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

Confirm ulcerative colitis with endoscopy showing continuous colonic inflammation from the rectum plus histology, after excluding infection with two-step CDI testing. Treat mild-moderate disease with 5-ASA by route and extent (suppository for proctitis, enema for left-sided, oral plus rectal for extensive); 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 - S1P modulators are weakest in exactly this group. Do not cycle within the anti-TNF class after primary non-response; switch mechanism. Apply treat-to-target (STRIDE-II) to endoscopic improvement (MES 0-1). Screen for acute severe UC by Truelove-Witts and admit for IV steroids. Begin CRC surveillance 8-10 years after DIAGNOSIS for extensive or left-sided disease; isolated proctitis follows average-risk screening.

Confirm ulcerative colitis with endoscopy showing continuous colonic inflammation from the rectum plus histology, after excluding infection with two-step CDI testing. Treat mild-moderate disease with 5-ASA by route and extent (suppository for proctitis, enema for left-sided, oral plus rectal for extensive); 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 - S1P modulators are weakest in exactly this group. Do not cycle within the anti-TNF class after primary non-response; switch mechanism. Apply treat-to-target (STRIDE-II) to endoscopic improvement (MES 0-1). Screen for acute severe UC by Truelove-Witts and admit for IV steroids. Begin CRC surveillance 8-10 years after DIAGNOSIS for extensive or left-sided disease; isolated proctitis follows average-risk screening.

Scope: this primary document covers portal hypertension and varices in cirrhosis ONLY. Everything else in the current entry (HCC surveillance, transplant referral, nutrition, vaccination, ascites/SBP/HE/HRS/ACLF management) belongs to the separate documents listed as supporting sources and must not be attributed to this guidance. Risk-stratify compensated advanced chronic liver disease (cACLD) with non-invasive tests before defaulting to endoscopy. By vibration-controlled transient elastography, liver stiffness (LSM) under 10 kPa excludes cACLD, 10 to 14.9 kPa is suggestive and warrants further testing, and 15 kPa or above rules cACLD in. Clinically significant portal hypertension (CSPH, i.e. HVPG above 10 mm Hg) is ruled in non-invasively by LSM at or above 25 kPa alone, or LSM 20 to 24.9 kPa with platelets below 150 x 10^9/L, or LSM 15 to 19.9 kPa with platelets below 110 x 10^9/L. Where spleen stiffness measurement is available, values below 21 kPa argue against CSPH and above 50 kPa argue for it. These non-invasive cutoffs are conditional probability thresholds, not universal diagnostic rules, and hold only when their derivation conditions are met. They were established in compensated advanced chronic liver disease of viral (treated or untreated HBV/HCV), alcohol-related, or non-obese (BMI under 30) MASLD etiology, and are not validated for and should not be applied to cholestatic (e.g. PBC, PSC), vascular, or other etiologies, in which different cutoffs apply. They also require a technically reliable liver stiffness measurement by vibration-controlled transient elastography, fasting, at least 10 valid acquisitions, and an IQR/median ratio below 30 percent, and are confounded by factors that raise liver stiffness independently of fibrosis, including ALT flares or acute hepatitis, extrahepatic cholestasis, hepatic congestion (right heart failure), and recent food intake; Baveno VII recommends confirming an LSM-based rule-in on a repeat measurement obtained on a separate day. The spleen stiffness cutoffs apply only to a dedicated 100 Hz spleen module, carry a higher technical failure rate, are machine-dependent, and are not interchangeable with values obtained using the standard 50 Hz liver probe. Where these population or acquisition conditions are not met, the numeric thresholds do not reliably classify CSPH, and HVPG measurement or endoscopy is required rather than a non-invasive determination. Preserve the gray zone: LSM 15 to 25 kPa without a qualifying platelet count is explicitly indeterminate (roughly 40 to 60 percent of cACLD patients) and calls for HVPG and/or endoscopy rather than assumption in either direction. Once CSPH is established, offer a non-selective beta-blocker, carvedilol preferred at 12.5 mg/day, to lower portal pressure and prevent FIRST decompensation, on the strength of PREDESCI. This is a treat-the-pressure strategy rather than a treat-the-varices one: because a patient already on NSBB for CSPH would not have management changed by the finding, screening endoscopy becomes unnecessary for most such patients. Screening EGD is still indicated where elastography is unavailable, technically difficult, or gives discordant results, and for patients who do not meet non-invasive criteria. Standard beta-blocker contraindications (severe asthma, advanced heart block, bradyarrhythmias) continue to apply. For varices needing treatment managed endoscopically, band ligation is repeated every 2 to 4 weeks until obliteration, with surveillance endoscopy at 6 months and annually thereafter. Gastric/cardiofundal varices are treated with cyanoacrylate injection or EUS-guided coil embolization rather than banding, with hepatology involvement. In acute variceal hemorrhage, consider preemptive (early) TIPS within 24 to 72 hours in high-risk patients: Child-Turcotte-Pugh class B with score above 7 and active bleeding at endoscopy despite vasoactive therapy, or CTP class C with score 10 to 13. Keep the document's own qualifier: there is no established universal MELD or CTP cutoff at which TIPS is mandatory, and the decision is case-by-case with hepatology consultation. Statin use in compensated cirrhosis is NOT a recommendation traceable to this document; the current entry's statin sentence needs its own source or removal. Verification note: the Hepatology full text is paywalled (402/403 on direct fetch). Document identity, title, year, volume, pages and authorship were confirmed via Crossref and PubMed metadata; the numeric thresholds above were corroborated from two independent peer-reviewed commentaries on this specific guidance and match the Baveno VII rule-of-five, but were not read verbatim from the primary PDF. A human should confirm the exact guidance-statement wording against the full text before this entry is treated as quotation-grade.

