Author name: Dr. Chetan Kalal

Monsoon Liver Health India: Hepatitis A, Gut Infections, and Why Liver Patients Need Extra Care

Dr Chetan Kalal — DM Hepatologist & Liver Transplant Physician, Gleneagles Hospital, Mumbai  |  July 2026 Monsoon Liver Health India: Hepatitis A, Gut Infections, and Why Liver Patients Need Extra Care Every July, Indian emergency rooms start filling with jaundice, profuse diarrhoea, and fever — illnesses that most patients trace back to something they ate, but whose real origin is the rain itself. This is what monsoon season does to water, what water does to the gut, and why patients with existing liver disease face a genuinely different level of risk. The monsoon brings relief — and a disruption of infrastructure that is invisible until someone gets sick. Flooding overwhelms drainage systems and contaminates drinking water supplies with faecal matter. Overhead tanks, borewells, and even municipal water that seems clean can carry hepatitis A virus, hepatitis E virus, the cholera bacterium, typhoid bacilli, and a range of other enteric organisms. All of them enter through the mouth. All of them target the gut, the liver, or both. What we informally call monsoon me pet ki bimari — stomach and gut illness in the rains — is, in most cases, one of these waterborne or foodborne infections expressing itself. The Infections That Concern Hepatologists Most Hepatitis A and hepatitis E dominate the hepatology clinic during July and August. Both travel by the faecal-oral route: contaminated water, shellfish (oysters and clams concentrate the virus efficiently), raw foods washed with untreated water, or hands that were not properly washed before a meal. Both cause acute hepatitis — fever, nausea, loss of appetite, jaundice — that can be clinically indistinguishable without blood tests. In an otherwise healthy adult, hepatitis A is self-limiting. The liver enzymes rise sharply, the patient feels genuinely unwell for several weeks, and recovery is complete in the overwhelming majority of cases. Hepatitis E in most healthy adults follows a broadly similar course — uncomfortable, but manageable at home with rest and hydration. The concern is in who falls outside those comfortable majorities. Cholera and typhoid complete the monsoon quartet. Cholera causes the dramatic, rapid fluid loss that can become dangerous within hours. Typhoid is more insidious — a persistent fever, abdominal discomfort, and intestinal complications that develop over days. Both are waterborne; both are preventable with the same precautions that protect against hepatitis A and E. Why Patients With Liver Disease Face a Different Risk For a patient managing cirrhosis, a hepatitis A or E infection is not a “you’ll recover, just rest” situation. The diseased liver has already lost functional reserve. An acute viral hepatitis superimposed on cirrhosis can trigger acute-on-chronic liver failure — a rapid, multi-organ deterioration that is life-threatening and requires intensive care. Monsoon-season viral hepatitis is a well-recognised precipitant of ACLF, and it is entirely preventable. Hepatitis E in pregnancy carries a risk that is worth stating plainly: severe hepatitis E can cause acute liver failure in pregnant women, and India has among the highest recorded rates of this complication in the world. Any pregnant woman who develops jaundice during the monsoon months needs urgent assessment — not a wait-and-see approach. For patients on immunosuppression after a liver transplant: the threshold for concern is lower than for everyone else on this page. The same drugs that prevent graft rejection dampen the immune response that would normally contain an infection. A gut illness that stays localised in a healthy person can become bloodstream infection in someone on tacrolimus or mycophenolate. If you have received a liver transplant and develop diarrhoea, fever, or any suggestion of jaundice during monsoon season — contact your transplant team the same day, not after a few days of waiting to see if it improves. Practical Prevention: What Actually Works Water is the central variable. Boiling water or using a reliable RO-UV purifier for drinking, cooking, and even rinsing raw vegetables removes the biological risk from the faecal-oral route. The filter on the tap achieves nothing if the water used to wash salad leaves or make ice is untreated — those are the routes that catch careful households off guard. Street food during peak monsoon months deserves genuine caution, particularly cut fruit, chaat items, and anything prepared with water of unknown provenance. Shellfish — oysters, clams, mussels — should be avoided from July through September. They concentrate hepatitis A virus from contaminated coastal water; even thorough cooking does not eliminate all risk if the raw shellfish was severely contaminated. Hepatitis A vaccination is safe, effective, and available across Mumbai. For any patient with chronic liver disease — cirrhosis, fatty liver disease, hepatitis B or C — vaccination against hepatitis A is not optional; it is a straightforward way to remove one serious risk from an already complicated clinical picture. If you are not sure whether you are vaccinated, a simple blood test can check immunity. Discuss it with your hepatologist at the next visit, or sooner if monsoon season has already arrived. Hand hygiene is not glamorous, but it is mechanically effective in a way that no supplement or herbal preparation can replicate. Consistent handwashing with soap — after using the toilet, before handling food, before eating — interrupts the faecal-oral chain for every organism on this list. When to Seek Medical Review Most gut infections during the monsoon are viral gastroenteritis — unpleasant, short-lived, manageable with oral rehydration salts and rest. But certain symptoms call for a doctor within 24 to 48 hours, not after a week of watching: yellowing of the eyes or skin (jaundice), dark urine the colour of tea or cola, high fever with abdominal pain, bloody diarrhoea, or inability to keep any fluids down for more than a day. If you are already under hepatology care — managing cirrhosis, recovering from a transplant, or on immunosuppression for any reason — the threshold is lower still. Do not wait for symptoms to worsen before making contact. A same-day call to your physician’s office is appropriate for any gastrointestinal illness that develops during the monsoon months, even if it

