The week in GI, filtered to what is worth knowing.

Outpatient positioning is unchanged from the ACG 2025 UC guideline and the AGA living guideline for moderate-to-severe UC. Confirm UC with endoscopy showing continuous colonic inflammation from the rectum plus histology, after excluding infection with two-step C. difficile testing. Treat mild-moderate disease with 5-ASA chosen by route and extent: suppository for proctitis, enema for left-sided disease, oral plus rectal for extensive disease. If 5-ASA fails, treat as moderate-to-severe rather than stepping up gradually. Position advanced therapy by efficacy tier, not by an anti-TNF-first rule. Advanced-therapy-naive, higher efficacy: infliximab, vedolizumab, ozanimod, etrasimod, upadacitinib, risankizumab, guselkumab. Intermediate: golimumab, ustekinumab, tofacitinib, filgotinib, mirikizumab. Lower: adalimumab. Previously TNF-exposed, higher efficacy: tofacitinib, upadacitinib, ustekinumab. Lower: adalimumab, vedolizumab, ozanimod, etrasimod. After anti-TNF primary non-response, switch mechanism rather than cycling within the class. Treat to target (STRIDE-II): endoscopic improvement, Mayo endoscopic subscore 0-1. Begin CRC surveillance 8-10 years after diagnosis for extensive or left-sided disease; isolated proctitis follows average-risk screening. Inpatient care now follows the 2026 AGA Clinical Practice Update (13 best-practice statements). Admit for severe symptoms refractory to outpatient therapy, suspected complications (obstruction, abscess, toxic megacolon) or significant malnutrition, and identify acute severe UC by Truelove-Witts. Give every patient admitted with diarrhea two-step C. difficile testing. Test for CMV, with early endoscopy, if symptoms worsen, the patient is systemically toxic or disease is steroid-refractory. Give routine VTE prophylaxis with LMWH or fondaparinux unless contraindicated, and individualize post-discharge extension. Give IV methylprednisolone 60 mg/day or equivalent; the AGA living guideline says 40-60 mg/day, and higher doses add no benefit. Do not give adjunctive antibiotics without infection. Involve surgery early. Assess response by day 3 (72 h) using stool frequency and CRP (Oxford criteria); do not continue IV steroids beyond about 7 days without response. Rescue steroid non-responders with infliximab (accelerated or intensified dosing in selected patients with high inflammatory burden or protein-losing colopathy), cyclosporine, or a JAK inhibitor at standard or intensified dosing, or with colectomy. Before discharge, the response should be stable and a transition plan should be in place.

Two current US guidelines govern Crohn's disease and should be read together. ACG 2025 (Lichtenstein et al.) remains the reference for diagnosis, mild-to-moderate disease, perianal, postoperative and abscess management. DIAGNOSIS: fecal calprotectin (>50-100 μg/g) separates inflammatory from noninflammatory disease of the colon. Workup is ileocolonoscopy with biopsies, including uninvolved mucosa, plus small-bowel imaging. CTE and MRE are comparable; prefer MRE in patients <35 y and when serial exams are likely. Intestinal ultrasound is an ungraded adjunct. Do routine CRC surveillance in Crohn's colitis. MILD-TO-MODERATE: recommend against oral mesalamine; sulfasalazine only for symptomatic mild colonic CD; ileal-release budesonide 9 mg for induction in ileocecal disease but not for maintenance. MODERATE-TO-SEVERE (AGA Living Guideline, Scott et al., Gastroenterology 2025;169(7):1397-1448, 16 recommendations: 1 strong, 9 conditional, 6 knowledge gaps; updated quarterly, adult outpatients only): RECOMMEND infliximab, adalimumab, ustekinumab, risankizumab, mirikizumab, guselkumab or upadacitinib over no treatment; SUGGEST certolizumab pegol or vedolizumab over no treatment. Advanced-therapy-naive: suggest higher-efficacy agents (infliximab, adalimumab, vedolizumab, ustekinumab, risankizumab, mirikizumab, guselkumab) over lower-efficacy ones (certolizumab pegol, upadacitinib). Prior advanced-therapy (especially anti-TNF) exposure: suggest higher- or intermediate-efficacy agents (adalimumab, risankizumab, guselkumab, upadacitinib; ustekinumab, mirikizumab) over lower-efficacy ones (vedolizumab, certolizumab pegol). Suggest against