Learning objectives
After this module you should be able to:
- Recognise compensated advanced chronic liver disease (cACLD) in MASLD using liver stiffness and platelets, and know where obesity makes the thresholds unreliable.
- Decide who needs endoscopy or a non-selective beta-blocker, and organise liver cancer surveillance.
- Adjust statins, glucose-lowering drugs, nutrition and weight-loss plans to the stage of cirrhosis.
- Explain the current place of bariatric surgery and MASH drugs in cirrhosis, and when to refer for transplant assessment.
Boxed recommendations are paraphrased from the EASL–EASD–EASO 2024 guideline, with its grades: evidence level from 1 (strongest) to 5; recommendation strong, weak or open; consensus is the panel's agreement (strong means at least 95%).
1Recognising advanced disease: cACLD
Cirrhosis in metabolic dysfunction-associated steatotic liver disease (MASLD) is often silent and is recognised less often than cirrhosis from other causes [1]. Once found, it changes care: patients need liver cancer surveillance, assessment for varices and monitoring for decompensation [2]. Each year, about 3–20% of people with cirrhosis decompensate [2].
Baveno VII uses the term compensated advanced chronic liver disease (cACLD) for the continuum of severe fibrosis and cirrhosis in a patient with ongoing liver injury. It is a practical, stiffness-based label that predicts risk at the bedside, whatever the histological stage. With transient elastography (TE), a liver stiffness measurement (LSM) below 10 kPa rules out cACLD when there are no other clinical or imaging signs; 10–15 kPa suggests it; and above 15 kPa makes it highly likely [3]. A first LSM of 10 kPa or more should be repeated fasting, or backed by a blood marker such as FIB-4 of 2.67 or more or ELF of 9.8 or more, because false-high readings occur [3].
Baveno VII also proposes a "rule of five": stiffness values of 10, 15, 20 and 25 kPa mark stepwise higher risks of decompensation and liver-related death, in any cause of chronic liver disease. In cACLD, LSM can be repeated every 12 months, and patients with cACLD should be seen by a liver specialist [3].
| Finding | Meaning | Caveat in MASLD |
|---|---|---|
| <10 kPa | cACLD ruled out (no other signs) | Check for clinical or imaging signs of cirrhosis |
| 10–15 kPa | Suggests cACLD | Repeat fasting or add FIB-4/ELF |
| >15 kPa | Highly suggests cACLD | Refer to a liver specialist |
| ≤15 kPa and platelets ≥150 ×10⁹/L | Rules out CSPH | Usable in MASLD (weak recommendation) |
| ≥20 kPa or platelets ≤150 ×10⁹/L | Screening endoscopy if no beta-blocker | Below both: missed treatable varices <5% |
| ≥25 kPa | Rules in CSPH | Only if BMI <30 kg/m² |
2Portal hypertension: rule it out, rule it in, treat it
Within cACLD, the key question is whether clinically significant portal hypertension (CSPH) is present, because it changes prognosis and treatment [3]. Hepatic venous pressure gradient measurement is the reference test, but non-invasive tools are accurate enough for daily practice.
In MASLD, a TE stiffness of 15 kPa or less together with a platelet count of 150 ×10⁹/L or more can be used to exclude CSPH. [1]
Ruling CSPH in is harder in MASLD. The 25 kPa rule-in threshold applies only to people with a BMI below 30 kg/m², because both obesity and underweight distort stiffness and give false-positive results. EASL states that the evidence does not yet show which non-invasive test should rule in CSPH in people with obesity [1,3]. The ANTICIPATE-NASH model, which combines LSM, platelets and BMI, can help estimate the risk, but it still needs validation [1,3].
When CSPH is present, a non-selective beta-blocker may be started if there is no contraindication. [1]
In the PREDESCI trial, non-selective beta-blockers in patients with CSPH reduced decompensating events in general, not only variceal bleeding [1]. Baveno VII names carvedilol as the preferred agent in compensated cirrhosis: it lowers portal pressure more, tends to be better tolerated and has improved survival compared with no treatment in compensated patients with CSPH [3]. If a patient has CSPH and tolerates a beta-blocker, it is reasonable to start it without first doing an endoscopy [1].
In cACLD with stiffness of 20 kPa or more and/or platelets below 150 ×10⁹/L, perform an upper endoscopy to look for varices, unless the patient already qualifies for a beta-blocker. [1]
Below both thresholds, fewer than 5% of varices needing treatment are missed, a finding confirmed in a cohort with MASH cirrhosis [1]. Patients who avoid endoscopy should have TE and a platelet count every year, and an endoscopy if stiffness reaches 20 kPa or platelets fall to 150 ×10⁹/L or less [3].