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What you should know about inflammatory gut condition

What is terminal ileitis and symptoms? Terminal Ileitis is inflammation (-itis) of the last part of the small intestine (terminal ileum). This is not a disease by itself but is rather a finding. It is often equated with Crohn’s disease, an autoimmune condition, but there are other common causes such as: Bacterial infections (e.g., Salmonella, Yersinia, Campylobacter) or intestinal tuberculosis or viral infections. Even some drugs such as pain reliever or NSAID can trigger this. It is necessary to identify the cause as this affects treatment, which differs widely, since treatment is based on the cause. Dr Chetan Kalal, Hepatologist and Liver Transplant Physician, Saifee Hospital, Mumbai shares that “It is important to note that the word ‘terminal ileitis’ does not necessarily indicate a dangerous disorder or a high risk (depending on the cause. Inflammatory disease of the terminal ileum can be mild and self-limited or severe. With the correct treatment, most people recover. In some cases, which are more severely inflamed, there may be dehydration, intense pain, the failure to eat, bleeding or, rarely, complications like intestinal blockage or perforation.” The doctor also elaborated on the symptoms, sharing: If, however, the inflammation is caused by conditions such as Crohn’s disease or TB of the intestines, then there is a possibility that treatment will be required on an ongoing basis to avoid complications. Anyone who has a persistent abdominal pain, prolonged diarrhoea, blood in stools, fever or unexplained weight loss should be evaluated by a medical professional before attempting any self-medicines.Symptoms depend on the cause but tend to have pain in the lower right side of the abdomen, diarrhoea (sometimes with blood in the stool), fever, loss of appetite, nausea or vomiting. The symptoms that last for weeks should be followed by additional tests, including colonoscopy or imaging and stool tests, for some infectious reasons. What are Lifestyle and Dietary changes? Dr Pramod Kadam, Consultant, General Surgery, Ruby Hall Clinic added, “Since there are a variety of causes of terminal ileitis, there is no single prevention method.All people can do to limit their risk from infectious causes is to: – Practising good hand hygiene. – Eating well cooked food and drinking safe water, particularly when travelling. – Rejection of raw or undercooked meats, poultry, egg and unpasteurized dairy. – Thoroughly washing fruits and vegetables. – Not using unnecessary antibiotics or painkillers (like ibuprofen or diclofenac) unless a doctor recommends them. – Don’t smoke, as smoking worsens and increases the risk of Crohn’s disease. While no food can cure terminal ileitis, a balanced diet can be beneficial in boosting overall gastrointestinal health, particularly when recovering from the disease. It is preferable to use oats, brown rice, green leafy vegetables, and fruits. Nuts and lentils aid also. Curd or Yogurt contains beneficial bacteria. And good hydration is crucial. Some patients may find it easier to tolerate a low fibre diet during an acute attack when there is a lot of pain or diarrhoea. Eating recommendations, then, should be personalised according to the diagnosis and severity of symptoms. However, anyone who has a persistent abdominal pain, prolonged diarrhoea, blood in stools, fever or unexplained weight loss should be evaluated by a medical professional before attempting any self-medicines.

