation.

And yet, the common pushback I hear is that --> metronidazole resistance in India is nearly 80%, so BQT won't work either. BQT's efficacy holds against metronidazole resistance when you use adequate doses (≥1500mg/day) for 14 days.

"I don't have local data so I'll assume it's okay" doesn't hold up anymore as per my understanding.

Has anyone had pushback from colleagues when trying to move away from triple therapy? As students - what is the status at your clinics/hospitals?

I've been thinking about this more than I should.

Most of us were trained on PPI + clarithromycin + amoxicillin as the default first move. It's still what gets prescribed in a huge chunk of Indian centres. But the resistance data is pretty hard to ignore at this point.

National clarithromycin resistance is sitting around 35–45%, and in some southern cities it's pushing 60-96% depending on whose data you trust.

The Maastricht VI threshold for abandoning empiric clarithromycin is 15%. We crossed that nationally years ago.

I am worried now! If you prescribe CLR triple empirically in Hyderabad or Chennai right now, you're statistically more likely to fail than succeed.

The ACG 2024 guideline made bismuth quadruple therapy its only strong first-line recommendation.

And yet, the common pushback I hear is that --> metronidazole resistance in India is nearly 80%, so BQT won't work either. BQT's efficacy holds against metronidazole resistance when you use adequate doses (≥1500mg/day) for 14 days.

"I don't have local data so I'll assume it's okay" doesn't hold up anymore as per my understanding.

Has anyone had pushback from colleagues when trying to move away from triple therapy? I am still processing all these!

I was going through my notes from the APASL conference 2026.

The goalposts in chronic HBV management have shifted enough that I wanted to organize it for myself.

Tried to map it out:

• HBsAg quant + pgRNA are now tracked alongside viral load
• Low HBsAg (<100 IU/mL) + undetectable pgRNA at end of NUC treatment = meaningfully higher chance of sustained HBsAg loss post-stop
• Functional cure (sustained HBsAg loss off therapy) is now the explicit target. Not just a virological suppression

From what I understand, the practical shift is that - every annual review should document HBsAg quantification, not just HBV DNA. Because if you're not measuring it, you can't identify which patients are positioning for finite treatment or stop eligibility.

Is this framework too simplified? Specifically, how much weight are people actually putting on pgRNA in clinical practice right now, given lab availability is inconsistent?

APASL 2026 in Istanbul had a whole session on liver transplantation in the MAFLD era and the framing was blunt. Centers are still using BMI cutoffs as a soft exclusion.

The argument made there was that MAFLD transplant patients who go through formal pre-listing metabolic evaluation are showing outcomes comparable to non-MAFLD etiologies at experienced centers.
Obesity alone isn't the variable that drives poor outcomes. The primary variable is uncontrolled metabolic risk, which is addressable.

The worry I have here is that this makes listing decisions significantly more subjective and resource-dependent. Centers without a formal MAFLD transplant protocol will apply different thresholds than those with one. That variation is going to matter a lot for patients.

How are people actually navigating this at their center? Is there a formal protocol, or is it still attending-dependent?

Have you all read about Rome V?

Rome IV required symptoms for at least 6 months before you could confidently diagnose IBS. Rome V (released recently) has formally introduced parallel "Clinical Criteria".

Qualitative symptom pattern is the same, but the 6-month requirement is gone. It is replaced by 8 weeks, with the real qualifying bar being whether the patient is bothered enough to seek care.

There's data showing ~25% of people with DGBI symptoms don't meet full Rome research criteria but still have meaningful quality-of-life impairment.

But here's a thing running in my mind. The 6-month threshold filtered out transient GI complaints. Shortening the window and leaning on "bothersome-ness" as the anchor NOW pushes more of that judgment back onto the clinician.

What do you think about this reform? Are you actually going to use 8 weeks as your threshold now? Or still defaulting to 6 months?

GBS, Rockall, AIMS65

These are the three scoring systems. They are all validated, and used interchangeably in most departments I've worked in.
It took me longer than I would like to admit to figure out they're actually asking different questions.