Evaluate suspected pancreatic adenocarcinoma with a dedicated pancreatic-protocol (multiphasic, contrast-enhanced) CT of the abdomen as the preferred imaging for diagnosis and staging (MRI/MRCP is an acceptable alternative); PET/CT may be added after, never as a substitute for, protocol CT/MRI in higher-risk situations. Obtain tissue confirmation, preferably by EUS-guided FNA/FNB with core biopsy where feasible; biopsy is generally required before neoadjuvant or palliative therapy, whereas patients with clearly resectable disease may proceed to surgery without preoperative biopsy. Measure baseline CA 19-9 (interpret after biliary decompression / with normal bilirubin; it can be falsely low in Lewis-antigen-negative patients and falsely elevated with cholestasis). Offer GERMLINE testing for inherited susceptibility to EVERY patient with confirmed pancreatic adenocarcinoma regardless of family history, using a comprehensive multi-gene panel; separately, for patients with locally advanced or metastatic disease who are candidates for anti-cancer therapy, obtain TUMOR/SOMATIC molecular profiling (broad NGS; RNA-based assays improve fusion detection; cell-free/liquid biopsy if tissue is insufficient). Assign resectability, resectable, borderline resectable, locally advanced (unresectable), or metastatic, by multidisciplinary review, ideally at a high-volume center. RESECTABLE disease: upfront resection (pancreaticoduodenectomy for head/uncinate; distal pancreatectomy ± splenectomy for body/tail) followed by adjuvant therapy, or neoadjuvant therapy in selected high-risk patients; preferred adjuvant regimen is modified FOLFIRINOX in patients able to tolerate it, ideally begun within 12 weeks of surgery, for a total of ~6 months of perioperative systemic therapy. BORDERLINE RESECTABLE and LOCALLY ADVANCED disease: neoadjuvant systemic therapy, with or without subsequent chemoradiation/RT, then restaging and reassessment for resection. METASTATIC disease by performance status: good PS (ECOG 0-1, adequate organ function), first-line FOLFIRINOX/modified FOLFIRINOX, NALIRIFOX, or gemcitabine + nab-paclitaxel, with clinical trial preferred; after ~4-6 months without progression, transition to a maintenance strategy (including olaparib for germline BRCA1/2 carriers who have NOT progressed on first-line platinum-based therapy), a clinical trial, or a treatment break; intermediate PS (ECOG 2), clinical trial preferred, otherwise less-intensive first-line therapy (preferred gemcitabine + nab-paclitaxel [category 1], or single-agent gemcitabine or capecitabine, or FOLFOX/FOLFIRI/CapeOx), since the intensive triplets (FOLFIRINOX/modified FOLFIRINOX and NALIRIFOX) are limited to ECOG 0-1 and are generally not appropriate at ECOG 2, with the same maintenance-versus-progression reassessment applied after ~4-6 months without progression; poor PS (ECOG 3-4), palliative/best supportive care, with single-agent chemotherapy or a biomarker-directed agent only if clinically appropriate. Treat by molecular target wherever an actionable alteration is present, across lines: pembrolizumab (or dostarlimab) for MSI-H/dMMR and pembrolizumab for TMB-H, olaparib for germline BRCA1/2 (maintenance after platinum), larotrectinib/entrectinib for NTRK fusions, selpercatinib for RET fusions, dabrafenib + trametinib for BRAF V600E, erdafitinib for FGFR2 alterations, fam-trastuzumab deruxtecan for HER2-positive disease, zenocutuzumab for NRG1 fusion-positive disease, and (in recent NCCN versions) KRAS G12C inhibitors (adagrasib/sotorasib), several of these after prior systemic therapy. Integrate supportive care throughout: relieve obstructive jaundice with an endoscopic self-expanding metal stent in non-operative or neoadjuvant pathways, but do NOT perform routine preoperative biliary drainage before planned upfront resection; treat exocrine insufficiency with pancreatic enzyme replacement titrated to symptoms (common starting dose ~40,000-50,000 units of lipase with main meals, roughly half with snacks, increased as needed); manage refractory pain with celiac plexus neurolysis or palliative RT; relieve gastric outlet obstruction with surgical or EUS-guided gastrojejunostomy (or enteral stenting); and provide VTE prophylaxis, nutritional support, and early palliative care.