3Liver cancer surveillance
Everyone with MASLD-related cirrhosis should be enrolled in a hepatocellular carcinoma surveillance programme, as for other causes of cirrhosis. [1]
The annual incidence of hepatocellular carcinoma (HCC) in MASH cirrhosis cohorts ranges from 0.2% to 2.6%, while surveillance is judged cost-effective above roughly 1.0–1.5% per year [1]. Risk is higher with long-standing diabetes or obesity, older age, alcohol or smoking, FIB-4 above 3.25, and stiffness above 10 kPa that keeps rising [1]. Without cirrhosis, EASL advises against surveillance below F3 and suggests an individual decision at F3 [1].
Ultrasound every 6 months remains the standard tool [1,4]. Its weakness in MASLD is poor visualisation with obesity: pooled sensitivity of ultrasound alone for early HCC is about 45%. Adding alpha-fetoprotein (AFP) raised it to 63% in a meta-analysis of 13,367 people, and a rising AFP over serial tests is more useful than a single value [1].
Because ultrasound misses many early tumours, especially in obese patients with MASLD cirrhosis, AFP can be added to ultrasound in high-risk people. [1]
MRI is more sensitive (85.7% vs 26.2% for early HCC in the PRIUS study) but costly, so EASL reserves it for high-risk patients with persistently poor ultrasound views, particularly those with nodules [1]. The global consensus agrees: ultrasound with or without AFP at least every 6 months, and MRI case by case [4].
4Metabolic drugs in cirrhosis
Baveno VII lists overweight, diabetes and alcohol as drivers of progression that still need treatment in advanced disease [3]. Most drugs remain usable in compensated cirrhosis; the main change comes with decompensation or worsening renal function.
Statins can be used in chronic liver disease, including compensated cirrhosis, and should be prescribed according to cardiovascular risk guidelines. [1]
Caution is needed in decompensated disease. In a European trial in Child-Pugh B or C cirrhosis, 19% of patients given simvastatin 40 mg daily developed liver toxicity and rhabdomyolysis [1]. AASLD notes limited data in decompensated cirrhosis but allows a statin with careful monitoring when cardiovascular risk is high [2].
Metformin can be used in compensated cirrhosis with preserved kidney function, but not in decompensated cirrhosis, especially with renal impairment, because of the risk of lactic acidosis. [1]
Observational data suggest that metformin may improve transplant-free survival in diabetes with advanced fibrosis or cirrhosis, so EASL advises against stopping it unless decompensation or renal failure requires it [1]. Table 2 summarises the other drug classes.
| Drug | Compensated (Child-Pugh A) | Child-Pugh B / decompensated | Note |
|---|---|---|---|
| Statin | Use per CV risk | Caution; avoid high doses | Toxicity reported with simvastatin 40 mg |
| Metformin | Yes, if kidney function preserved | No | eGFR >30 mL/min in Fig. 4 |
| GLP-1 RA | Yes, for its indication | No recommendation; data limited | Watch muscle mass |
| SGLT2 inhibitor | Yes | Child-Pugh B: yes | Exposure rises in Child-Pugh C; caution in severe renal impairment |
| Sulfonylurea | Not preferred | Avoid | Hypoglycaemia |
| Insulin | If needed | Preferred in decompensation | Global 2025 prefers insulin in cirrhosis with T2D |
Guidelines differ here. EASL allows GLP-1 receptor agonists in Child-Pugh A and SGLT2 inhibitors in Child-Pugh A and B, and keeps insulin for decompensated cirrhosis [1]. The 2025 global consensus names insulin as the recommended treatment for diabetes in MASLD cirrhosis, without separating compensated from decompensated disease [4].
5Nutrition, weight, muscle and alcohol
Sarcopenia affects 50–60% of people with cirrhosis awaiting transplant, and sarcopenic obesity, low muscle with excess fat, is found in 20–35% of people with cirrhosis around transplant, mainly in MASH [1]. Both worsen outcomes. A large waist does not mean good nutrition.
People with sarcopenia, sarcopenic obesity or decompensated cirrhosis should receive a high-protein diet and a late-evening snack. [1]
Most nutrition plans in cirrhosis aim for protein of 1.2–1.5 g/kg per day. Fasting gaps should be short, with meals every 4–6 hours and a late-evening snack containing complex carbohydrate and protein [1]. In compensated cirrhosis with obesity, moderate weight loss through modest calorie restriction and supervised exercise has lowered portal pressure, provided protein intake and physical activity protect muscle [1,2]. EASL gives this a weak recommendation (LoE 3) and advises caution with weight loss in decompensated disease [1].