So, I am trying to simplify it for my own department:

• GBS → pre-endoscopy, admission vs. discharge decision. GBS ≤1 = strong case for sending home or outpatient scope
• Rockall → post-endoscopy, rebleeding and mortality risk. Needs the endoscopic findings to be meaningful. Rockall ≤2 = safe to discharge after scoping. Not to use the pre-scope version alone
• AIMS65 → in-hospital mortality prediction, not triage. Albumin, INR, mental status, BP, age >65. Useful for deciding who needs ICU-level monitoring, not great just for admissions

From what I understand is that if we use GBS to triage, then scope, then Rockall to decide disposition is actually a logical sequential workflow. The problem is most places are just picking one score.

AIMS65 ≥2 in a patient already admitted probably warrants a more senior conversation about their care.

Is this a reasonable way to frame it, or am I oversimplifying the overlap between GBS and Rockall?

GBS, Rockall, AIMS65

These are the three scoring systems. They are all validated, and used interchangeably in most departments I've worked in.
It took me longer than I would like to admit to figure out they're actually asking different questions.

So, I am trying to simplify it for my own department:

• GBS → pre-endoscopy, admission vs. discharge decision. GBS ≤1 = strong case for sending home or outpatient scope
• Rockall → post-endoscopy, rebleeding and mortality risk. Needs the endoscopic findings to be meaningful. Rockall ≤2 = safe to discharge after scoping. Not to use the pre-scope version alone
• AIMS65 → in-hospital mortality prediction, not triage. Albumin, INR, mental status, BP, age >65. Useful for deciding who needs ICU-level monitoring, not great just for admissions

From what I understand is that if we use GBS to triage, then scope, then Rockall to decide disposition is actually a logical sequential workflow. The problem is most places are just picking one score.

AIMS65 ≥2 in a patient already admitted probably warrants a more senior conversation about their care.

Is this a reasonable way to frame it, or am I oversimplifying the overlap between GBS and Rockall?

Cirrhotic patients with ascites make me hell nervous. The window to act is generally narrow. And the albumin decision is sometimes confusing.

I have made a framework for myself (which is kind of WIP).

1. Tap anyone with cirrhosis + ascites + any clinical suspicion
2. PMN ≥ 250/mm³ → SBP. In this case, I don't wait for culture. Treat.
3. Blood-tinged fluid? Subtract 1 PMN per 250 RBCs (otherwise, it can be false positive)
4. Community-acquired → cefotaxime 2g q8h × 5 days
5. Healthcare-associated or unit has MDRO signal → skip to pip-tazo or carbapenem upfront
6. Albumin 1.5 g/kg day 1 + 1 g/kg day 3 if Cr > 1, BUN > 30, or bili > 4
7. Repeat tap at 48h. PMN fall < 25% → not responding, escalate and rule out secondary peritonitis
8. Discharge → secondary prophylaxis starts that day, every time

The part that trips me the most in practice is the albumin criteria. The Sort trial numbers (HRS 33% → 10%, mortality 29% → 10%) are hard to argue with.

Is my thought process an oversimplification? How are you making calls in real-life practice?

Cirrhotic patients with ascites make me hell nervous. The window to act is generally narrow. And the albumin decision is sometimes confusing.

I have made a framework for myself (which is kind of WIP).

1. Tap anyone with cirrhosis + ascites + any clinical suspicion
2. PMN ≥ 250/mm³ → SBP. In this case, I don't wait for culture. Treat.
3. Blood-tinged fluid? Subtract 1 PMN per 250 RBCs (otherwise, it can be false positive)
4. Community-acquired → cefotaxime 2g q8h × 5 days
5. Healthcare-associated or unit has MDRO signal → skip to pip-tazo or carbapenem upfront
6. Albumin 1.5 g/kg day 1 + 1 g/kg day 3 if Cr > 1, BUN > 30, or bili > 4
7. Repeat tap at 48h. PMN fall < 25% → not responding, escalate and rule out secondary peritonitis
8. Discharge → secondary prophylaxis starts that day, every time

The part that trips me the most in practice is the albumin criteria. The Sort trial numbers (HRS 33% → 10%, mortality 29% → 10%) are hard to argue with.

Is my thought process an oversimplification? How are you making calls in real-life practice?