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What Is Portal Hypertension? The portal vein carries blood from the intestines and spleen to the liver. Portal hypertension is a rise in pressure within this system — defined as a hepatic venous pressure gradient (HVPG) above 5 mmHg. When HVPG reaches 10 mmHg or more, it becomes clinically significant: the point at which varices begin to form and ascites can develop. At 12 mmHg or above, the risk of variceal bleeding rises sharply. Portal hypertension is not a disease in itself but a consequence — most often of cirrhosis, but sometimes of vascular or inflammatory conditions that obstruct blood flow before it enters the liver. Understanding what has blocked the portal circulation determines both the prognosis and the treatment. Causes and Who Is at Risk In India, cirrhosis is responsible for the majority of portal hypertension cases. Alcohol-related liver disease, hepatitis B, hepatitis C, and metabolic-associated steatotic liver disease (MASLD) are the leading drivers. As the liver scars over years, its architecture distorts, vascular resistance rises, and the portal system bears the brunt. India has a higher burden of non-cirrhotic portal hypertension (NCPH) than most Western countries. Two forms are especially relevant here: Extrahepatic portal vein obstruction (EHPVO): A clot in the portal vein, often from a neonatal infection or a prothrombotic disorder, that obstructs flow before it enters the liver. Common in children and young adults. The liver itself may be entirely normal. Non-cirrhotic intrahepatic portal hypertension (NCIPH): A heterogeneous group of conditions — including nodular regenerative hyperplasia and porto-sinusoidal vascular disorder — where resistance is raised within the liver without classical cirrhosis. Less common causes include Budd-Chiari syndrome (hepatic vein thrombosis), right heart failure causing back-pressure, and schistosomiasis (relevant in parts of eastern India). Risk factors across all causes: prothrombotic states, long-term exposure to certain medications or toxins, and chronic viral hepatitis without adequate treatment. Symptoms and Complications Portal hypertension is often silent for years. When it declares itself, it does so through its complications: Gastroesophageal varices: Dilated veins in the oesophagus and stomach that form as the portal system seeks alternative drainage routes. They bleed without warning — and when they do, it is a medical emergency. Ascites: Fluid accumulating in the abdomen. Patients notice abdominal swelling, weight gain, and breathlessness as the diaphragm is pushed upward. Hepatic encephalopathy: Confusion, altered sleep, flapping tremor (asterixis), and — in severe cases — coma, driven by ammonia and other toxins bypassing the liver. Splenomegaly and hypersplenism: An enlarged spleen sequesters platelets and white cells, causing thrombocytopenia and increased infection risk. Hepatorenal syndrome: Kidney failure secondary to circulatory dysfunction, one of the gravest complications of decompensated disease. Diagnosis Diagnosis begins with clinical suspicion — a patient with known liver disease, an unexpectedly low platelet count, or a spleen that has grown too large. From there, the workup is layered: Doppler ultrasound is the first investigation. It can visualise the portal vein, estimate flow velocity, detect splenomegaly, and identify ascites. It is non-invasive, widely available, and the standard initial step. Liver stiffness measurement (FibroScan/transient elastography) is increasingly used to predict clinically significant portal hypertension non-invasively. A liver stiffness above 25 kPa in a patient with known liver disease has a high specificity for HVPG ≥ 10 mmHg, per EASL guidance. When combined with platelet count — the Baveno VII criteria — it can safely avoid endoscopy in a substantial proportion of compensated patients. Upper GI endoscopy remains essential for directly visualising varices, grading their size, and identifying high-risk stigmata (red wale marks, cherry red spots) that predict imminent bleeding. HVPG measurement — via transjugular hepatic venography — is the gold standard. It guides treatment decisions, particularly in clinical trials and refractory cases, but is performed selectively in India given its invasive nature. CT or MRI of the abdomen is used when vascular anatomy needs clarification — especially for portal vein thrombosis, Budd-Chiari syndrome, or pre-transplant assessment. Treatment Management is stratified by the clinical stage — compensated, decompensated, or acutely bleeding — and by the underlying cause. Primary prophylaxis (preventing the first bleed): For patients with medium or large oesophageal varices, or small varices with high-risk features, the APASL consensus on portal hypertension and EASL clinical practice guidelines recommend non-selective beta-blockers (NSBBs) as first-line pharmacological therapy. Carvedilol (12.5 mg daily) is preferred over propranolol in many centres because of its dual action — blocking both portal blood flow and intrahepatic resistance. Endoscopic variceal ligation (EVL) is an effective alternative when beta-blockers are not tolerated. Acute variceal