WCOG 2026, New Delhi. Post Graduate Course

• Do not dismiss concerning symptoms because a patient is young. Persistent rectal bleeding, iron-deficiency anaemia, altered bowel habit or unexplained weight loss warrant appropriate investigation.

• Take family history seriously, while recognising that young-onset colorectal cancer also occurs without an obvious inherited syndrome.

• Consider hereditary cancer assessment. Young age at diagnosis should prompt attention to genetic evaluation and implications for relatives.

• The microbiome is an important research direction. Certain bacteria can produce genotoxic substances capable of damaging epithelial DNA.

• Colibactin findings are particularly relevant. Characteristic mutational signatures have been identified in colorectal cancers and associated with younger-onset disease.

• Association does not establish a clinical screening test. Stool microbiome testing cannot currently determine who will develop early-onset CRC.

• Do not present salicylate deficiency as an established cause. This remains a hypothesis rather than a basis for routine treatment.

• Avoid recommending aspirin broadly from these notes. Prevention decisions require a defined indication and assessment of bleeding risk.

Take-home: The immediate clinical priority is timely symptom evaluation; microbiome-based prevention remains investigational.

• Investigate beyond diarrhoea. Coeliac disease may present with iron deficiency, weight loss, osteoporosis, unexplained liver-test abnormalities or other extraintestinal features.

• Test while the patient is eating gluten. Starting a gluten-free diet beforehand can reduce the sensitivity of both serology and biopsy.

• Use tissue transglutaminase IgA with total IgA as the usual initial approach. IgA deficiency requires an appropriate IgG-based testing strategy.

• Use duodenal biopsy when indicated. Take adequate samples because mucosal involvement may be patchy.

• Do not diagnose coeliac disease from symptom improvement alone. Response to gluten withdrawal is not sufficiently specific.

• Apply adult no-biopsy pathways carefully. Eligibility depends on the guideline, antibody results and clinical circumstances; it is not appropriate for every adult.

• Use HLA testing selectively, particularly when results are discordant or the patient has already restricted gluten.

• After diagnosis, address nutrition and follow-up. Dietitian support, correction of deficiencies and assessment of persistent symptoms are essential.

Take-home: Secure the diagnosis before recommending lifelong dietary restriction.

• State the definition being used. APASL/AARC and EASL-CLIF approaches differ; their diagnostic criteria and grading systems should not be mixed.

• Search actively for precipitants. Infection, alcohol-associated hepatitis, viral reactivation and gastrointestinal bleeding are important possibilities.

• Assess all relevant organs. Renal, cerebral, circulatory, respiratory and coagulation abnormalities influence immediate care and prognosis.

• Use serial assessment rather than a single score. Improvement or worsening over the first few days helps guide treatment intensity and transplant decisions.

• Start appropriate organ support early. Infection treatment, haemodynamic care, renal support and nutrition are core components.

• Use albumin for a defined indication. A fixed paracentesis volume or routine halfway infusion should not be generalised from brief lecture notes.

• Consider transplantation early in suitable patients. Successful stabilisation may make a previously unsuitable patient eligible.

• Keep extracorporeal therapies appropriately qualified. Plasma exchange has emerging trial evidence; albumin-replacement devices and other approaches are not interchangeable or universal treatments.

Take-home: ACLF management depends on rapid trigger control, organ support and repeated assessment of transplant suitability.

• Recognise the emergency early. Acute liver injury with coagulopathy and encephalopathy requires urgent specialist assessment and consideration of transfer to a transplant centre.

• Identify the cause promptly. Drug toxicity, viral hepatitis, autoimmune disease and other causes require targeted investigation and treatment.

• Support organ function while assessing recovery. Monitor glucose, haemodynamics, renal function, infection and neurological status closely.

• Ammonia trends matter. Significant hyperammonaemia raises concern for cerebral oedema, but ammonia should not be used as the only prognostic measure.

• Consider CRRT in appropriate patients, including those with renal indications or concerning hyperammonaemia. Its role extends beyond correcting creatinine.

• Interpret early-CRRT evidence carefully. A recent pilot trial provides encouraging findings but does not establish a universal protocol for every ALF patient.