thiopurine monotherapy for induction; suggest it for maintenance of remission. Suggest SC/IM methotrexate monotherapy; suggest against oral methotrexate. In thiopurine-naive patients starting infliximab, suggest infliximab + thiopurine over infliximab alone. No recommendation on IFX + MTX, adalimumab + immunomodulator, or non-TNF biologic + immunomodulator. After ≥6 months of steroid-free remission on anti-TNF + immunomodulator, suggest withdrawing the immunomodulator and suggest against withdrawing the anti-TNF. SUGGEST upfront advanced therapy over step-up therapy (corticosteroids and/or immunomodulator first). No recommendation on treating to endoscopic vs symptomatic remission. The ACG 2025 moderate-to-severe recommendations (anti-TNF, IFX + thiopurine combination and IL-12/23/IL-23 agents, each strong/moderate; upadacitinib after anti-TNF exposure; steroids for short-term induction only; TPMT/NUDT15 testing before thiopurines) still stand alongside AGA. ACG perianal (infliximab first; drain abscesses and place setons before escalating), postoperative (endoscopy at 6-12 months; anti-TNF strong, vedolizumab conditional in high-risk patients) and intra-abdominal abscess (>2 cm: antibiotics plus drainage, hold immunosuppression) positions are unchanged. THERAPEUTIC ENDOSCOPY (AGA Clinical Practice Update, CGH 2026; details below come from AGA news coverage, not the full text, and are ungraded advice): get cross-sectional imaging before the procedure. Endoscopic balloon dilation is first-line for short strictures (about ≤4-5 cm) with few risk factors (fistula, prestenotic dilation >5 cm, high CRP, prior anti-TNF). Longer or multiple strictures, or ≥3 risk factors, favor surgery.

Outpatient positioning is unchanged from the ACG 2025 UC guideline and the AGA living guideline for moderate-to-severe UC. Confirm UC with endoscopy showing continuous colonic inflammation from the rectum plus histology, after excluding infection with two-step C. difficile testing. Treat mild-moderate disease with 5-ASA chosen by route and extent: suppository for proctitis, enema for left-sided disease, oral plus rectal for extensive disease. If 5-ASA fails, treat as moderate-to-severe rather than stepping up gradually. Position advanced therapy by efficacy tier, not by an anti-TNF-first rule. Advanced-therapy-naive, higher efficacy: infliximab, vedolizumab, ozanimod, etrasimod, upadacitinib, risankizumab, guselkumab. Intermediate: golimumab, ustekinumab, tofacitinib, filgotinib, mirikizumab. Lower: adalimumab. Previously TNF-exposed, higher efficacy: tofacitinib, upadacitinib, ustekinumab. Lower: adalimumab, vedolizumab, ozanimod, etrasimod. After anti-TNF primary non-response, switch mechanism rather than cycling within the class. Treat to target (STRIDE-II): endoscopic improvement, Mayo endoscopic subscore 0-1. Begin CRC surveillance 8-10 years after diagnosis for extensive or left-sided disease; isolated proctitis follows average-risk screening. Inpatient care now follows the 2026 AGA Clinical Practice Update (13 best-practice statements). Admit for severe symptoms refractory to outpatient therapy, suspected complications (obstruction, abscess, toxic megacolon) or significant malnutrition, and identify acute severe UC by Truelove-Witts. Give every patient admitted with diarrhea two-step C. difficile testing. Test for CMV, with early endoscopy, if symptoms worsen, the patient is systemically toxic or disease is steroid-refractory. Give routine VTE prophylaxis with LMWH or fondaparinux unless contraindicated, and individualize post-discharge extension. Give IV methylprednisolone 60 mg/day or equivalent; the AGA living guideline says 40-60 mg/day, and higher doses add no benefit. Do not give adjunctive antibiotics without infection. Involve surgery early. Assess response by day 3 (72 h) using stool frequency and CRP (Oxford criteria); do not continue IV steroids beyond about 7 days without response. Rescue steroid non-responders with infliximab (accelerated or intensified dosing in selected patients with high inflammatory burden or protein-losing colopathy), cyclosporine, or a JAK inhibitor at standard or intensified dosing, or with colectomy. Before discharge, the response should be stable and a transition plan should be in place.

