Fatty liver (MASLD): the normal ALT that isn't
So. Fifty-four year old man, came in about his knee, and somewhere in the workup somebody did liver function tests. One clinical scenario, worked through by Sarah and Ben. Every claim in this episode is taken from our own Ocean article "Metabolic dysfunction-associated steatotic liver disease (MASLD)", last reviewed 6 August 2026.
Clinical Rounds, the GPAtlas podcast. Gastroenterology (GIT). 20 minutes. Published 31 August 2026. Free to listen.
Clinical source: our own Ocean article "Metabolic dysfunction-associated steatotic liver disease (MASLD)", last reviewed 6 August 2026.
Transcript
Sarah: Hello, and welcome to GPAtlas Clinical Rounds. I'm Sarah, and this is the podcast where we take one thing you'll genuinely see this week, and work out together what to do about it.
Ben: And I'm Ben. I'm the one who's been through the guidance, so when Sarah tells you what she did, I'll tell you whether the evidence agrees with her. Today, the liver result you were about to reassure someone about.
Sarah: So. Fifty-four year old man, came in about his knee, and somewhere in the workup somebody did liver function tests. His ALT is normal. Completely normal. And there's a line on an old ultrasound report from two years ago that says bright liver, probably fatty change. His BMI is thirty-three. And the thing I would have done, and I think most of us would have done, is glance at the normal ALT and move on to the knee. That is the mistake. Because in this condition, a normal ALT tells you almost nothing.
Ben: Three things today. Why the name changed and why that's a clinical instruction rather than a label. The one number that actually matters, which is not the ALT and not the ultrasound. And what you do with it, which is mostly not a referral.
Sarah: So, the name first. What we all learned as non-alcoholic fatty liver disease is now MASLD. Metabolic dysfunction-associated steatotic liver disease. And NICE has already moved. They renamed and updated NG49 in July, so this isn't something coming down the line, it's the current guideline. Our own article puts it well: the old name was inaccurate and potentially stigmatising, and you should use the change to open the alcohol and weight conversation, not to avoid it.
Ben: And the rename matters clinically, not just politically. Calling it non-alcoholic defined a disease by what it wasn't. Calling it metabolic dysfunction-associated tells you what it is and what to do about it, which is to treat the metabolic problem. And that reframing leads straight to the single most important sentence about this condition. Most people with MASLD die of cardiovascular disease, not liver disease. So the medical priority is aggressive cardiometabolic risk reduction, running alongside fibrosis risk-stratification. Those two things, together.
Sarah: So that's the first one. It's MASLD now, NICE has already changed, and the new name is telling you where to aim.
Sarah: Now the number, and this is the part that changed how I read a liver screen. Routine liver function tests cannot rule this out. The ALT is normal in roughly half of people with MASLD, and that includes some who already have advanced fibrosis. So a normal ALT is not reassurance. Neither is a soft abdomen, neither are absent spider naevi, and neither is a normal-looking liver edge, because palpation is insensitive.
Ben: And two more things that catch people out. The ultrasound tells you about fat, not about scarring, so it is insensitive to fibrosis and to mild steatosis. And it is not a disease of large people only: up to around seven per cent of people with a normal BMI have MASLD, so a normal weight does not exclude it. Which is why the number that matters is a fibrosis score. Our article is blunt about it: the single most important number is the fibrosis- risk score, not the degree of steatosis and not the ALT, because fibrosis stage is the strongest predictor of both liver-related and all-cause mortality.
Sarah: And the good news is you almost certainly already have it. FIB-4 is calculated from results you've got: age, the transaminases and the platelets. It's free, it's automated in most systems, and it takes seconds. So for my man with the normal ALT, I'm not ordering anything new. I'm calculating a score from bloods that are already on the screen.
Sarah: Normal ALT means nothing here. Calculate the FIB-4.
Ben: So here are the bands, and they're worth knowing properly because they decide everything that follows. Below one point three, low risk, advanced fibrosis unlikely. Between one point three and two point six seven, indeterminate, and you arrange a second-line test, either an ELF or a FibroScan. Above two point six seven, high risk, refer to hepatology. On the ELF, the number is ten point five one: at or above that, refer. Two age caveats. Over sixty-five the low-risk threshold moves up to two point oh, and under thirty-five you confirm with elastography. And check your local pathway, because some UK areas use a higher referral threshold of three point two five.
Sarah: And here's the trap at the other end, which I think is the one we'll actually fall into. Don't lose the low-risk patient. If his FIB-4 comes back under one point three, that is not a discharge. He still needs his cardiometabolic risk managed, and he needs the score repeating in about three years. Low risk today is not low risk forever.