haemorrhage: This is a life-threatening emergency. The priority is resuscitation, restrictive blood transfusion (targeting haemoglobin of 7–8 g/dL), and immediate vasoactive therapy — terlipressin is the vasoactive drug of choice in India and is supported by AASLD and APASL guidelines. Emergency endoscopy within 12 hours, with EVL as the preferred technique, is standard. Prophylactic antibiotics — ceftriaxone 1g intravenously daily for up to seven days — reduce the risk of infection and rebleeding and are recommended by all major societies. In high-risk patients (Child-Pugh C or HVPG ≥ 20 mmHg), early TIPS within 72 hours of the index bleed has been shown to substantially improve survival. Secondary prophylaxis (preventing rebleeding): The combination of NSBBs plus EVL is the standard of care. Neither alone is as effective as the two together. Ascites: Salt restriction (less than 2g sodium daily), spironolactone (starting at 50–100 mg daily, titrated up), and furosemide as needed. Large-volume paracentesis with intravenous albumin infusion (8g per litre of ascites removed) for refractory cases. TIPS (Transjugular Intrahepatic Portosystemic Shunt): A stent placed between the hepatic and portal veins that decompresses the portal system. Used for refractory variceal bleeding, refractory ascites, and certain cases of hepatic hydrothorax. PTFE-covered stents have significantly improved patency rates. TIPS is not appropriate in all patients — hepatic encephalopathy, advanced heart failure, and polycystic liver disease are relative contraindications. Liver transplantation is the definitive treatment for portal hypertension secondary to end-stage liver disease. At Gleneagles Hospital Mumbai, Dr. Chetan Kalal’s programme offers transplant evaluation and listing for patients with

What is ACLF? Acute-on-Chronic Liver Failure (ACLF) is one of the most severe and rapidly fatal syndromes in hepatology. It is defined by the APASL (Asian Pacific Association for the Study of the Liver) as an acute hepatic insult superimposed on a previously diagnosed or undiagnosed chronic liver disease, presenting with jaundice (serum bilirubin ≥5 mg/dL) and coagulopathy (INR ≥1.5), complicated within 4 weeks by clinical ascites and/or encephalopathy in a patient without previous decompensation. Dr. Chetan Kalal is one of India’s foremost experts in ACLF, has co-authored research contributing to the APASL AARC (ACLF Research Consortium) consensus, and manages ACLF cases at Gleneagles Hospital Mumbai. AARC Score and Grading The AARC score (0–15 points) uses six parameters to grade ACLF severity and predict 28-day mortality: Serum bilirubin INR (coagulation) Serum lactate Creatinine Hepatic encephalopathy grade Presence of infection Grade 1 ACLF (AARC score 5–7): 28-day mortality approximately 15–20% with optimal medical therapy. Grade 2 ACLF (AARC score 8–10): Intermediate mortality; intensive care mandatory. Grade 3 ACLF (AARC score 11–15): 28-day mortality exceeds 70% without liver transplantation. Common Precipitants of ACLF in India Hepatitis B reactivation (most common in Asia) Alcohol-related liver disease acute decompensation Bacterial infections — spontaneous bacterial peritonitis (SBP), pneumonia Superimposed drug-induced or herbal-induced liver injury (DILI/HILI) Superimposed hepatitis A or E on chronic liver disease Treatment of ACLF Grade 1: Intensive medical management — treat the precipitant, nutritional support (high-protein diet, BCAA supplementation if encephalopathy), lactulose, rifaximin for encephalopathy, prophylactic antibiotics for infection, and careful fluid management. Grade 2–3: Refer immediately to a tertiary liver centre with ICU and liver transplant capabilities. Evaluate urgently for liver transplantation. The window for transplant is narrow — decisions must be made within 7–10 days of presentation. Liver transplantation is the only definitive treatment for Grade 2–3 ACLF that does not respond to medical therapy. Living donor liver transplant (LDLT) is the preferred route in India given the limited deceased-donor pool. Frequently Asked Questions about ACLF Can ACLF patients survive without a liver transplant? Grade 1 ACLF patients have a meaningful chance of survival with aggressive medical management, particularly if the precipitant is identified and treated early. Grade 2–3 ACLF carries high mortality without transplantation. Early AARC scoring on admission is essential to determine the trajectory and escalate care promptly. How quickly does ACLF progress? ACLF is a rapidly evolving condition. The AARC score should be reassessed at 72 hours and day 7 — an increasing score despite treatment is an indicator to expedite transplant referral. Some patients deteriorate from Grade 1 to Grade 3 within days. Which hospital in Mumbai treats ACLF? Dr. Chetan Kalal at Gleneagles Hospital Mumbai specialises in ACLF management including intensive medical care and liver transplant evaluation for Grade 2–3 ACLF. Referrals from physicians across India and internationally are accepted. Author: Dr. Chetan Kalal — First DM Hepatologist of Maharashtra, AASLD Foundation Award 2016 and 2017. ORCID: 0000-0002-5284-7890. Read more about ACLF treatment at Gleneagles Hospital Mumbai.