First exclude emergency/secondary causes (cauda equina/cord compression, fecal impaction with overflow) with a mandatory digital rectal exam, screen for eating disorder before dietary restriction, and classify the subtype (urge, passive, overflow, mixed) since it drives therapy. Work up loose-stool FI for inflammatory, infectious, and bile-acid drivers before labeling idiopathic. Manage with a stepwise ladder: optimize stool consistency (fiber, loperamide, bile-acid sequestrant, or TCA neuromodulator), pelvic floor PT plus biofeedback, skin protection and bridge devices, then escalate to surgical therapy. Prescribe the antimotility/neuromodulator agents with their indications, dosing, and safety limits: loperamide is first-line for loose-stool/urge FI, start low (e.g., 2 mg before meals or as needed) and titrate to stool consistency while staying within the FDA-approved maximum (8 mg/day OTC, 16 mg/day prescription), because the FDA warns that higher-than-recommended doses cause QT prolongation, torsades de pointes, and cardiac arrest; the TCA neuromodulator (e.g., amitriptyline, typically low-dose ~20 mg) is an off-label option reserved for loose-stool/idiopathic FI, and the AGS Beers Criteria recommend avoiding TCAs such as amitriptyline in older adults given their strong anticholinergic burden, sedation, orthostatic hypotension, and fall risk. Per the dedicated ASCRS 2023 fecal-incontinence guideline (updating ASCRS 2007, superseding reliance on ACG's broader 2021 anorectal-disorders guideline as the primary specialty source), sacral neuromodulation is a first-line surgical option for incontinent patients WITH OR WITHOUT a defined anal sphincter defect (conditional recommendation, low-quality evidence), it is not gated on documenting a sphincter defect. Sphincteroplasty remains appropriate for symptomatic patients with a defined external anal sphincter defect; repeat sphincteroplasty after a failed overlapping repair should generally be avoided in favor of other modalities. Antegrade continence enemas are an option before colostomy, which remains last resort.

Per AGA best practice advice: dietary intervention is most appropriate for IBS patients who have insight into meal-related symptoms and are motivated to make dietary changes. Soluble fiber (e.g., psyllium/ispaghula) is efficacious for global IBS symptoms and is a reasonable initial option, most suitable in constipation-predominant IBS; insoluble fiber (wheat bran) is NOT. The low-FODMAP diet is currently the most evidence-based diet intervention for IBS and is delivered as a structured 3-phase protocol, NOT lifelong restriction: (1) restriction of high-FODMAP foods lasting NO MORE than 4-6 weeks, (2) reintroduction of FODMAP foods, and (3) personalization based on reintroduction results. Any specific diet intervention should be attempted for a predetermined length of time; if there is no clinical response, the diet should be ABANDONED and a different diet or therapy tried, rather than continued indefinitely. Refer willing and appropriate patients to a GI registered dietitian nutritionist (RDN) to implement and supervise the diet. Poor candidates for restrictive diet interventions include patients who already consume few culprit foods, those at risk for malnutrition, those who are food insecure, and those with an eating disorder or uncontrolled psychiatric disorder; routine screening for disordered eating/eating disorders by careful dietary history is critical before starting a restrictive diet.