This standard applies to MASLD: hepatic steatosis on imaging or biopsy, at least one cardiometabolic criterion, no other liver disease, and alcohol below the MetALD range. The AGA 2026 MetALD update sets MetALD at about 140-350 g/week of alcohol in women and 210-420 g/week in men, averaged over at least 3 months. MASLD therefore means under about 140 g/week (women) or 210 g/week (men), and drinking above the MetALD range is ALD. Assess alcohol use in every patient with steatotic liver disease at diagnosis and at least once a year, by interview, a validated questionnaire (e.g., AUDIT-C) and/or biomarkers such as phosphatidylethanol (PEth). Advise every patient with steatotic liver disease to stop drinking. Screen people with type 2 diabetes, people with overweight or obesity plus at least one more metabolic risk factor, and anyone with incidental steatosis or raised aminotransferases. Use FIB-4 first. A score below 1.3 (below 2.0 at age 65 or older) is low risk: the patient stays in primary care and repeats FIB-4 every 1-2 years. A score at or above the cutoff goes to a second-line test: VCTE, or ELF if elastography is not available. VCTE below 8 kPa is low risk. VCTE of 8 kPa or more, or ELF of 9.2 or more, means clinically significant fibrosis is likely and the patient should be referred to hepatology. Read liver stiffness with caution if the patient is actively drinking. Reserve biopsy for discordant or unclear results. Lifestyle change is the base of treatment for everyone: at least 5% weight loss improves steatosis, and 10% or more is usually needed for fibrosis to improve. Pharmacotherapy is recommended for adults with non-cirrhotic MASH and F2-F3 fibrosis (by non-invasive tests or biopsy), alongside structured lifestyle intervention and optimised management of comorbidities. The NIT ranges that stand in for F2-F3 differ by society. AASLD uses VCTE 8-15 kPa, MRE 3.1-4.4 kPa or ELF 9.2-10.5. EASL-EASD-EASO 2026 frames the treatable high-risk group as, for example, VCTE 10-20 kPa, MRE 3.1-5.0 kPa or ELF 9.8-11.3. Two drugs are approved: resmetirom (80 mg oral daily, or 100 mg at body weight of 100 kg or more; AASLD Oct 2024 guidance) and semaglutide 2.4 mg subcutaneously once weekly (FDA accelerated approval Aug 2025, AASLD Nov 2025 guidance; in ESSENCE, MASH resolved without fibrosis worsening in 62.9% vs 34.3% on placebo). EASL-EASD-EASO 2026 says to choose between them by patient preference, risks and cardio-renal-metabolic profile. Semaglutide may be preferred with obesity, type 2 diabetes, established cardiovascular disease or high cardiovascular risk. Resmetirom may be prioritised without obesity, or when the patient is already on or cannot tolerate a GLP-1 receptor agonist. On semaglutide, monitoring includes nutrition and sarcopenia assessment, and fibrosis NITs are used over time to judge response. In MASH cirrhosis, resmetirom and semaglutide appear safe but should not be used as MASH-targeted treatment until liver-related benefit is shown. Pioglitazone or vitamin E remain options under the AASLD 2023 guidance. Neither resmetirom nor semaglutide has been formally studied in MetALD. Manage cardiometabolic risk in every patient whatever the fibrosis stage, including statins for ASCVD and control of glucose and blood pressure. On semaglutide, watch for GI side effects and rare risks (AKI, gallbladder disease, pancreatitis, retinopathy, loss of lean mass). For MetALD, treat moderate or severe alcohol use disorder with medication plus behavioural therapy, correct micronutrient deficiencies (folate, thiamine, vitamin D), and do not offer bariatric or endobariatric procedures. HCC surveillance with ultrasound, with or without AFP, every 6 months is indicated only when cirrhosis is present.