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Monsoon is here, but is your gut monsoon-ready? 6 simple changes that can keep infections away

The monsoons each year are a welcome respite from the summer heat. As a gastroenterologist, however, I know it also coincides with a typical increase in stomach infections. My clinic begins to see patients with cases of hepatitis A, hepatitis E, acute gastroenteritis, typhoid and severe food poisoning within a few weeks of the first rains. Unfortunately, many of these diseases are 100% preventable. Bacteria, viruses and parasites flourish with the monsoon. Gut infections can happen if the pipelines are flooded, if water is contaminated, if food is not stored properly, and if poor hygiene is practiced. Fortunately, there are a number of simple habits that can go a long way toward keeping your digestive system healthy. Water, food and hygiene issues The first and foremost rule is awareness of drinking water. Contamination can be caused by damaged or flooded pipelines, even if the city supply is treated. Use boiled water or water treated by a good RO-UV purifier. Whenever purchasing packaged water, inspect it for seal and a valid water quality certification. The foods that are eaten also have an impact. Though street food can be very attractive during the rainy season, all that exposed food, cut fruit, fresh juice and food made under unhygienic conditions can carry bad bacteria like Salmonella and E. coli. Medical intervention Lastly, be familiar with when to seek medical attention. If the child vomits often, has a high temperature, is severely ill with diarrhoea, eyes become yellow or dark coloured urine or if the child has a high fever, this is not something to be ignored. Prompt diagnosis and treatment is key to avoiding complications, especially if it involves the presence of hepatitis and/or highly dehydration. The monsoon should be fun not avoided because you catch an illness that is preventable. There are a few conscious alterations in how you eat, drink and take care of your personal hygiene that can make a huge difference. The gut is your body’s first line of defence and you need to protect it, and it will protect you this rainy season. Dr. Chetan Kalal, DM Hepatology & Liver Transplant Specialist, Saifee Hospital, Mumbai Already managing cirrhosis or a liver transplant? Your monsoon risk profile is different from the general public’s — a hepatitis A or E infection that a healthy adult shrugs off can trigger acute-on-chronic liver failure in a cirrhotic patient, or bloodstream infection in someone on post-transplant immunosuppression. Read Monsoon Liver Health India: Hepatitis A, Gut Infections, and Why Liver Patients Need Extra Care for the risk-specific guidance.

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Portal Hypertension: Causes, Diagnosis, Varices, and Treatment in India

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

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Fatty liver disease (NAFLD/NASH) — hepatology consultation, Mumbai

Fatty Liver: ना वजन जास्त, ना मधुमेह… तरीही फॅटी लिव्हर का होतो? जाणून घ्या खरं कारण