Sarah: Under one point three, you keep him and recheck in three years. Over two point six seven, you refer. In between, second-line test.
Sarah: And what do I actually do for him, because most of this is mine, not the hepatologist's. Weight is the single most effective intervention. Seven to ten per cent of body weight can reduce the fat, resolve the inflammation and even regress fibrosis, and even three to five per cent improves liver fat. A Mediterranean-style diet, and cut the sugary drinks. A hundred and fifty minutes a week of moderate activity plus resistance training twice a week, and that helps even if he doesn't lose weight. Alcohol within fourteen units, and abstinence if there's significant fibrosis. And unsweetened coffee, genuinely, is associated with less fibrosis.
Ben: And the one that people get wrong, because it feels counterintuitive. Continue the statin. Do not stop or withhold a statin because of MASLD. It is safe and it is beneficial, and remember what he is most likely to die of. The only reason to reconsider is if the liver enzymes double within three months of starting. That's the rule. Not a vague sense that the liver is unhappy.
Sarah: Before we get to the fibrosis score, there's a step it's tempting to skip, and skipping it is how you end up treating the wrong disease for two years. MASLD is a diagnosis of exclusion. So you do the liver screen. Hepatitis B and C serology. An autoimmune profile. Ferritin and transferrin saturation for haemochromatosis. Alpha-1 antitrypsin. Coeliac serology. Thyroid function. It feels like a lot of bottles for someone whose ultrasound just says fatty liver. But fatty liver on a scan plus metabolic risk factors is a very easy story to accept, and haemochromatosis and autoimmune hepatitis both hide comfortably underneath it.
Ben: And the FIB-4 has a property most people don't know about, which is that the cut-off moves with age. Below one point three is low risk, but that becomes below two point zero if the patient is sixty-five or over. Our article says it's less reliable at the extremes of age: recalibrate at sixty-five and above, and if the patient is under thirty-five, confirm with elastography rather than trusting the score. So the same number means different things in a thirty year old and a seventy year old, and applying one threshold to everybody will over-refer the old and falsely reassure the young.
Ben: Then there's the middle band, between one point three and two point six seven, which is where a lot of patients land and where people get stuck. That's indeterminate, and it has a defined next step: a second-line test, either an ELF blood test or transient elastography, a FibroScan. The ELF is the NICE-recommended test for advanced fibrosis, and a score of ten point five one or above diagnoses it. So indeterminate is not a reason to refer, and it is definitely not a reason to do nothing. It's a reason to do the second test.
Sarah: And check your local pathway, genuinely, because our own article flags that some UK pathways use a higher FIB-4 referral threshold, above three point two five. If you work to the guideline number and your service works to theirs, your referrals come back and the patient waits another three months for a letter that says do the test you already did.
Ben: The cut-off moves at sixty-five. And indeterminate means do the second test.
Ben: There are also results that override the score completely. If you see a prolonged INR, a falling albumin, or platelets below a hundred and fifty, that's portal hypertension or advanced fibrosis and it goes for referral regardless of what the FIB-4 says. And separately, an ALT or ALP at five times the upper limit of normal, or rapidly rising transaminases, is not a fatty liver conversation at all. That's urgent investigation for acute liver injury.
Sarah: And at the other end, the patient whose score is low, who is the one I used to quietly lose. Our article puts it well: don't lose the low-risk patient. They still need cardiometabolic management, and re-testing in about three years. Not discharge. Because low risk today is a statement about today, and the whole point of this disease is that it moves slowly enough for us to stop watching.
Ben: Low risk is a three-year recall, not a discharge.
Sarah: So what do you actually offer him, given there's no tablet for the liver itself? And this is where I've changed how I talk about it, because the numbers are genuinely motivating if you give them properly. A gradual loss of seven to ten per cent of body weight can reduce the fat, resolve the inflammation, and even regress fibrosis. And even three to five per cent improves liver fat. That second number is the one to lead with, because seven to ten per cent sounds impossible to somebody who has failed at diets for twenty years, and three per cent doesn't.
Sarah: And the part I like most, because it rescues the patient whose weight won't shift: a Mediterranean-style diet, cutting sugary drinks, refined carbohydrate and ultra-processed food, lowers liver fat even without weight loss. Same for exercise. Aim for a hundred and fifty minutes a week of moderate activity plus resistance work twice a week, and our article says exercise reduces liver fat independent of weight change. So when he stands on the scales in six months and nothing has moved, that is not a failed consultation. His liver may already be better. And regular unsweetened coffee is associated with less fibrosis, which is the one piece of advice anybody ever takes.
