WCOG, New Delhi 2026

• Define the intended use precisely. A detection tool, diagnostic system and treatment adviser have different functions and risks.

• Evaluate clinically relevant performance. Accuracy alone is insufficient; missed disease, false positives and consequences for patient management matter.

• Require independent validation. Testing should represent the populations, hospitals and equipment where the system will actually operate.

• Examine performance across patient groups. An acceptable average can conceal important weaknesses in under-represented populations.

• Make limitations visible. Users need to understand suitable inputs, excluded situations and the degree of human oversight required.

• Distinguish regulatory status from general endorsement. Authorisation concerns a specified product and intended use, not every claim made about it.

• Monitor after implementation. Changes in data, workflow or software can alter performance and require reassessment.

• Plan updates and failure responses. Hospitals need clear processes for incident reporting, version control and withdrawal when necessary.

• Protect patient information. Data handling and cybersecurity are part of clinical safety.

Take-home: Safe clinical AI requires validation, clear accountability and continued monitoring throughout its lifecycle.

• AI already assists polyp detection. Computer-aided detection systems can draw attention to lesions that might otherwise be overlooked.

• Detection and diagnosis are different tasks. Identifying a polyp does not automatically establish its histology or determine the correct treatment.

• Higher detection is not the final outcome. More small adenomas do not necessarily translate into fewer interval cancers or lower cancer mortality.

• Maintain examination quality. Good preparation, complete examination, careful inspection and appropriate resection remain essential.

• Assess performance in the intended setting. Results may differ between expert centres, community practice, equipment platforms and patient populations.

• Monitor unintended consequences. False alerts, removal of low-risk lesions, additional pathology and altered surveillance recommendations can increase workload and cost.

• Guard against over-reliance. Endoscopists should retain independent inspection skills and review AI suggestions critically.

• Evaluate implementation beyond accuracy. Workflow, training, access and cost-effectiveness determine practical value.

• Keep responsibility clear. The clinician remains accountable for the examination and resulting decisions.

Take-home: AI is a useful assistant, but its value should be judged by meaningful patient outcomes.

• ACLF requires treatment of the precipitant and failing organs. Extracorporeal therapy supplements these measures rather than replacing them.

• Understand what each system does. Renal replacement, plasma exchange and albumin-based devices remove different substances and have different clinical objectives.

• CRRT has established renal indications. Its broader use should depend on physiology, organ dysfunction and the treating centre’s protocol.

• Plasma exchange has emerging evidence. Recent trial findings are encouraging, but patient selection, durability of benefit and procedural tolerance remain important.

• DIALIVE targets albumin dysfunction and inflammatory mediators. Early randomised evidence showed physiological improvements and faster ACLF resolution.

• Improved markers do not automatically mean improved survival. The small DIALIVE study did not demonstrate a mortality reduction.

• Assess procedural burden. Haemodynamic instability, vascular access, infection risk and resource requirements may limit treatment.

• Evaluate transplantation early. A support device should not delay referral or definitive treatment in an eligible patient.

• Reassess the trajectory repeatedly. Continuing therapy should have a clear clinical purpose.

Take-home: Select extracorporeal support according to the patient’s needs, evidence and realistic recovery or transplantation pathway.

• Use the current adult criteria explicitly. Rome V provides a diagnostic framework; avoid assuming that every previously used definition remains unchanged.

• Recognise the functional dyspepsia pattern. Bothersome meal-related fullness, early satiation, epigastric pain or burning are central symptoms.

• Identify the dominant subtype. Postprandial distress and epigastric pain patterns may overlap, influencing the treatment discussion.

• Exclude plausible alternative explanations. Structural, systemic and metabolic disease should be assessed according to presentation and risk.

• Distinguish dyspepsia from vomiting disorders. Chronic nausea and vomiting, cyclic vomiting, cannabinoid hyperemesis and rumination require separate clinical consideration.

• Ask specifically about regurgitation and cannabis exposure. These details may reveal a diagnosis missed by a general symptom checklist.

• Use adult and paediatric criteria appropriately. Their duration requirements and definitions should not be interchanged.

• Do not label normal investigations as absence of disease. Explain altered gut–brain function and offer a positive management plan.

• Avoid unsupported diagnostic changes. Exact frequency and duration requirements should be checked against the published criteria.

Take-home: Rome V supports precise symptom classification followed by focused evaluation and individualised treatment.