Manage portal hypertension without cirrhosis by confirming portal hypertensive features while excluding cirrhosis (liver biopsy is the gold standard), then performing a comprehensive etiology workup (drug history, MPN/thrombophilia/PNH screen, autoimmune, CVID, HIV, schistosomiasis). Treat portal hypertension complications the same as cirrhosis, variceal prophylaxis with NSBB (carvedilol preferred) or EVL, TIPS for refractory or recurrent bleeding, and address the underlying cause by discontinuing offending drugs and treating the specific etiology. For concurrent portal vein thrombosis, anticoagulation decisions should be individualized based on thrombus acuity (recent vs. chronic), bleeding risk, and underlying etiology; liver transplantation is reserved for refractory complications, and HCC surveillance is not routine without cirrhosis.

ACG 2025 (GRADE) is still the governing guideline. The ASGE 2026 consensus Part 2 (modified Delphi, 28 statements at ≥80% agreement; not GRADE) adds endoscopic and pediatric detail without contradicting it. DIAGNOSIS: symptoms of esophageal dysfunction plus ≥15 eos/hpf after excluding other causes of esophageal eosinophilia. A PPI trial is not a diagnostic criterion (PPI-REE abandoned). Do the initial diagnostic EGD off PPI, topical steroid and dietary therapy (ACG key concept; ASGE consensus, which gives no washout duration). Initial assessment is a standard EGD, not a less-invasive modality, so that full biopsies and dilation are possible (ASGE). Take ≥6 esophageal biopsies from ≥2 levels in anyone with symptoms or endoscopic findings consistent with EoE, targeting visible lesions. In CHILDREN with suspected EoE, also biopsy the stomach and duodenum (ASGE). Use EREFS at every endoscopy and report a quantified peak eosinophil count (ACG strong/low; ASGE). TREATMENT (ACG): swallowed topical steroids STRONG/moderate; high-dose PPI CONDITIONAL/low; empiric elimination diet CONDITIONAL/low. Choose a single initial therapy by shared decision-making. Fluticasone or budesonide are both reasonable. Adult doses: PPI double the reflux dose (e.g., omeprazole 20 mg BID or 40 mg daily); budesonide 2-4 mg/day (BOS 2 mg BID); fluticasone 1,760 mcg/day divided. Pediatric doses: PPI 2 mg/kg/day; budesonide 1-2 mg/day; fluticasone 110-880 mcg/day. Allergy testing is not used to direct diets. A 1FED/2FED step-up diet with a dietitian is acceptable, with endoscopic and biopsy confirmation after each reintroduced food. Dupilumab is CONDITIONAL for PPI-nonresponsive patients aged ≥12 (moderate) and for ages 1-11 at ≥15 kg (low). Weight-band dosing: 15-<30 kg 200 mg q2w; 30-<40 kg 300 mg q2w; ≥40 kg 300 mg weekly. Recommendations AGAINST: omalizumab, cromolyn, montelukast. No recommendation for cendakimab, benralizumab, lirentelimab, mepolizumab or reslizumab. DILATION: an adjunct to anti-inflammatory therapy for strictures causing dysphagia (ACG conditional/low). Start low and go slow; target ≥16 mm in adults and adolescents over ≥1 session. In children, ASGE supports dilation of symptomatic strictures or a narrow-caliber esophagus regardless of disease activity, using the same start-low/go-slow approach. MAINTENANCE: continue effective therapy (ACG STRONG despite low evidence) at the lowest effective dose. MONITORING: judge