Fatty liver Real Causes: सामान्य वजन, नियमित व्यायाम आणि मधुमेह नसतानाही अनेक तरुणांमध्ये फॅटी लिव्हरचे निदान होत असून ही समस्या वाढत आहे. पारंपरिक जोखीम घटकांबाहेरही यकृतात चरबी साचण्याचे प्रमाण वाढत असल्याचे तज्ज्ञांचे निरीक्षण आहे. यामागचे कारण काय, जाणून घ्या ना वजन जास्त, ना मधुमेहतरीही फॅटी लिव्हर का होतो?जाणून घ्या खरं कारण कल्पना करा, तुमचे वय तिशीच्या आसपास आहे. तुमचे वजन सामान्य आहे, तुम्ही नियमित व्यायाम करता, मधुमेह किंवा उच्च रक्तदाबाचा कोणताही इतिहास नाही. तरीही नियमित तपासणीत तुमच्या यकृतात (liver) चरबी साचल्याचे निदान होते. आजच्या घडीला अशी परिस्थिती काही अपवादात्मक राहिलेली नाही. भारतातील यकृतविकार तज्ज्ञांना अशा रुग्णांची संख्या सातत्याने वाढताना दिसत आहे, जे फॅटी लिव्हरच्या पारंपरिक जोखीम गटात बसत नाहीत. पूर्वी फॅटी लिव्हर हा आजार प्रामुख्याने लठ्ठपणा, मधुमेह आणि अतिमद्यपानाशी संबंधित मानला जात होता. मात्र, आता संशोधनातून असे स्पष्ट झाले आहे की मेटाबॉलिक डिसफंक्शन-असोसिएटेड स्टिएटोटिक लिव्हर डिसीज (MASLD) हा आजार बाहेरून पूर्णपणे निरोगी दिसणाऱ्या व्यक्तींनाही होऊ शकतो. सैफी हॉस्पिटलचे डीएम (हेपॅटोलॉजी) व लिव्हर ट्रान्सप्लांट तज्ज्ञ, डॉ. चेतन कलाल यांनी फॅटी लिव्हर होण्यामागचे खरं कारण सांगितले आहे, जाणून घेऊयात. Dizziness Causes: वारंवार चक्कर येतेय? दुर्लक्ष करू नका; असू शकतात ‘हे’ गंभीर आजार यामागचे कारण काय?यामागे सर्वात महत्त्वाचे कारण म्हणजे अनुवांशिकता (Genetics). काही व्यक्तींमध्ये PNPLA3 सारख्या जनुकांमधील बदलांमुळे यकृतात चरबी साचण्याची प्रवृत्ती जन्मतःच अधिक असते. ही प्रवृत्ती दक्षिण आशियाई लोकांमध्ये, विशेषतः भारतीयांमध्ये, अधिक आढळते. त्यामुळे अनेक भारतीयांचे वजन सामान्य असतानाही त्यांना फॅटी लिव्हर होऊ शकतो. याशिवाय, आहाराचा दर्जा देखील अत्यंत महत्त्वाचा ठरतो. कॅलरींचे प्रमाण योग्य असले तरी वारंवार साखरयुक्त पेये, मैद्याचे पदार्थ, पॅकेज्ड स्नॅक्स आणि प्रक्रिया केलेले (Processed) अन्न खाल्ल्यास यकृत अतिरिक्त साखरेचे चरबीत रूपांतर करते. ही प्रक्रिया हळूहळू सुरू राहते आणि वजन न वाढताही कालांतराने फॅटी लिव्हर होऊ शकतो. सध्या संशोधक आतडे आणि यकृत यांच्या परस्पर संबंधावर (Gut-Liver Axis) विशेष भर देत आहेत. प्रक्रिया केलेले अन्न, वारंवार प्रतिजैविकांचा (Antibiotics) वापर, सततचा ताण आणि अपुरी झोप यांमुळे आतड्यांतील उपयुक्त जीवाणूंचे संतुलन बिघडते. त्यामुळे शरीरातील दाह (Inflammation) वाढतो आणि यकृतातील चरबीच्या प्रक्रियेवर परिणाम होतो. त्यामुळे पारंपरिक जोखीम नसलेल्या व्यक्तींमध्येही फॅटी लिव्हरचा धोका वाढू शकतो. याशिवाय, हार्मोनल आणि चयापचयाशी (Metabolic) संबंधित समस्या देखील कारणीभूत ठरू शकतात. हायपोथायरॉईडीझम, पॉलीसिस्टिक ओव्हरी सिंड्रोम (PCOS), इन्सुलिन रेझिस्टन्स आणि कोलेस्टेरॉलमधील बिघाड यांमुळे मधुमेह होण्यापूर्वीच यकृतात चरबी साचण्यास सुरुवात होऊ शकते. सर्वात चिंतेची बाब म्हणजे फॅटी लिव्हरच्या सुरुवातीच्या टप्प्यात कोणतीही लक्षणे जाणवत नाहीत. अनेकांना अल्ट्रासाऊंड किंवा नियमित रक्ततपासणीदरम्यानच हा आजार असल्याचे समजते. सुरुवातीच्या टप्प्यात योग्य जीवनशैलीतील बदलांमुळे हा आजार पूर्णपणे नियंत्रणात आणता येतो. मात्र दुर्लक्ष केल्यास पुढे यकृताची सूज, फायब्रोसिस, सिरोसिस, लिव्हर फेल्युअर आणि अगदी लिव्हर कर्करोगासारख्या गंभीर आजारांचा धोका निर्माण होऊ शकतो. महत्त्वाचा संदेश असा की, शरीराने सडपातळ किंवा निरोगी दिसत असल्याचा अर्थ यकृतही तितकेच निरोगी आहे, असे नाही. तुमचे वजन आणि रक्तातील साखर सामान्य असली, तरी तपासणीत फॅटी लिव्हर आढळल्यास त्याकडे दुर्लक्ष करू नका. यकृतातील फायब्रोसिसची तपासणी आणि मेटाबॉलिक जोखीम मूल्यांकन करून त्यामागील कारण शोधणे आवश्यक आहे. वेळेवर निदान आणि जीवनशैलीतील योग्य बदल केल्यास यकृताचे गंभीर नुकसान टाळता येऊ शकते.यकृताच्या आरोग्याचा विचार करताना केवळ वजनकाट्यावर दिसणारा आकडा पुरेसा नसतो.