• Food processing and nutrient composition both matter. Ultra-processed products often combine high energy density, convenience and features that encourage rapid consumption.

• Controlled feeding research supports an effect on intake. Participants consumed more energy and gained weight on an ultra-processed diet in a short randomised study.

• Do not overextend short-term findings. Evidence for overeating does not establish that every product causes every chronic gastrointestinal disease.

• Long-term disease associations need cautious interpretation. Dietary patterns, socioeconomic factors and other behaviours can confound observational research.

• Focus on achievable substitutions. Replace frequent sugary drinks and packaged snacks with water, fruit, legumes, nuts and suitable home-prepared foods.

• Consider affordability and access. Advice should fit the patient’s household rather than depend on expensive specialist products.

• Avoid excessive restriction. Patients with malnutrition, IBD or limited intake need adequate nutrition, not blanket food exclusion.

• Assess the overall dietary pattern. Preparation, fibre, protein, portion size and frequency are more useful than a label alone.

Take-home: Encourage sustainable dietary improvement while separating established effects from uncertain disease claims.

• Confirm the diagnosis carefully. Document the extent of suspected Barrett’s and obtain appropriate histology rather than relying on appearance alone.

• Use high-definition inspection with chromoendoscopy. Carefully examine the segment for subtle visible abnormalities before taking surveillance biopsies.

• Follow a structured biopsy protocol. Target visible lesions and sample the remaining segment systematically.

• Dysplasia should receive expert pathological review. Misclassification can lead to unnecessary treatment or missed opportunities for prevention.

• Individualise surveillance intervals. Segment characteristics, histology, previous findings and the patient’s health influence follow-up.

• Do not routinely ablate non-dysplastic Barrett’s. Treatment intensity should reflect the risk of progression.

• Refer confirmed dysplasia or early neoplasia for expert assessment. Visible lesions generally require resection before decisions about treating residual Barrett’s mucosa.

• Manage reflux appropriately. Acid suppression supports care but does not replace surveillance when indicated.

• Review whether surveillance remains beneficial. Consider comorbidity, life expectancy and willingness to undergo treatment.

Take-home: Accurate pathology and careful examination are the foundations of effective cancer prevention.

• Define the diagnostic objective before sampling. Cytology, tissue architecture, immunohistochemistry and molecular profiling have different specimen requirements.

• Choose the needle for the lesion. Current ESGE guidance favours end-cutting fine-needle biopsy needles for solid pancreatic lesions.

• FNA retains selected uses. It may remain appropriate when rapid on-site evaluation is available and the clinical question can be answered by cytology.

• Target viable tissue. Avoid predominantly necrotic areas and select a safe trajectory that minimises vascular injury.

• Technique influences yield. Appropriate lesion sampling, needle movement and specimen handling matter alongside needle design.

• Coordinate with pathology in advance. Suspected lymphoma, neuroendocrine tumour or molecular testing may require specific processing.

• A negative sample does not always exclude malignancy. Reconsider adequacy when imaging and clinical suspicion remain concerning.

• Plan the next step after an inconclusive result. Repeat sampling, a different technique or multidisciplinary assessment may be necessary.

• Avoid unnecessary procedures. Tissue acquisition should change diagnosis, staging or treatment.

Take-home: Diagnostic success depends on planning, technique and pathology coordination—not needle selection alone.

• Clinically significant portal hypertension predicts complications. Its recognition helps identify patients at risk of ascites, variceal bleeding and other decompensating events.

• Use non-invasive assessment in suitable patients. Liver stiffness combined with platelet count can reduce reliance on invasive pressure measurements.

• Apply thresholds to the correct population. Established Baveno criteria use stiffness of ≤15 kPa with platelets ≥150,000/µL to exclude CSPH in appropriate compensated disease.

• A stiffness value ≥25 kPa can support CSPH in validated groups. Applicability varies with aetiology and obesity; this is not a universal threshold.

• Intermediate results require further assessment. Clinical findings, additional tests and specialist interpretation help resolve uncertainty.

• Separate CSPH assessment from variceal screening. The questions are related but are not interchangeable.

• Consider non-selective beta-blockers when indicated. The aim includes preventing decompensation, with attention to blood pressure and tolerance.

• Use current consensus guidance. Baveno VIII extends the framework for individualised assessment and management.

Take-home: Identify portal hypertension early and connect risk assessment to preventive treatment.

• Monitor liver tests during immunotherapy. Immune-mediated injury may be detected before symptoms develop.