Scope: individuals with suspected or confirmed idiopathic or diabetic gastroparesis, including medically refractory disease. All 12 recommendations are CONDITIONAL ('suggests'), at low or very low certainty of evidence; none are strong. DIAGNOSIS (Rec 1): AGA suggests against a 2-hour (or shorter) gastric emptying study and in favour of a 4-hour study [conditional, low certainty], because patients with normal emptying at 2 hours may be reclassified as delayed at 4 hours. The 4-hour value must be measured directly at 4 hours, not mathematically derived from earlier time points. Testing should be done without confounders: hyperglycaemia and drugs that alter emptying (opioids, GLP-1 receptor agonists, prokinetics). Two meals have well-established normal values: the low-fat Tougas/EggBeaters meal (liquid egg white, bread, jam, water; 250 kcal, 2% fat) and the Mayo Clinic meal (two whole eggs, bread, skim milk; 320 kcal, 30% fat), the latter more thoroughly validated. PHARMACOTHERAPY: AGA suggests USING metoclopramide (Rec 2) and USING erythromycin (Rec 3), each conditional/very low certainty. Metoclopramide, oral tablet/liquid or intranasal, start 5 mg before meals, may increase up to 10 mg before meals; discuss potential side effects before starting (tardive dyskinesia risk noted, absolute risk low; higher risk of adverse events leading to discontinuation in older patients and those on psychotropics); assess efficacy and side effects at 4-8 weeks to decide on continuation, then monitor for the duration of therapy. Patients placing higher value on adverse-event risk and lower value on symptom improvement may reasonably decline it. Erythromycin, low dose (e.g. 100-150 mg by mouth, 30 min before meals) to reduce side effects seen at 250-500 mg; ethylsuccinate oral suspension allows smaller doses since tablets come only in high strengths; prokinetic via motilin agonism with no direct antiemetic effect; tachyphylaxis with prolonged continuous use is managed by drug holidays (e.g. 3 weeks on, 1 week off); cautions include QT prolongation, CYP3A interactions and antibiotic resistance. AGA suggests AGAINST, as first-line therapy, with shared-decision carve-outs, domperidone (Rec 4), prucalopride (Rec 5), aprepitant (Rec 6), nortriptyline (Rec 7.1) and buspirone (Rec 7.2) [conditional; low to very low certainty], and against cannabidiol EXCEPT in the context of a clinical trial (Rec 8, conditional/low certainty). Each carries an explicit shared-decision-making carve-out naming who may still reasonably use it: domperidone for patients who had neurological side effects on metoclopramide or who have movement disorders such as Parkinson's disease (US use requires an FDA expanded-access IND, and the sole US supplier is exiting; obtain baseline potassium, magnesium and ECG QTc, monitor on therapy, reassess at 4-8 weeks); prucalopride particularly in idiopathic gastroparesis (patients with diabetic or connective-tissue-disease-related gastroparesis are less likely to respond) and in those with coexisting chronic idiopathic constipation, noting the depression/suicidality monitoring warning; aprepitant for nausea and vomiting not helped by 5-HT3 antagonists such as ondansetron, recognising it has no effect on gastric motor function; nortriptyline for coexisting IBS or significant abdominal pain, started at low dose and titrated slowly, framed to patients as a peripheral neuromodulator; buspirone for predominant early satiety and bloating. For cannabidiol the panel notes the single positive trial used pharmaceutical-grade Epidiolex, which is not available for clinical use in gastroparesis, that commercial formulations are unregulated and variable in potency, and that THC-containing products raise cannabinoid hyperemesis concern. PROCEDURES (medically refractory disease): AGA suggests against G-POEM EXCEPT for selected patients with medically refractory disease (Rec 9, conditional/low certainty), candidates should have gastroparesis confirmed on an appropriately performed 4-hour gastric emptying study, generally with at least moderate delay (20% retention at 4 hours with the EggBeaters meal), at least six months of moderate cardinal symptoms (nausea, vomiting and/or postprandial fullness), and a prior trial of other treatments including a prokinetic such as metoclopramide plus an antiemetic. AGA suggests against pyloric botulinum toxin injection (Rec 11, conditional/very low certainty), noting that retreatment as often as every 3 months limits cost-effectiveness and that repeat treatment may cause pyloric scarring complicating later G-POEM; patients placing higher value on endoscopic intervention and lower value on chronic medical therapy may reasonably attempt it. AGA suggests against the ROUTINE INITIAL use of gastric electrical stimulation (Rec 12, conditional/very low certainty), reserving it, as with G-POEM, for select patients whose symptoms are refractory to medical therapy; patients placing higher value on potential nausea/vomiting improvement and lower value on the increase in serious adverse events may reasonably select GES, and should be told it aims to improve nausea and vomiting, not abdominal pain. For surgical pyloric interventions (pyloromyotomy or pyloroplasty) AGA makes NO recommendation and designates a knowledge gap, advising use only in the context of clinical trials (Rec 10). NON-GRADED adjuncts appear only as implementation considerations, not recommendations: panel content experts use small-particle, low-fat, low-residue diets before or alongside pharmacotherapy, and as-needed antiemetics (5-HT3 antagonists e.g. ondansetron, H1 antagonists e.g. promethazine, D2 antagonists e.g. prochlorperazine); efficacy of pharmacological interventions is assessed at 4-8 weeks. The guideline does NOT address exclusion of mechanical obstruction, enteral/J-tube nutrition, glycaemic targets, or perioperative GLP-1 RA management, those remain with the supporting documents.