Why NRI Patients Choose India for Liver Transplant India has emerged as one of the world’s leading destinations for liver transplantation — combining internationally trained hepatologists, high-volume transplant centres, and costs that are a fraction of those in the UK, USA, UAE, Canada, or Australia. For NRI patients (Non-Resident Indians) living abroad, Mumbai offers a particular advantage: familiar language, family support networks, direct international flights, and world-class medical care at Gleneagles Hospital and other premier centres. Dr. Chetan Kalal, the first DM Hepatologist of Maharashtra and a liver transplant physician at Gleneagles Hospital Mumbai, coordinates liver transplant programmes for patients arriving from the UK, USA, UAE, Gulf (GCC), Canada, Australia, New Zealand, and Africa. Cost Comparison: India vs UK, USA, UAE Country Approximate Liver Transplant Cost United States (USA) USD 300,000 – 500,000+ United Kingdom (NHS — waitlist only; private) GBP 150,000 – 250,000 United Arab Emirates (UAE) USD 150,000 – 250,000 Canada CAD 200,000 – 350,000 Australia AUD 200,000 – 350,000 India (Mumbai — premier centre) USD 25,000 – 40,000 Note: Costs vary by centre, donor type, and patient complexity. These are approximate ranges for comparison only. Living Donor vs Deceased Donor Transplant for International Patients Living Donor Liver Transplant (LDLT) is the preferred and most common route for international patients visiting India. A compatible family member (parent, sibling, child, spouse) donates approximately 60% of their liver, which is transplanted into the recipient. Both livers regenerate to near-full size within 6–8 weeks. LDLT avoids the deceased-donor waitlist entirely. Deceased Donor Liver Transplant (DDLT) is available via the ZTCC Maharashtra waitlist but involves waiting periods that are impractical for international patients visiting specifically for transplantation. DDLT is more suitable for patients who are Mumbai residents. How to Arrange a Liver Transplant in Mumbai from Abroad Initial teleconsultation — Send blood reports (LFT, INR, CBC, creatinine, viral markers), imaging (MRI abdomen or CT triphasic), and any biopsy reports. Dr. Kalal reviews and advises whether transplant is indicated. Donor evaluation — The proposed living donor undergoes blood group, liver volumetry, and fitness assessment. This can be partially done in the home country. Travel to Mumbai — Patient and donor travel together. Most evaluations are completed in 5–7 days before listing. Surgery and recovery — ICU stay typically 5–7 days; hospital stay 2–3 weeks. Most patients return home 4–6 weeks post-transplant. Follow-up — Immunosuppression management can be coordinated with a local physician back home, with teleconsultation follow-up with Dr. Kalal. Frequently Asked Questions Can patients from Dubai get a liver transplant in Mumbai? Yes. Mumbai is a 3-hour direct flight from Dubai. Many patients from the UAE, Saudi Arabia, Kuwait, and other Gulf countries receive liver transplants at Gleneagles Hospital Mumbai. Dr. Chetan Kalal provides initial teleconsultation before the patient travels. What documents are needed for international patients? Passport, medical visa (Indian Medical Visa — MED), sponsor letter from the hospital, all medical records, and proof of relationship with the living donor. Gleneagles Hospital Mumbai has an international patient services team that assists with documentation. Is the quality of liver transplant in India comparable to the UK or USA? India’s top liver transplant centres perform thousands of transplants annually with 1-year survival rates of 85–90%, comparable to leading Western centres. Indian surgeons and hepatologists at premier centres are internationally trained, many holding fellowships from the USA, UK, and Germany. Author: Dr. Chetan Kalal — Hepatologist and Liver Transplant Physician, Gleneagles Hospital Mumbai. ORCID: 0000-0002-5284-7890. For international consultation: Contact Dr. Kalal.