Ben: Alcohol is two-tiered and worth being precise about. Stay within the UK low-risk limits, fourteen units a week. But advise abstinence where there is significant fibrosis or cirrhosis, because alcohol accelerates progression. So the advice genuinely changes once you know the fibrosis stage, which is another reason to finish the risk assessment rather than leave it at fatty liver.
Sarah: Three to five per cent already helps. Say that number first.
Ben: And the statin question, which comes up every single time, usually from the patient. Continue it, or offer it, for cardiovascular risk. It is safe and beneficial in MASLD. Our article says plainly: do not stop or withhold statins on account of MASLD. There is exactly one stopping rule and it's numerical, which is to consider stopping only if the liver enzymes double within three months of starting.
Ben: And the reason that matters is the sentence that should frame the whole consultation. Most people with MASLD die of cardiovascular disease, not liver disease. So the medical priority is aggressive cardiometabolic risk reduction, weight, glycaemic control, blood pressure and lipids with the statin continued, running alongside the fibrosis risk- stratification. Stopping a statin to protect a liver, in a patient whose liver is not what will kill them, is a bad trade twice over.
Sarah: On the new drug, because patients are reading about it. Resmetirom, brand name Rezdiffra, is the first medicine licensed for MASH, MHRA-authorised in June this year, for non- cirrhotic MASH with moderate to advanced fibrosis. But a NICE technology appraisal is still pending, so it is not yet routinely available on the NHS. That's the honest answer to give: it exists, it's real, and we can't prescribe it here yet. Pioglitazone or vitamin E are options in advanced fibrosis but they're off-label and specialist-initiated, and pioglitazone is contraindicated in heart failure and in bladder cancer or uninvestigated visible haematuria.
Ben: Do not stop the statin. The liver is not what most of them die of.
Sarah: Three last traps. Lean MASLD: up to around seven per cent of people with a normal BMI have this, so a normal weight does not exclude it. Surveillance: six-monthly ultrasound for liver cancer is for established cirrhosis only, and non-cirrhotic MASLD does not need it, so don't commit somebody to twice-yearly scans forever out of diligence. And children with suspected MASLD go to paediatric hepatology, not to us.
Ben: Two more. There's no population screening, and NICE doesn't recommend it, so you case-find in the at-risk groups, type 2 diabetes and metabolic syndrome, and you investigate incidental steatosis or abnormal liver tests when they turn up. And on driving, hepatic encephalopathy was added to the DVLA standards in November twenty twenty-five, but it's narrow: it only applies in advanced decompensated cirrhosis. Early MASLD carries no notification duty at all.
Sarah: A normal BMI does not exclude it. Seven per cent of them are lean.
Sarah: One last thought on how this lands for him, because I think it's the part we handle worst. He came in for a routine blood test and he's leaving with a liver condition he's never heard of, a new acronym, and no tablet for it. That combination reads as serious but untreatable, which is the worst of both. So I try to say the opposite explicitly: this is common, we have found it early, the treatment is real even though it isn't a pill, and the thing we are protecting is mostly your heart. Otherwise he goes home and searches for the acronym, and what he finds is cirrhosis.
Ben: Right, exam corner. Sarah, and everybody driving, a few seconds. Fifty-eight year old woman with type two diabetes and a BMI of thirty-four. Incidental fatty liver on ultrasound. ALT is within the normal range. Her FIB-4 comes back at one point nine. What is the next step? A, reassure her, the ALT is normal. B, refer to hepatology. C, arrange an ELF test or a FibroScan. Or D, repeat the liver function tests in six months.
Ben: It's C. One point nine sits in the indeterminate band, between one point three and two point six seven, and that band means a second-line test, not a referral and not reassurance. A is the trap the whole episode is about, because her normal ALT is meaningless here. B sends someone to hepatology who may well not need it, which is exactly what the two-tier approach exists to prevent. And D wastes six months watching a test that was never going to answer the question.
Sarah: So. Three things for Monday. One. A normal ALT does not exclude advanced fibrosis. Half of them have a normal ALT. Two. The number that matters is the FIB-4, and you can calculate it from bloods you already have. And three. Continue the statin. Stop it only if the enzymes double within three months.
Sarah: One thing to reflect on, if you're logging this. Think about the last time you saw fatty liver mentioned on an ultrasound report. Did you calculate a fibrosis score, or did you look at the ALT and move on? The full transcript and the references are on the episode page. Ben and I are synthetic voices. The medicine isn't. See you next week.
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