response on symptoms, endoscopy and histology together, never symptoms alone. Assess response endoscopically at 8-12 weeks after starting a PPI or topical steroid. For diet, ACG says 8-12 weeks and ASGE says 6-8 weeks. For dupilumab or biologics, assess at 12-24 weeks (ASGE: up to 24 weeks). Allow appropriate washout or timing after any treatment change before the follow-up EGD (ASGE). Take monitoring biopsies from the most severe-appearing lesions (rings, furrows, exudates) (ASGE). Monitoring biopsies may be limited to the esophagus when prior gastric and duodenal biopsies were normal and nothing new suggests other pathology (ASGE). The histologic response threshold of <15 eos/hpf is a 'may consider' target, read alongside endoscopic and symptom findings. Shorten follow-up after complications. Care gaps of ≥2 years are associated with fibrostenosis. PEDIATRIC (ACG): esophagram for children with dysphagia to assess fibrostenotic disease; feeding therapy and dietitian for feeding dysfunction; growth, development and nutrition are treatment goals.

Diagnose acute pancreatitis (AP) by the Atlanta criteria (2 of 3: characteristic epigastric/LUQ pain, lipase or amylase >3x ULN [lipase preferred for specificity/duration], or characteristic imaging). ACG 2024 stratifies severity risk using SIRS on admission plus bedside risk factors, rising/elevated BUN, rising/elevated hematocrit (>44), obesity (BMI>30), extrapancreatic fluid collections/pleural effusion/infiltrates, altered mental status, and older age/comorbidities, rather than mandating a formal BISAP or APACHE II composite score. Give moderately aggressive lactated Ringer's, most important in the first 6-12 hours, reassessing volume status/BUN/HCT at 6 hours (further aggressive hydration has little added benefit after 24-48h). Start oral low-fat solid food within 24-48h as tolerated in mild disease; if enteral feeding is needed for moderately severe/severe disease, prefer nasogastric over nasojejunal with small-peptide/medium-chain-triglyceride formula and continuous (not bolus/cyclic) feeding; avoid parenteral nutrition if possible. Do not give prophylactic antibiotics, even in severe disease or sterile necrosis; reserve antibiotics for suspected infected necrosis (typically arising 10-14 days in), and choose agents that penetrate pancreatic necrosis while together covering both gut-derived gram-negative enterics and anaerobes, a carbapenem supplies this as monotherapy, whereas a fluoroquinolone or a third-or-higher-generation cephalosporin must be combined with metronidazole; metronidazole alone (anaerobic cover only), or a cephalosporin or a quinolone alone, does not adequately treat infected necrosis. Perform cholecystectomy preferably before discharge for mild acute biliary pancreatitis, and after a second unexplained AP episode even without identified gallstones; reserve ERCP within 24h for AP complicated by cholangitis, with rectal indomethacin +/- pancreatic duct stent and periprocedural hydration to reduce post-ERCP pancreatitis risk. Check triglycerides when gallstones/alcohol are absent (>1000 mg/dL supports a hypertriglyceridemia etiology). For stable pancreatic necrosis, defer surgical, radiological, or endoscopic intervention 4-6 weeks to allow walling-off (step-up approach).