• Plasma exchange may be useful in selected settings. Your note that it has little benefit should not become a blanket conclusion.

• Do not postpone transplant assessment while trying supportive therapies. These may serve as bridges to recovery or transplantation.

Take-home: Early referral and coordinated organ support preserve the opportunity for recovery or transplantation.

• Do not screen the general population routinely. Current surveillance is directed towards selected high-risk individuals.

• Take a detailed family history. Record affected relatives, their relationship to the patient and age at diagnosis; genetic counselling may clarify eligibility.

• Recognise relevant inherited risks. Peutz–Jeghers syndrome, CDKN2A mutations and hereditary pancreatitis are important examples. Other mutations require consideration of family history and applicable guidance.

• Use MRI/MRCP and EUS in expert programmes. These provide complementary assessment of pancreatic lesions.

• Individualise the starting age. The responsible syndrome and youngest affected relative influence when surveillance should begin.

• CA19-9 is not a standalone screening test. A normal result does not exclude early pancreatic cancer.

• Treat new-onset diabetes as a risk signal, not an automatic screening indication. Weight loss and worsening glycaemia may justify further evaluation; END-PAC can support risk enrichment.

• Keep AI tools in perspective. Their clinical role requires validation and a defined pathway for acting on results.

Take-home: Surveillance is most useful when risk selection and downstream management are both well organised.

• Recognise evolving organ failure early. Reassess haemodynamics, oxygenation, urine output and laboratory trends; deterioration requires appropriate monitored or intensive care.

• Use fluids with frequent reassessment. Avoid indiscriminate aggressive hydration, particularly in patients with cardiac or renal disease.

• Provide nutrition early. Oral feeding is preferred when tolerated; enteral feeding is favoured over parenteral nutrition when oral intake is inadequate.

• Do not prescribe prophylactic antibiotics for sterile necrosis. Treat suspected or confirmed infection and investigate its source.

• Reserve early CT for a clear indication. Imaging is useful when diagnosis is uncertain or improvement fails to occur, rather than automatically at admission.

• Perform urgent ERCP for associated cholangitis. Gallstone pancreatitis alone does not require urgent ERCP in every patient.

• Delay necrosis intervention when the patient is stable, allowing collections to organise where possible.

• Use a step-up strategy. Drainage followed by further intervention only when needed can reduce unnecessary procedural harm.

Take-home: Repeated assessment, appropriate nutrition and selective intervention are central to reducing complications.

• Establish the diagnosis and disease extent. Ileocolonoscopy with appropriate biopsies helps distinguish UC, Crohn’s disease and important mimics.

• Consider local mimics before immunosuppression. Intestinal tuberculosis is particularly relevant in India; CMV, drug injury and ischaemia may also resemble IBD.

• Do not equate symptom improvement with mucosal healing. Clinically well patients can still have active inflammation, especially in Crohn’s disease.

• Plan objective reassessment after treatment begins. Timing should reflect disease severity, the therapy used and whether findings will change management.

• Monitor after ileocolonic resection. Early endoscopic assessment can detect Crohn’s recurrence before symptoms become prominent.

• Use high-quality surveillance for dysplasia. Careful inspection, appropriate enhanced imaging and targeted sampling are central.

• Select strictures carefully for dilation. Length, accessibility, inflammation, associated fistula or abscess, and malignancy risk determine suitability.

• Use capsule endoscopy selectively. Assess retention risk when a stricture is suspected; capsule examination is not suitable for every patient.

Take-home: Endoscopy should answer a defined clinical question and lead to a clear management decision.

• Confirm active inflammation before escalating treatment. Persistent symptoms may arise from infection, IBS overlap, bile acid diarrhoea or structural complications.

• Use objective assessment. Combine symptoms with faecal calprotectin, blood markers, endoscopy and imaging according to disease location.

• Recognise the limits of calprotectin. It is useful in colonic disease but may be less sensitive in isolated small-bowel Crohn’s disease.

• Distinguish inadequate drug exposure from mechanistic failure. Drug levels and anti-drug antibodies can guide selected decisions, especially after loss of response to anti-TNF treatment.