Fatty Liver: ना वजन जास्त, ना मधुमेह… तरीही फॅटी लिव्हर का होतो? जाणून घ्या खरं कारण Read More »

Dr. A P J Abdul Kalam Health Award 2024 — Excellence in Hepatology | Dr. Chetan Kalal

Dr. Chetan Kalal, DM Hepatology, has been conferred the Dr. A P J Abdul Kalam Health Award for Excellence in Hepatology (Liver Care) and Community Health. The award was announced by Nandish Communication on the occasion of Doctor’s Day 2024 and published by TheHealthSite.com on 27 June 2024. Dr. Chetan Kalal, Associate Director — Hepatology & Liver Transplant at Gleneagles Hospital Mumbai, received the Dr. A P J Abdul Kalam Health Award 2024 for Excellence in Hepatology (Liver Care) and Community Health. The award was conferred on Doctor’s Day (July 1) by Nandish Communication to honor outstanding doctors who have shown exceptional commitment to their profession and patients. About the Award The Dr. A P J Abdul Kalam Health Awards are named in memory of India’s beloved scientist-president and are presented to honor healthcare professionals across specialties who have demonstrated outstanding commitment to patient care and community health. The awards are announced annually on Doctor’s Day — July 1 — which in India commemorates Dr. Bidhan Chandra Roy, the renowned physician and statesman. Dr. Kalal’s recognition in the category of Hepatology (Liver Care) and Community Health reflects his decade-long dedication to advancing liver disease management in India, with a particular focus on: Acute-on-Chronic Liver Failure (ACLF) — India’s leading cause of liver-related mortality Liver transplantation (living donor and deceased donor) MASLD/fatty liver disease — a rapidly growing public health burden Nutrition and sarcopenia in cirrhosis Making specialist hepatology care accessible to patients across Maharashtra and India About Dr. Chetan Kalal Dr. Chetan Kalal is the first DM Hepatologist of Maharashtra and Associate Director — Hepatology & Liver Transplant at Gleneagles Hospital, Mumbai. He completed his DM Hepatology from the Institute of Liver and Biliary Sciences (ILBS), New Delhi (2016) under the mentorship of Prof. Shiv Kumar Sarin. He has 26 PubMed-indexed publications, has won two EASL International Abstract Awards (Barcelona and Amsterdam), and serves on the Advisory Panels of Novo Nordisk and Eli Lilly for metabolic liver disease. Source: TheHealthSite.com — Tribute to Dedication: Celebrating Healthcare Excellence on Doctor’s Day (Published 27 June 2024)

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Résultats de la Transplantation Hépatique à 1 An : Guide Complet pour les Patients