Risk-stratify suspected choledocholithiasis (high >50%, intermediate 10-50%, low <10% probability). HIGH-risk criteria, any of which should directly prompt ERCP: (1) CBD stone on ultrasound or cross-sectional imaging; (2) ascending cholangitis; (3) total bilirubin >4 mg/dL AND dilated CBD (>6 mm in adults with gallbladder in situ, >8 mm after cholecystectomy). Gallstone pancreatitis was deliberately REMOVED as a high-risk criterion in the 2019 revision. INTERMEDIATE risk (abnormal liver biochemical tests, age >55 y, or bile-duct dilation on imaging): the panel suggests confirmation with either EUS or MRCP (conditional recommendation, low-quality evidence; choice by patient preference, local expertise, availability), laparoscopic intraoperative cholangiography (IOC) or intraoperative US are equally sanctioned alternatives. LOW risk: cholecystectomy with or without IOC/intraoperative US if indicated for symptomatic cholelithiasis; no ERCP and no mandatory advanced biliary imaging. In gallstone pancreatitis WITHOUT cholangitis or biliary obstruction/choledocholithiasis, the panel recommends AGAINST urgent (<48 h) ERCP (strong recommendation, low-quality evidence). Same-admission cholecystectomy is recommended for patients with MILD gallstone pancreatitis (consensus, PONCHO-based); ERCP with prophylactic sphincterotomy should not be used as an alternative to cholecystectomy unless surgery is absolutely contraindicated (e.g., recurrent pancreatitis in end-stage liver disease). For large bile-duct stones, the panel suggests endoscopic sphincterotomy followed by large-balloon dilation (ES-LBD) rather than sphincterotomy alone (conditional, moderate); for large AND difficult stones, it suggests intraductal therapy (cholangioscopy-guided EHL or laser lithotripsy) or conventional therapy with papillary dilation, chosen by local expertise, cost, and patient/physician preference (conditional, very low). Timing versus cholecystectomy: pre- or postoperative ERCP or laparoscopic bile-duct clearance for patients at high risk or with positive IOC, depending on local surgical and endoscopic expertise (consensus).

For acute variceal hemorrhage in cirrhosis, resuscitate conservatively with a restrictive RBC transfusion strategy targeting hemoglobin 7-8 g/dL, start a vasoactive agent as soon as bleeding is suspected and before endoscopy (terlipressin, somatostatin, or octreotide; octreotide is the agent available for this indication in US practice) and continue it 2-5 days, and give empiric IV ceftriaxone 1 g every 24 hours in patients with advanced cirrhosis. Perform upper endoscopy within 12 hours of presentation once resuscitated, or as soon as safely possible if the patient is unstable, with band ligation for esophageal varices and for GOV1 (which is treated as an esophageal varix); cardiofundal varices (GOV2 and IGV1) are treated with cyanoacrylate injection, with EUS-guided coil placement with or without cyanoacrylate increasingly used as first-line where expertise exists, and TIPS or BRTO as alternatives or salvage. PPIs started empirically should be stopped immediately after endoscopy unless there is a separate strict indication. Evaluate every patient at presentation for pre-emptive (early) TIPS with a PTFE-covered stent, placed within 72 hours and ideally within 24 hours, in high-risk patients defined as Child-Pugh class C with score under 14 (that is, 10-13) or Child-Pugh class B with score above 7 who have active bleeding at initial endoscopy despite vasoactive drugs; the decision is individualized and multidisciplinary, weighing age, frailty, comorbidity, heart failure, HCC, portal vein thrombosis, and transplant candidacy. For uncontrolled bleeding, a self-expanding covered esophageal metal stent is as effective as balloon tamponade and is the safer option; both are a bridge to definitive therapy (PTFE-covered TIPS) and neither is definitive therapy. Balloon tamponade must NOT be left in place for more than 24 hours, 24 hours is the ceiling, not a range: Baveno VI states it "should only be used in refractory oesophageal bleeding, as a temporary bridge (for a maximum of 24 h) with intensive care monitoring and considering intubation, until definitive treatment can be instituted", because severe esophageal injury/necrosis, perforation and aspiration rise sharply beyond that point. The 72-hour figure in this standard belongs to the pre-emptive TIPS window and must not be read as a permissible tamponade duration. Secondary prophylaxis is mandatory in all survivors and is combination therapy: a nonselective beta-blocker, either a traditional NSBB (propranolol or nadolol) or carvedilol, which Baveno VII endorses as an equivalent rather than clearly superior option in this specific indication, plus serial EVL every 2 to 8 weeks until variceal eradication, with surveillance endoscopy thereafter. TIPS is the treatment of choice for patients who rebleed despite NSBB plus EVL.