• Do not treat proactive monitoring as mandatory for everyone. Its role depends on the therapy, clinical setting and available evidence.

• Aim for steroid-free remission and endoscopic healing. Histological healing provides additional information in UC but is not a universal formal escalation target.

• Consider earlier effective treatment in high-risk Crohn’s disease to reduce cumulative bowel damage.

• Reserve combined advanced therapies for carefully selected patients. Dual biologic or biologic–small-molecule treatment requires expert oversight and safety monitoring.

Take-home: Identify the mechanism of failure before changing the dose, drug or treatment strategy.

• Treat acute severe ulcerative colitis as an inpatient emergency. Assess stool frequency, bleeding, systemic toxicity, hydration and nutritional status.

• Exclude infection early. Test for Clostridioides difficile and perform careful flexible sigmoidoscopy with biopsies when appropriate, including assessment for CMV.

• Correct electrolytes, especially potassium. Monitor for abdominal distension and toxic megacolon; use abdominal imaging when clinically indicated.

• Give intravenous corticosteroids and pharmacological thromboprophylaxis, unless a specific contraindication exists. Avoid opioids, antidiarrhoeals and other drugs that may worsen colonic dilatation.

• Review response formally by day 3. Stool frequency and inflammatory markers help identify patients needing rescue therapy.

• Infliximab and ciclosporin are established rescue options. Selection depends on contraindications, previous treatment and local expertise; infliximab is not universally superior.

• Higher-dose infliximab is not routinely better. PREDICT-UC did not establish overall superiority of intensified induction.

• Involve colorectal surgery early. Deterioration, complications or failed rescue treatment should not lead to repeated delays.

Take-home: Timely reassessment and coordinated medical–surgical care protect both the colon and the patient.

• Consider post-infectious IBS when new bowel symptoms follow gastroenteritis. Persistent abdominal pain with altered bowel habit may continue after the infection has resolved.

• Risk is greater after severe infection. Younger age, female sex and psychological distress are recognised associations; bacterial and protozoal infections are important triggers.

• Exclude relevant alternatives. Persistent giardiasis, coeliac disease, inflammatory bowel disease and post-infectious lactose intolerance can resemble IBS.

• Look for alarm features, including bleeding, weight loss, anaemia or progressive symptoms, before making a positive diagnosis.

• Mechanisms extend beyond altered microbiota. Immune activation, changed serotonin signalling and increased intestinal permeability have supporting evidence; permeability should not be described as invariably unchanged.

• Treat the dominant bowel pattern. Dietary advice, appropriate fibre, symptom-directed medication and gut–brain therapies may be combined.

• Avoid presenting antibiotics or glutamine as universal treatment. Benefits are selective and evidence varies.

• Antibody tests are not established routine diagnostic tools. Clinical assessment remains central.

Take-home: Recognise the post-infectious pattern, exclude treatable mimics and provide an individualised treatment plan. PMC

• Recognise the symptom pattern. Early satiety and post-meal fullness suggest postprandial distress; epigastric pain or burning suggests an epigastric pain pattern. Overlap is common.

• Assess alarm features and cancer risk. Endoscopy decisions should reflect age, symptoms, family history and local epidemiology rather than a universal age threshold.

• Test for and treat Helicobacter pylori when appropriate before settling on a functional diagnosis.

• Explain the diagnosis positively. Functional dyspepsia involves altered gut–brain signalling and sensitivity; symptoms are real even when routine investigations are normal.

• Use acid suppression as an initial option, particularly for pain or burning. Selected patients may benefit from a prokinetic.

• Consider low-dose tricyclic treatment for persistent symptoms, with clear explanation of its role as a gut–brain neuromodulator.

• Avoid excessive dietary restriction. Small, regular meals and individual trigger identification are more practical than broad elimination diets.

• Include behavioural treatment when available. Persistent symptoms often require combined approaches and planned review.

Take-home: A clear explanation and symptom-directed treatment are preferable to repeated investigations without a management plan.

Identify patients who need surveillance. Cirrhosis and selected chronic hepatitis B populations are key groups; surveillance is not automatically indicated for every patient with fatty liver.