🌐 Language / ਭਾਸ਼ਾ / اللغة / Langue / ભાષા:   English العربية Français ગુજરાતી ਪੰਜਾਬੀ Résultats de la Transplantation Hépatique à 1 An : Guide Complet pour les Patients Le Dr Chetan Kalal, hépatologiste DM et médecin spécialiste de la transplantation hépatique à l’Hôpital Gleneagles de Mumbai, est reconnu comme le premier hépatologiste DM du Maharashtra. Avec 26 publications indexées sur PubMed dans les domaines de la transplantation hépatique, de l’insuffisance hépatique aiguë-sur-chronique (ACLF) et de la nutrition en soins intensifs, il accompagne les patients atteints d’une maladie hépatique avancée — y compris ceux venant du Maroc, d’Algérie, de Tunisie et d’Afrique de l’Ouest — tout au long du parcours de greffe et du suivi post-transplantation. Ses consultations sont disponibles en présentiel à Mumbai ou en téléconsultation internationale. La transplantation hépatique représente aujourd’hui l’une des interventions chirurgicales les plus complexes et les plus porteuses d’espoir en médecine moderne. Lorsqu’un patient reçoit un nouveau foie, la première année qui suit est déterminante : c’est durant cette période que le corps s’adapte, que le système immunitaire est le plus sollicité, et que les fondations d’une longue survie sont posées. Comprendre ce qui se passe au cours de cette première année — les succès, les défis et les stratégies pour y faire face — est essentiel pour les patients et leurs familles. Pour les patients francophones d’Afrique du Nord et d’Afrique de l’Ouest qui envisagent une transplantation hépatique, Mumbai s’impose comme une destination de référence mondiale. L’Inde a développé une expertise chirurgicale et hépatologique de premier rang, avec des coûts bien inférieurs à ceux de l’Europe ou des États-Unis, et une accessibilité facilitée par des liaisons aériennes directes depuis Casablanca, Tunis, Alger, Lagos ou Abidjan. Le Dr Chetan Kalal, à l’Hôpital Gleneagles de Mumbai, accompagne ces patients à chaque étape du processus. Qu’est-ce que la survie à 1 an après une transplantation hépatique ? La survie à 1 an est le principal indicateur de succès en transplantation hépatique. Selon les données des grands registres mondiaux (European Liver Transplant Registry, UNOS/OPTN), les taux de survie à 1 an pour une transplantation hépatique réalisée dans un centre expérimenté dépassent 90 % pour les receveurs adultes, quelle que soit l’indication principale. Ces résultats reflètent les progrès considérables réalisés depuis les débuts de la chirurgie de transplantation dans les années 1960–70 : meilleure sélection des donneurs et des receveurs, perfusion de préservation avancée, immunosuppression ciblée, et soins intensifs post-opératoires spécialisés. À l’Hôpital Gleneagles de Mumbai, les taux de survie à 1 an sont comparables aux standards internationaux des centres de référence. Les principales causes de complications dans la première année La première année après la greffe concentre la majorité des risques. Les causes les plus fréquentes de complication ou de perte du greffon sont : Le rejet aigu : survient typiquement dans les premières semaines ou les premiers mois. Il est traité par bolus de corticoïdes (méthylprednisolone) ou, en cas de rejet résistant, par des immunosuppresseurs plus puissants comme les anticorps anti-thymocytes (ATG). Selon les lignes directrices de l’EASL, un rejet aigu bien pris en charge n’affecte pas la survie à long terme s’il est diagnostiqué rapidement. Les infections : l’immunosuppression nécessaire pour protéger le greffon augmente le risque d’infections bactériennes (dans les 30 premiers jours), fongiques (surtout dans les 2 premiers mois) et virales — notamment le cytomégalovirus (CMV). Une prophylaxie antivirale par valganciclovir est systématique dans les centres modernes. Les complications biliaires : sténoses ou fuites de la voie biliaire surviennent dans 5 à 20 % des cas selon les séries. Elles peuvent être traitées par cholangiopancréatographie rétrograde endoscopique (CPRE) ou par radiologie interventionnelle. Les complications vasculaires : la thrombose de l’artère hépatique (TAH) est la plus redoutée, survenant dans 2 à 5 % des cas. Elle peut nécessiter une retransplantation d’urgence si elle n’est pas détectée précocement. Un suivi echo-doppler hebdomadaire est indispensable durant les premières semaines. La récidive de la maladie initiale : l’hépatite C, autrefois une cause majeure de perte du greffon, est aujourd’hui maîtrisée grâce aux antiviraux à action directe (DAA) avec des taux de guérison supérieurs à 95 %. La stéatohépatite non alcoolique (NASH/MASLD) peut récidiver si le syndrome métabolique n’est pas contrôlé. L’immunosuppression : équilibre délicat et suivi rigoureux L’immunosuppression post-transplantation repose généralement sur une trithérapie initiale : inhibiteur de calcineurine (tacrolimus ou ciclosporine), mycophénolate mofétil (MMF), et corticoïdes. Le tacrolimus est aujourd’hui le pilier central, avec des niveaux cibles stricts mesurés par dosage sanguin (taux résiduels). Les lignes directrices de l’AASLD et de l’EASL recommandent une décroissance progressive des corticoïdes, généralement stoppés dans les 3 à 6 mois après la greffe, afin de réduire le risque de diabète post-transplantation, d’hypertension, d’ostéoporose et d’infections. Le suivi des taux de tacrolimus, la surveillance de la fonction rénale et la détection précoce du rejet sont les piliers du suivi à 1 an. Il est crucial de ne jamais interrompre ou modifier son immunosuppression sans avis médical. Même une seule dose oubliée peut déclencher un épisode de rejet. Les patients qui voyagent à l’étranger après leur transplantation — notamment ceux qui retournent au Maroc, en Algérie, en Tunisie ou en Afrique de l’Ouest — doivent emporter leur carnet de suivi, une liste de leurs médicaments (nom générique et posologie), et les coordonnées de leur centre référent à Mumbai. Nutrition et style de vie dans la première année après la greffe La sarcopénie (perte de masse musculaire) est fréquente chez les patients atteints de cirrhose avancée avant la greffe. La récupération nutritionnelle post-transplantation est un déterminant majeur de la survie à long terme. Les recommandations de l’ESPEN (European Society for Clinical Nutrition and Metabolism) préconisent : Un apport protéique de 1,2 à 1,5 g/kg/jour dans la phase de récupération immédiate Une reprise précoce de la nutrition orale ou entérale dès le premier jour post-opératoire si possible La supplémentation en vitamine D, calcium et magnésium (déplétion fréquente sous tacrolimus et corticoïdes) Une activité physique progressive, supervisée par un kinésithérapeute dès la sortie des soins intensifs Le Dr Kalal est co-auteur de travaux publiés