• Do not assume every elevation is immune-related. Exclude viral infection, other drug toxicity, biliary obstruction, tumour progression and vascular or ischaemic causes.

• Assess severity beyond aminotransferases. Bilirubin, INR, symptoms and the rate of deterioration influence urgency and management.

• Recognise different injury patterns. Hepatocellular injury and immune-mediated cholangitic disease may have different investigations and treatment responses.

• Coordinate with oncology early. Decisions to continue, interrupt or discontinue checkpoint therapy must balance liver risk against cancer control.

• Use corticosteroids according to severity and clinical assessment. Mild abnormalities may need close monitoring; more significant injury often requires treatment.

• Reassess inadequate response promptly. Specialist-directed additional immunosuppression, commonly mycophenolate, may be needed after reconsidering the diagnosis.

• Use liver biopsy selectively. Atypical, severe or treatment-resistant cases may benefit from tissue assessment.

• Individualise rechallenge. Recovery does not automatically make restarting immunotherapy appropriate.

Take-home: Accurate diagnosis and coordinated hepatology–oncology care are essential before increasing immunosuppression.

• Monitor liver tests during immunotherapy. Immune-mediated injury may be detected before symptoms develop.

• Do not assume every elevation is immune-related. Exclude viral infection, other drug toxicity, biliary obstruction, tumour progression and vascular or ischaemic causes.

• Assess severity beyond aminotransferases. Bilirubin, INR, symptoms and the rate of deterioration influence urgency and management.

• Recognise different injury patterns. Hepatocellular injury and immune-mediated cholangitic disease may have different investigations and treatment responses.

• Coordinate with oncology early. Decisions to continue, interrupt or discontinue checkpoint therapy must balance liver risk against cancer control.

• Use corticosteroids according to severity and clinical assessment. Mild abnormalities may need close monitoring; more significant injury often requires treatment.

• Reassess inadequate response promptly. Specialist-directed additional immunosuppression, commonly mycophenolate, may be needed after reconsidering the diagnosis.

• Use liver biopsy selectively. Atypical, severe or treatment-resistant cases may benefit from tissue assessment.

• Individualise rechallenge. Recovery does not automatically make restarting immunotherapy appropriate.

Take-home: Accurate diagnosis and coordinated hepatology–oncology care are essential before increasing immunosuppression.

• Suspect infection when the clinical course deteriorates. Sepsis, persistent organ dysfunction and suggestive imaging findings warrant reassessment, while excluding other infection sources.

• Do not give prophylactic antibiotics for sterile necrosis. Antimicrobial treatment is reserved for suspected or established infection.

• Choose antibiotics appropriately. Consider tissue penetration, local resistance, culture results and the need for subsequent narrowing.

• Support nutrition and organ function. Enteral feeding and management of haemodynamic, respiratory and renal problems remain essential.

• Delay intervention when clinically safe. Allowing collections to organise can make drainage and subsequent treatment more effective and less hazardous.

• Use a step-up approach. Begin with suitable endoscopic or percutaneous drainage; proceed to necrosectomy when the response is inadequate.

• Match the route to anatomy. Collection location, maturity, extension and local expertise determine the safest approach.

• Avoid rigid waiting periods in unstable patients. Uncontrolled sepsis or deterioration may require earlier source control.

• Coordinate care across specialties. Endoscopy, radiology, surgery and critical care should work from a shared plan.

Take-home: Individualise timing and use the least invasive effective intervention.

• Assess alcohol exposure without judgement. Record quantity, pattern, duration and recent changes, alongside metabolic and other liver-disease risks.

• Alcohol and metabolic dysfunction can coexist. Avoid assuming that every patient belongs to a single, mutually exclusive disease category.

• Use blood-based scores and elastography to assess fibrosis. These tests can identify patients requiring specialist evaluation without immediate biopsy.

• Inflammation can increase liver stiffness. Active alcohol-related hepatitis and recent heavy drinking may produce measurements that overestimate fibrosis.

• Interpret stiffness with laboratory and clinical findings. An isolated high value should not automatically establish irreversible cirrhosis.

• Repeat testing when appropriate. Reassessment after reduced drinking and improvement in inflammation may clarify the underlying disease stage.

• Do not miss decompensation. Ascites, jaundice, encephalopathy or bleeding requires urgent clinical management rather than further screening tests.

• Link diagnosis to treatment. Alcohol-use disorder care, nutritional support and management of metabolic risks should accompany liver assessment.