• Use six-monthly ultrasound with AFP under AASLD guidance. Check whether ultrasound visualisation is adequate rather than accepting a technically limited examination.

• Escalate suspicious findings promptly. A concerning lesion or AFP trend requires appropriate diagnostic imaging.

• AFP alone cannot diagnose HCC. Diagnosis depends on characteristic imaging in suitable at-risk patients or tissue confirmation when necessary.

• Assess tumour burden and liver reserve together. Performance status, portal hypertension and hepatic function influence treatment as much as tumour size.

• Consider curative options early. Resection, ablation and transplantation should be evaluated before disease progression closes the opportunity.

• Use multidisciplinary review to select locoregional or systemic treatment and reassess response.

• Avoid blanket treatment rules. The best option depends on disease stage, liver function, comorbidities and patient preferences.

Take-home: Reliable surveillance and timely staging create the greatest opportunity for curative treatment.

• Assess more than ALT. Treatment decisions require HBV DNA, fibrosis or cirrhosis assessment, age, comorbidities and relevant family history.

• Established oral antivirals remain central. Tenofovir-based treatment and entecavir provide effective viral suppression with a high barrier to resistance.

• Match treatment to the patient. Renal function, bone health, pregnancy and previous antiviral exposure influence drug selection and monitoring.

• Treatment eligibility has expanded. Updated guidance aims to identify more patients who would benefit, including those with significant fibrosis and important clinical risk factors.

• Suppression does not equal cure. Patients may require prolonged treatment and continued follow-up even when HBV DNA becomes undetectable.

• Continue HCC surveillance when indicated. Antiviral therapy reduces risk but does not eliminate it.

• Test for hepatitis D where appropriate, and offer screening and vaccination to susceptible household and sexual contacts.

• Keep emerging therapies in perspective. New approaches target viral products and host immunity, but their availability and clinical role require verification.

Take-home: Expand access to effective treatment while maintaining surveillance, adherence and prevention.

• Fibrosis assessment matters more than documenting fatty liver alone. Patients with diabetes, abdominal obesity and additional metabolic risks deserve particular attention.

• Use a stepwise assessment. Start with FIB-4, followed by transient elastography or another validated second-line test when indicated. Interpret results in the context of age and clinical circumstances.

• Normal liver enzymes do not exclude advanced disease. Avoid reassurance based solely on an apparently normal ALT.

• Set practical weight-loss goals. Sustained loss of approximately 5% improves liver fat; greater reductions are usually needed to improve inflammation and fibrosis.

• Treat the whole patient. Address diabetes, obesity, hypertension, dyslipidaemia, cardiovascular risk and alcohol intake alongside liver disease.

• Exercise remains beneficial even without major weight loss. Combine aerobic activity with resistance training and achievable dietary changes.

• Choose medication according to the clinical indication. Obesity and diabetes therapies can support metabolic management; liver-directed treatment requires appropriate disease staging and eligibility.

• Protect muscle in advanced disease. Weight reduction should not worsen sarcopenia or nutritional status.

Take-home: MASLD management combines fibrosis risk assessment with sustained metabolic care.

• Stabilise first. Assess haemodynamic status, establish intravenous access and arrange timely endoscopic haemostasis. Record the antithrombotic drug, indication, last dose and renal function.

• Distinguish primary from secondary prevention. Aspirin prescribed after myocardial infarction, stroke or established vascular disease carries a different interruption risk from aspirin used for primary prevention.

• Continue secondary-prevention aspirin when possible. If interrupted, resume it on the day endoscopic haemostasis is confirmed.

• Avoid stopping both antiplatelet agents without specialist discussion, particularly after recent coronary stenting. Coordinate decisions with cardiology.

• Anticoagulant reversal is selective. Consider bleeding severity, ongoing drug activity and thrombotic risk rather than reversing every patient automatically.

• Do not routinely transfuse platelets simply to reverse antiplatelet treatment in patients without thrombocytopenia.

• Plan anticoagulant resumption before discharge. Timing depends on haemostasis, rebleeding risk and the original indication; one fixed interval does not fit every patient.

Take-home: Control the bleeding while minimising avoidable cardiovascular and thromboembolic harm. gi.org