Am I a Good Candidate for a Liver Transplant? A hepatologist explains who needs one and why timing decides the outcome.

Am I a Good Candidate for a Liver Transplant? A Hepatologist Explains Who Needs One — and Who Doesn’t

Patients ask me two opposite questions in the same week: “Doctor, am I sick enough to need a transplant?” and “Doctor, am I too sick for one?” Both are the right question, because a liver transplant is a timing decision, not a last resort or a default treatment for every damaged liver. In my practice, I evaluate a patient when living with the diseased liver has become more dangerous than the surgery itself — that single principle drives every test, score, and conversation below. One correction I make early with almost every patient: most of what you’ll read online about transplant eligibility is written for the American deceased-donor system. In India, roughly 8 in 10 liver transplants are living donor (LDLT) — a family member gives part of their liver. That changes the eligibility conversation substantially. It isn’t “how sick do you have to be to move up a waiting list” — it’s “is transplant the right call, and do you have a donor.” I’ll flag where this distinction matters throughout. Does Everyone With Cirrhosis Need a Transplant? No. Cirrhosis has two clinically distinct phases, and only one puts transplant on the table. Compensated cirrhosis — the liver is scarred but still functioning. Patients are often working, asymptomatic, with no fluid buildup or confusion. This group needs monitoring, not transplant evaluation. Decompensated cirrhosis — the liver has stopped keeping up. This is the group I actually start evaluating: Recurrent ascites (fluid buildup) Spontaneous bacterial peritonitis Jaundice Hepatic encephalopathy (confusion) Variceal bleeding Worsening kidney function Sarcopenia (muscle wasting) Repeated hospital admissions for any of the above If you’ve already been evaluated and told no, see what actually disqualifies you from a transplant. Case — early referral changed the outcome. A 55-year-old male presented with acute-on-chronic liver failure, deteriorating rapidly — the kind of presentation where the decision window can be as tight as 2 to 3 days. His wife came forward as donor; she wasn’t a blood-group match, so the transplant proceeded as ABO-incompatible, within a selected-cohort protocol where survival outcomes run 80–85% in appropriately selected, desensitized cases. Early recognition and early transplant, not last-minute rescue, was what made survival possible. What Actually Causes the Liver Disease That Leads Here MASLD (formerly NAFLD/fatty liver) — the fastest-growing indication in India right now Alcohol-related liver disease Chronic hepatitis B and C Autoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis Wilson disease, hemochromatosis, alpha-1 antitrypsin deficiency Acute liver failure (days-long deterioration in a previously healthy liver — this one moves fast) Selected hepatocellular carcinoma (HCC) How I Actually Decide — Beyond the Lab Numbers This is the part that separates a real evaluation from a checklist. Disease severity numbers matter — bilirubin, INR, creatinine, sodium, albumin, platelets, imaging. But how MELD gets used changes entirely depending on whether we’re considering DDLT or LDLT, and this is where most patient-facing content gets it backwards. DDLT (Deceased Donor) LDLT (Living Donor) Role of MELD score Drives allocation — “sickest first” on a waitlist Measures surgical risk, not queue position Ideal patient state Higher MELD moves you up the list Moderate/lower MELD often tolerates surgery better Waiting Determined by organ availability Planned around donor readiness Risk of waiting too long Patient may not survive to allocation Patient may become too sick to safely undergo LDLT India relevance ~20% of transplants ~80% of transplants Wait too long for MELD to climb, and an LDLT candidate can become too sick to safely survive the surgery — the opposite of how DDLT logic works. This is exactly why early evaluation, long before a patient is critically ill, matters more in India’s LDLT-majority reality than it does in a pure allocation-queue system. On cancer eligibility specifically: I don’t work off a rigid checklist like Milan criteria alone. Tumor size and number are a starting point, not the whole picture — vascular invasion, response to bridging therapy, and overall liver reserve all factor into whether transplant is the right call for a given patient. Physical fitness for major surgery — heart, lung, kidney function, nutritional status, frailty, infection status all get assessed. Psychological and family readiness — lifelong medication adherence isn’t optional after transplant, and I look for whether a patient and their support system understand that before, not after, listing. Case — delayed referral, severe alcoholic hepatitis. One of the most heartbreaking patterns I see: patients with severe alcoholic hepatitis reaching a tertiary center only after multi-organ failure has already set in. By the time they arrive in the ICU, the critical window for intervention has closed — infection often rules out standard therapy, and an unstable patient can’t safely undergo transplant evaluation. This pattern disproportionately hits patients in their 30s and 40s with young families. Severe alcoholic hepatitis is a medical emergency, not a wait-and-watch diagnosis — early referral to a specialized liver unit is the decisive factor between a second chance and a preventable outcome. When You Do NOT Need a Transplant Compensated, stable cirrhosis Reversible liver injury Early fibrosis Successfully treated hepatitis MASLD without decompensation Case — recovered without transplant. A young male came in with a first episode of severe alcoholic hepatitis — Maddrey discriminant function above 80, a picture that looked transplant-bound. A sepsis screen was negative. With steroid therapy and aggressive nutritional support, he recovered fully without transplantation. Evaluation isn’t a pipeline toward surgery. Sometimes the right call is intensive medical management, and a first-episode presentation with good support behind it is exactly where that call gets made. When Transplant Isn’t Possible Yet (Not Never) Active uncontrolled infection Ongoing alcohol or substance use Severe uncontrolled cardiac disease Malignancy outside transplant criteria Not currently fit for major surgery Most of these are reversible with treatment first — this is a “not now,” not a permanent door closing, and I make a point of telling patients that distinction explicitly. Living Donor vs. Deceased Donor — The Part Most Articles Underweight In India, this is usually the real fork in the road, not MELD-based queue position.