Take-home: Non-invasive tests are useful when interpreted within the patient’s drinking history, inflammatory state and clinical presentation.

• Early lesions may be subtle. Small changes in colour, surface pattern, depression or elevation can be missed during a hurried examination.

• Prepare the stomach for inspection. Adequate cleaning, distension and careful examination improve visibility and diagnostic confidence.

• Use a systematic inspection sequence. Examine all gastric regions and document relevant findings rather than limiting attention to obvious lesions.

• Use image enhancement when available. Virtual chromoendoscopy can help characterise suspicious areas and guide targeted biopsies.

• Assess the background mucosa. Atrophy and intestinal metaplasia provide important information about future cancer risk.

• Obtain appropriate biopsies. Target suspicious lesions and use recommended mapping protocols when assessing precancerous conditions.

• Select surveillance according to risk. Extensive or advanced precancerous changes deserve different follow-up from limited low-risk findings.

• Refer potentially curable lesions early. Expert assessment can determine suitability for endoscopic resection or surgery.

• Resources matter, but technique remains fundamental. Better equipment cannot compensate for incomplete inspection.

Take-home: A clean, systematic and well-documented examination is the foundation of early gastric cancer detection.

• Treat confirmed infection with an effective regimen. Selection should reflect local resistance, previous antibiotic exposure, allergy and availability.

• Avoid empirical clarithromycin triple therapy when susceptibility is unknown. Resistance can substantially reduce eradication success.

• Optimised bismuth quadruple therapy for 14 days is an important option. Other regimens, including selected rifabutin- or potassium-competitive acid blocker-based approaches, depend on clinical context and access.

• Explain the regimen clearly. Complex schedules, adverse effects and incomplete adherence are frequent preventable reasons for failure.

• Confirm eradication in every treated patient. Symptom improvement does not establish microbiological cure.

• Time testing correctly. Perform a urea breath or stool antigen test at least four weeks after antibiotics; withhold PPIs or PCABs for two weeks beforehand.

• Do not use serology to confirm cure. Antibodies can persist after successful treatment.

• After failure, review the original regimen. Avoid simply repeating antibiotics likely to be ineffective; consider susceptibility-guided treatment where available.

Take-home: Successful management requires both appropriate antibiotic selection and a documented test of cure.

• Precision care starts with accurate phenotyping. Disease location, behaviour, severity, previous complications and extraintestinal manifestations influence treatment decisions.

• Symptoms alone are insufficient. Combine the patient’s experience with inflammatory markers, faecal calprotectin, endoscopy and imaging where appropriate.

• Separate inflammation from other causes of symptoms. Infection, functional overlap, bile acid diarrhoea and structural damage may require different treatment.

• Clarify why a therapy has failed. Inadequate exposure, immunogenicity and failure of the drug’s mechanism should not lead to the same response.

• Use reactive drug monitoring selectively. In active disease during anti-TNF treatment, drug levels and antibodies can help guide optimisation or switching.

• Set measurable goals. Steroid-free remission and objective healing are more informative than symptom improvement alone.

• Incorporate patient priorities. Treatment burden, access, reproductive plans and tolerance can determine whether an otherwise effective strategy is sustainable.

• Keep novel predictive tests in perspective. Many molecular approaches remain investigational and do not yet reliably identify the best drug for every patient.

Take-home: Precision IBD means informed individualisation and objective monitoring, rather than routine use of expensive experimental tests.

• Moderate-to-severe UC often requires advanced treatment. Repeated steroid courses should trigger reassessment rather than become a long-term management strategy.

• Confirm inflammatory activity and severity. Symptoms, biomarkers and endoscopic findings help establish the need for escalation and provide a baseline for monitoring.

• Consider earlier advanced therapy. Prolonged step-up treatment may expose patients with substantial disease to ongoing inflammation and steroid-related harm.

• Drug selection depends on more than efficacy. Previous exposure, comorbidities, infection risk, pregnancy plans, route of administration, affordability and patient preference all matter.

• Different mechanisms offer different opportunities. Anti-TNF, anti-integrin, interleukin-targeted and small-molecule therapies should be selected according to the individual clinical setting.

• Complete safety screening before treatment. Assess relevant infections, vaccination status and therapy-specific risks.

• Define success in advance. Aim for steroid-free symptom control and objective improvement, with scheduled review after induction.

• Change ineffective treatment promptly. Persistent disease requires an explanation and a revised plan.