NAFLD is Now Called MASLD — Here is What Changed and Why In 2023, the global hepatology community officially renamed Non-Alcoholic Fatty Liver Disease (NAFLD) to MASLD — Metabolic dysfunction-Associated Steatotic Liver Disease. The rename followed a multi-society consensus (EASL, AASLD, ALEH, APASL) and reflects a more precise understanding of the disease. Key changes in terminology: NAFLD → MASLD (Metabolic dysfunction-Associated Steatotic Liver Disease) NASH → MASH (Metabolic dysfunction-Associated Steatohepatitis) NAFLD cirrhosis → MASH cirrhosis The biology is identical. The new name removes the stigmatising “non-alcoholic” label, emphasises the role of metabolic syndrome (obesity, type 2 diabetes, hypertension, dyslipidaemia), and creates a clearer taxonomy for patients who have both metabolic liver disease and some alcohol use. How Common is MASLD in India? MASLD is the most common liver disease in India, with prevalence estimated at 25–38% of the adult population based on ultrasound-based surveys. The rising rates of obesity, type 2 diabetes, and sedentary lifestyles are driving a parallel epidemic of fatty liver disease. Importantly, MASLD affects non-obese individuals too — so-called “lean MASLD” — which is particularly prevalent in the Indian subcontinent. When Does Fatty Liver Become Dangerous? Most patients with MASLD have simple steatosis (fat accumulation without inflammation) and do not progress to serious liver disease. The danger lies in progression to MASH with fibrosis: Simple steatosis (F0–F1): Usually benign; reversible with lifestyle modification MASH without significant fibrosis (F1–F2): Mildly elevated risk; lifestyle change and close monitoring MASH with advanced fibrosis (F3–F4/cirrhosis): High risk of liver failure, portal hypertension, and hepatocellular carcinoma (HCC). Approximately 10–20% of patients with F3 fibrosis develop cirrhosis over 10 years. Annual FibroScan (transient elastography) is recommended for all MASLD patients to track fibrosis progression without repeated liver biopsies. Can Fatty Liver Be Reversed? Yes — with the right approach: Lifestyle modification (first-line, most evidence): A 7–10% reduction in body weight resolves MASH in most patients and reduces fibrosis by at least one stage in many Mediterranean diet: high in vegetables, legumes, whole grains, olive oil, fish; low in added sugar, refined carbohydrates, and saturated fat Avoid fructose and sugar-sweetened beverages entirely 150–300 minutes of moderate aerobic exercise per week Complete alcohol abstinence Pharmacological options (2024–2025): Semaglutide (GLP-1 agonist): Significant evidence for weight loss and MASH resolution Resmetirom (Rezdiffra): FDA-approved in March 2024 — the first approved drug specifically for MASH with liver fibrosis (F2–F3). Not yet widely available in India. Pioglitazone: Useful in patients with type 2 diabetes and MASH; reduces liver inflammation Vitamin E: Evidence in non-diabetic MASH; limited to specific patient subgroups Frequently Asked Questions Does fatty liver cause pain? Most patients with MASLD/fatty liver have no symptoms. Some experience mild right upper quadrant discomfort or fatigue. Significant pain is unusual in simple steatosis and may indicate complications such as hepatomegaly, MASH with inflammation, or an alternative diagnosis. Any significant abdominal pain warrants evaluation by a hepatologist. Can I drink alcohol if I have fatty liver? No. Alcohol worsens MASLD at any stage. Even moderate alcohol consumption in a patient with metabolic fatty liver increases the risk of progression to MASH and fibrosis. Complete abstinence is strongly recommended by all current guidelines. How is MASLD diagnosed? Liver ultrasound showing increased echogenicity is the standard initial test. FibroScan quantifies liver fat (CAP score) and fibrosis (liver stiffness measurement). Liver biopsy remains the gold standard for definitive diagnosis and fibrosis staging but is reserved for cases where non-invasive tests are inconclusive. Author: Dr. Chetan Kalal — Hepatologist, Gleneagles Hospital Mumbai. MASLD and metabolic liver disease is one of Dr. Kalal’s key clinical areas. Learn more about MASLD management at Gleneagles Hospital Mumbai. ORCID: 0000-0002-5284-7890.