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

Not Overweight, Not Diabetic — So Why Do You Have Fatty Liver?

MASLD & Fatty Liver / Dr. Chetan Kalal

A clinical overview by Dr. Chetan Kalal, DM (Hepatology), Associate Director — Hepatology & Liver Transplant, Gleneagles Hospital, Mumbai Picture this: you are in your early thirties, your weight is normal, you exercise three times a week, and your last blood test came back unremarkable. Then an abdominal ultrasound — done incidentally during a routine health check — shows something unexpected. Fat in the liver. Fatty liver disease, in a person who does not fit a single conventional risk factor for it. This scenario is no longer rare. Hepatology clinics across India are seeing a steady increase in exactly this kind of patient. The condition has a name — lean MASLD, part of the broader spectrum now called Metabolic Dysfunction-Associated Steatotic Liver Disease — and understanding why it happens is not an academic question. Without the right explanation, there is no right treatment plan. The Old Risk Profile No Longer Tells the Whole Story Fatty liver was historically associated with obesity, type 2 diabetes, and heavy alcohol intake. Those associations are real, but they are not the complete picture. A substantial proportion of patients with confirmed hepatic steatosis carry a normal BMI, have no diabetes, and drink little or no alcohol. In Indian clinical practice, this pattern is common enough that lean MASLD is now considered a distinct and important entity — one that is underdiagnosed precisely because patients and clinicians alike assume that a normal weight rules out the diagnosis. Why It Happens: The Real Causes 1. Genetics — PNPLA3, TM6SF2, and the South Asian disadvantage The most significant driver of lean MASLD is genetic. Variants in the PNPLA3 gene impair the liver’s ability to export triglycerides, causing fat to accumulate within liver cells even when dietary intake and body weight are entirely normal. The TM6SF2 variant works through a related mechanism, reducing hepatic lipid secretion. Both are associated with a higher risk of not just fatty liver but also more advanced liver disease — fibrosis and cirrhosis — independent of weight or metabolic status. These risk variants are substantially more prevalent in South Asian populations than in Europeans. This genetic reality helps explain a pattern that has puzzled many Indian patients: fatty liver diagnosed in a lean, fit individual with no obvious lifestyle risk factor. The liver did not malfunction because of what the patient ate or weighed — the predisposition was written into their genetics from the start. 2. Visceral fat and sarcopenic obesity — the hidden adiposity BMI measures total body weight relative to height. It does not tell you where the fat is stored. A person with a perfectly normal BMI can carry significant amounts of visceral fat — fat that accumulates around the abdominal organs, rather than under the skin — and visceral fat is metabolically far more harmful than subcutaneous fat. It drives insulin resistance, systemic inflammation, and hepatic fat deposition at levels that body weight alone would not predict. A related but distinct phenomenon is sarcopenic obesity: low skeletal muscle mass combined with excess body fat, occurring in a person who appears thin or normal. With less muscle available to absorb and metabolise glucose, the liver compensates by converting the excess into fat. The result is fatty liver in someone who looks lean — and who may never be flagged for further investigation because their outward appearance suggests good metabolic health. 3. Insulin resistance before the diabetes label Many patients with lean MASLD have measurable insulin resistance — meaning their tissues respond poorly to insulin — even when their fasting blood glucose and HbA1c fall within normal limits. This is a pre-diabetic metabolic state that does not yet meet the diagnostic threshold for type 2 diabetes, so it is rarely tested for in the context of a routine health check. The liver is exquisitely sensitive to insulin signalling. When that signalling is impaired, the liver receives conflicting instructions: it upregulates fat synthesis and simultaneously reduces fat export. The combination produces steatosis in the absence of overt hyperglycaemia — a condition that a standard blood glucose test will entirely miss. 4. Diet quality, not just calorie count Two people can consume similar total calories and have very different liver outcomes depending on what those calories consist of. Fructose — found in soft drinks, packaged fruit juices, and added sugars in processed food — is metabolised almost exclusively in the liver, and in excess, it is shunted directly into fat synthesis. Refined carbohydrates and ultra-processed foods drive similar hepatic lipogenic pathways. A person eating what they would describe as a “normal” diet — not overeating, not obviously unhealthy — can still be delivering a daily fructose and refined carbohydrate load that a genetically susceptible liver cannot handle. No visible weight gain is required for this process to cause measurable liver damage over years. 5. Hormonal triggers — hypothyroidism and PCOS Hypothyroidism reduces the rate at which the liver clears fat; even subclinical hypothyroidism (where thyroid hormone levels are low-normal but TSH is elevated) can be sufficient to cause steatosis. This is reversible with appropriate thyroid treatment, making it one of the most important and under-recognised causes of fatty liver in lean patients — particularly in women. Polycystic ovarian syndrome (PCOS) is independently associated with insulin resistance and elevated androgens, both of which promote hepatic fat accumulation. Young women with PCOS carry a meaningful risk of developing fatty liver even at normal body weight, and liver assessment is warranted as part of their long-term metabolic monitoring. 6. Medications that cause hepatic steatosis Several commonly used drugs can cause or worsen fatty liver as a direct effect, regardless of the patient’s baseline metabolic risk. The list includes corticosteroids used for inflammatory conditions, tamoxifen prescribed for breast cancer, valproate for epilepsy, and methotrexate used in rheumatological disease. Patients on any of these agents who develop raised liver enzymes deserve formal hepatological evaluation — not simply a repeat blood test in three months. 7. The gut-liver connection The gut microbiome communicates directly with the liver via the

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

Uncategorized / Dr. Chetan Kalal

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

Uncategorized / Dr. Chetan Kalal

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

Uncategorized / Dr. Chetan Kalal

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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