Take-home: The best initial advanced therapy combines appropriate efficacy, acceptable safety and a realistic monitoring strategy.

• The key question is fibrosis risk. Finding steatosis is the beginning of assessment; advanced fibrosis predicts clinically important liver outcomes.

• Prioritise high-risk populations. Type 2 diabetes, abdominal obesity with additional metabolic risks and persistently abnormal liver enzymes should prompt structured evaluation.

• Use sequential testing. FIB-4 is a practical first step, followed by elastography or another validated second-line test when indicated.

• Interpret results in context. Age and acute illness can affect blood-based scores; a single abnormal result should not automatically establish advanced fibrosis.

• Normal ALT does not exclude significant disease. Avoid reassurance based solely on liver enzymes when metabolic risk is substantial.

• Refer patients with concerning or discordant findings. Specialist evaluation can clarify disease stage, follow-up needs and eligibility for liver-directed treatment.

• Address metabolic disease simultaneously. Weight management, diabetes care, physical activity and cardiovascular prevention should begin while fibrosis assessment proceeds.

• Plan reassessment. Low-risk patients still need follow-up according to their metabolic profile and subsequent clinical changes.

Take-home: Replace incidental fatty-liver reporting with a clear fibrosis assessment and follow-up pathway. pmc.ncbi.nlm.nih.gov

• Gallstones are an important association, but absolute cancer risk remains low. Most people with gallstones never develop gallbladder cancer.

• Do not attribute every abnormality to stones. A gallbladder mass, suspicious wall changes or unexplained biliary obstruction needs further assessment.

• Symptoms may be non-specific. Persistent upper abdominal pain, jaundice or progressive constitutional symptoms warrant attention, particularly when the clinical course is atypical.

• Imaging should assess the entire gallbladder. The purpose is to identify suspicious lesions and involvement of adjacent structures, rather than simply confirm calculi.

• Cancer can be discovered incidentally after cholecystectomy. A malignant histopathology result requires staging and specialist review; the initial operation may not constitute complete treatment.

• Resectability is central to management. Early disease may be treated surgically, while advanced disease needs coordinated oncological and supportive care.

• Avoid translating association into universal surgery. Decisions for asymptomatic stones require individual assessment rather than cancer anxiety alone.

Take-home: Recognise suspicious gallbladder findings early while explaining that uncomplicated gallstones usually do not progress to cancer.

• Established explanations can be incomplete. Marshall and Warren’s work demonstrated the role of Helicobacter pylori in gastritis and peptic ulcer disease, changing both understanding and treatment.

• Observation is the starting point. Unexpected pathological findings or clinical patterns deserve investigation rather than dismissal because they conflict with prevailing beliefs.

• A convincing hypothesis still requires evidence. Reproducible observations, microbiological confirmation and treatment studies are essential before changing clinical practice.

• Treat causes when they are established. The H. pylori discovery shifted ulcer management beyond acid suppression towards eradication of the underlying infection.

• Distinguish scepticism from resistance to evidence. Clinicians should question new claims while remaining willing to revise established views.

• Apply the same discipline to emerging technologies. AI, biomarkers and microbiome interventions require validation, not acceptance based on novelty.

• Research should answer a clinical question. The most useful discoveries improve diagnosis, treatment or prevention rather than merely producing an interesting association.

Take-home: Remain curious, test assumptions and change practice when reliable evidence justifies it

• Colorectal cancer before age 50 is an increasing concern. Young age should not reassure clinicians when symptoms suggest significant colorectal disease.

• Investigate persistent warning symptoms. Rectal bleeding, iron-deficiency anaemia, unexplained weight loss and a sustained change in bowel habit require appropriate assessment.

• Separate screening from diagnosis. A symptomatic patient needs diagnostic evaluation even when below the age recommended for population screening.

• Document family history carefully. Record colorectal and related cancers, affected relatives and age at diagnosis; arrange hereditary cancer assessment when indicated.

• The causes are probably multifactorial. Metabolic, dietary, environmental and microbial exposures are under investigation rather than a single established explanation.

• Colibactin research provides a biological clue. Genotoxic bacteria can leave characteristic DNA changes, but these findings do not yet support routine microbiome screening.

• Avoid unproven prevention strategies. Antibiotics, microbiome treatments or aspirin should not be prescribed solely because of concern about early-onset cancer.

Take-home: The immediate opportunity is earlier recognition and investigation of symptoms, alongside appropriate family-risk assessment.