Diagnose acute pancreatitis (AP) by the Atlanta criteria (2 of 3: characteristic epigastric/LUQ pain, lipase or amylase >3x ULN [lipase preferred for specificity/duration], or characteristic imaging). ACG 2024 stratifies severity risk using SIRS on admission plus bedside risk factors, rising/elevated BUN, rising/elevated hematocrit (>44), obesity (BMI>30), extrapancreatic fluid collections/pleural effusion/infiltrates, altered mental status, and older age/comorbidities, rather than mandating a formal BISAP or APACHE II composite score. Give moderately aggressive lactated Ringer's, most important in the first 6-12 hours, reassessing volume status/BUN/HCT at 6 hours (further aggressive hydration has little added benefit after 24-48h). Start oral low-fat solid food within 24-48h as tolerated in mild disease; if enteral feeding is needed for moderately severe/severe disease, prefer nasogastric over nasojejunal with small-peptide/medium-chain-triglyceride formula and continuous (not bolus/cyclic) feeding; avoid parenteral nutrition if possible. Do not give prophylactic antibiotics, even in severe disease or sterile necrosis; reserve antibiotics for suspected infected necrosis (typically arising 10-14 days in), and choose agents that penetrate pancreatic necrosis while together covering both gut-derived gram-negative enterics and anaerobes, a carbapenem supplies this as monotherapy, whereas a fluoroquinolone or a third-or-higher-generation cephalosporin must be combined with metronidazole; metronidazole alone (anaerobic cover only), or a cephalosporin or a quinolone alone, does not adequately treat infected necrosis. Perform cholecystectomy preferably before discharge for mild acute biliary pancreatitis, and after a second unexplained AP episode even without identified gallstones; reserve ERCP within 24h for AP complicated by cholangitis, with rectal indomethacin +/- pancreatic duct stent and periprocedural hydration to reduce post-ERCP pancreatitis risk. Check triglycerides when gallstones/alcohol are absent (>1000 mg/dL supports a hypertriglyceridemia etiology). For stable pancreatic necrosis, defer surgical, radiological, or endoscopic intervention 4-6 weeks to allow walling-off (step-up approach).

The thresholds on file still hold, and the 2026 AGA Clinical Practice Update (Calderwood, Yoshida, Das, Falk; Clin Gastroenterol Hepatol, online 2026-08-03) agrees with them while adding to them. Average-risk adults are screened routinely from age 45 to 75 (USPSTF 2021: Grade B for 45-49, Grade A for 50-75; USMSTF and ACS agree). For ages 76-85 the decision is individualized (USPSTF Grade C). Under USMSTF, people who are up to date with negative prior screening, especially a high-quality colonoscopy, should consider stopping at 75 or when life expectancy falls below 10 years. People who were never adequately screened may be screened up to 85, depending on age and comorbidity. Screening is not recommended at 86 or older. The 2026 AGA update adds four things. (1) After age 75, the decision to continue screening (BPA 6) or polyp surveillance (BPA 7) should be individualized by weighing benefit, screening or polyp history, comorbidities and risks; this now explicitly covers post-polypectomy surveillance, not only screening. (2) Formal comorbidity assessment and life-expectancy tools may help separate older adults likely to benefit from those likely to be harmed (BPA 1). (3) Colonoscopy adverse events rise with age whatever the indication, so the reasoning behind any colonoscopy decision in someone over 75 should be documented in the EHR (BPA 8). (4) For Barrett's esophagus, continuing surveillance is a shared decision, and a patient who could not tolerate endoscopic, surgical or oncologic treatment should stop surveillance at any age (BPA 3 and 5). The AGA statements are expert-opinion Best Practice Advice without formal evidence grades, and they set no new numeric age or life-expectancy cutoffs. New alarm features (iron-deficiency anemia, GI bleeding, change in bowel habit, weight loss) still warrant diagnostic workup at any age; this is general practice, not a guideline statement.