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Role of Nutritional Therapy in Alcoholic Hepatitis — Dr. Chetan Kalal at Juhu IMA 2026

Dr. Chetan Kalal’s invited lecture at Juhu IMA 2026. Evidence-based nutritional therapy in severe alcoholic hepatitis: protein targets, NG tube feeding, BCAAs, zinc repletion, late evening snack, and why nutrition outperforms corticosteroids at 90 days.

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Weight Loss and Beyond: The Comprehensive Benefits of Treating MASH — Dr. Chetan Kalal at IMPA 2026

Dr. Chetan Kalal’s invited lecture at IMPA 2026 — GLP-1 RAs in MASH, fibrosis regression, cardiovascular risk reduction, HCC prevention, and the practical algorithm for treating metabolic-associated steatohepatitis beyond weight loss alone.

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Obesity Masterclass 2026 — Dr. Chetan Kalal, Invited Faculty | MASLD, Metabolic Liver Disease & Bariatric Hepatology

Dr. Chetan Kalal was invited as Faculty to Obesity Masterclass 2026. A comprehensive review of MASLD, liver fibrosis assessment in obese patients, bariatric surgery and the liver, emerging MASH pharmacotherapy (resmetirom, semaglutide), and MASLD-related liver transplant.

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Book AppointmentDr. Chetan Kalal · Hepatologist