Surveillance practice is now defined by the AGA 2025 surveillance guideline (Wani et al., Gastroenterology 2025;169:1184-1231; endorsed by the Canadian Association of Gastroenterology). Its 8 GRADE recommendations are: (1) endoscopic surveillance for nondysplastic BE rather than none (conditional, low certainty); (2) NO endoscopic surveillance for columnar-lined esophagus <1 cm, even with intestinal metaplasia, when there is no neoplasia (conditional); (3) high-definition white-light endoscopy PLUS chromoendoscopy over white light alone (STRONG); (4) no recommendation for or against wide-area transepithelial sampling (WATS-3D) as an adjunct to structured biopsy; (5) no recommendation on p53 IHC and (6) no recommendation on TissueCypher as adjuncts to histopathology in NDBE, indefinite for dysplasia (IND), or LGD; (7) daily PPI over no PPI to prevent neoplastic progression (conditional); (8) PPI over antireflux surgery to prevent progression to HGD/EAC (conditional). Implementation statements require a high-quality exam, a structured (Seattle-type) biopsy protocol, confirmation of any BE-related dysplasia by an expert GI pathologist, intervals tailored to segment length and dysplasia grade, and shared decision-making. Surveillance should stop when a patient could not tolerate endoscopic therapy, surgery, or oncologic treatment for EAC, at any age. The AGA 2025 interval table could not be read directly (full text paywalled). Until it is, the intervals below are the ACG 2022 intervals, which remain consistent with AGA's segment-length framing: NDBE <3 cm every 5 years; NDBE >=3 cm every 3 years; IND, after a second-pathologist read, optimize to twice-daily PPI, repeat EGD within 6 months, then annually if IND persists; confirmed LGD on surveillance, EGD at 6 and 12 months, then annually. Diagnosis (IM plus >=1 cm columnar mucosa, no biopsy of a normal or <1 cm irregular Z line, >=8 biopsies), endoscopic eradication therapy (EET over esophagectomy for HGD/T1a (strong); EET suggested for confirmed LGD with surveillance an acceptable alternative; resect visible lesions before RFA; sm1 low-risk T1b may be considered for EET) and post-EET intervals (baseline LGD: 1 year, 3 years, then every 2 years; baseline HGD/T1a: 3, 6, 12 months, then annually) are still governed by ACG 2022. The AGA surveillance guideline does not address them, and AGA has said a separate screening guideline will follow in 2026.

Begin evaluation of abdominal pain with a rapid risk assessment: identify hemodynamic instability, signs of peritonitis, or pain out of proportion to examination findings, these patients need urgent resuscitation or surgical evaluation. Pursue specific life-threatening causes (ruptured AAA, aortic dissection, mesenteric ischemia, ectopic pregnancy, myocardial ischemia) when presentation and risk factors raise suspicion for them, rather than as a universal rule-out before assigning a GI cause. In stable patients, apply a localization-driven differential (RUQ/epigastric/LUQ/RLQ/LLQ/diffuse/periumbilical/suprapubic) with stepwise workup: history and exam with red flags (fever, protracted vomiting, syncope/presyncope, GI blood loss), labs (CBC, CRP, hepatobiliary markers, electrolytes/creatinine/glucose, urinalysis, lipase; pregnancy test in all premenopausal women, including those using reliable contraception; lactate when sepsis or mesenteric ischemia is suspected, may be normal early; ECG/troponin when a cardiac cause is suspected), imaging by location (ultrasound first for RUQ pain; CT with IV contrast for RLQ, LLQ, and generalized pain; CTA when mesenteric ischemia is suspected; in pregnancy, ultrasound first with MRI when ultrasound is inconclusive), then endoscopy and specialty referral by suspicion.