The same applies to drug-induced weight loss. With semaglutide, lean mass makes up about 39% of the weight lost, so AASLD advises checking for muscle loss, resistance exercise and protein of 1.2–1.5 g/kg per day [5].
People with advanced fibrosis or cirrhosis must stop all alcohol completely and permanently. [1]
6Bariatric surgery in cirrhosis
In MASLD-related cACLD or compensated cirrhosis with an approved indication, bariatric surgery can be considered, but only after careful review by an experienced multidisciplinary team of the indication, the procedure and the presence of CSPH. [1]
Risk rises sharply with liver disease severity. After bariatric surgery, death is about ten times more likely in decompensated than in compensated cirrhosis, and surgery should be avoided with CSPH (above 10 mmHg) except in highly selected patients at expert centres [1]. In transplant candidates, sleeve gastrectomy is the accepted option; gastric bands and Roux-en-Y bypass are avoided [1].
All three main guidelines agree that decompensated cirrhosis is a contraindication, unless surgery is combined with liver transplantation at an experienced centre [1,2,6].
7MASH drugs and cirrhosis: where we stand
No MASH-targeted drug can currently be recommended for people with MASH cirrhosis. [1]
Resmetirom and semaglutide are licensed in some countries for non-cirrhotic MASH with F2–F3 fibrosis [4,5]. The global consensus advises against resmetirom when cirrhosis is shown on biopsy, when TE stiffness exceeds 20 kPa, or when there are clinical or laboratory signs of portal hypertension [4]. AASLD states that semaglutide is not approved to treat MASH cirrhosis (TE above 20 kPa, MRE above 5.0 kPa, ELF above 11.3 or portal hypertension), but people with compensated cirrhosis who take it for diabetes or obesity should be monitored carefully [5].
GLP-1 receptor agonists remain appropriate in compensated cirrhosis for their own indications [1]. In a small trial of 71 people with compensated MASH cirrhosis, semaglutide 2.4 mg weekly was well tolerated and improved liver fat, enzymes, weight and HbA1c, but did not improve histology [1]. Always check local (SFDA) approval and label before prescribing any MASH drug; the Saudi consensus notes that resmetirom was not approved in Saudi Arabia at the time it was written [6].
8Decompensation, transplant and general care
Watch at every visit for ascites, variceal bleeding and hepatic encephalopathy, and follow standard cirrhosis guidelines when they appear [4]. Baveno VII advises that every patient with decompensated cirrhosis be considered for liver transplantation [3]. MASLD candidates differ from others: in 68,950 European transplant recipients, those transplanted for MASH were older, heavier and more often had HCC [1].
Transplant candidates with MASLD should have a multidisciplinary assessment of cardiovascular and metabolic comorbidities to reduce major cardiovascular events before, during and after transplantation. [1]
EASL proposes a stepwise cardiac work-up: history, ECG and echocardiography for all, then stress imaging or CT coronary angiography if baseline tests are abnormal, age is over 50 or there are two or more cardiovascular risk factors [1]. Stress tests can mislead: a meta-analysis found sensitivities of only 28% for stress echocardiography and 61% for perfusion scintigraphy in transplant candidates [1]. Before listing, aim for dietary change and supervised exercise to bring BMI below 40, ideally below 35 kg/m², without worsening sarcopenia. After transplant, MASLD often recurs, especially with several metabolic risk factors [1].
Finally, the global consensus advises considering hepatitis A and B vaccination for all people with MASLD when feasible [4].
9The Saudi 2026 consensus
The Saudi modified-Delphi consensus takes a broader view of liver cancer surveillance than EASL. It recommends regular surveillance for patients with FIB-4 above 2.67, LSM above 12 kPa or MRE above 5.0 kPa (low-level evidence, 100% agreement), and its text advises 6-monthly HCC screening once non-invasive tests suggest F3 or worse, although its formal statement for F3 asks for an individual risk assessment, as EASL does [6]. It notes the disagreement itself: AASLD limits surveillance to cirrhosis, while EASL asks for an individual risk assessment at F3 [6,1,2].
| Guideline | Cirrhosis | F3 without cirrhosis | Tools |
|---|---|---|---|
| EASL–EASD–EASO 2024 | Yes | Individual decision | US every 6 months; AFP and MRI in selected |
| AASLD 2023 | Yes | No | Twice-yearly |
| Global 2025 | Yes | Individualised by risk profile | US ± AFP at least every 6 months |
| Saudi 2026 | Yes | Consider after individual risk assessment (its text advises 6-monthly once NITs suggest F3 or worse) | Every 6 months |
On surgery, the Saudi panel requires multidisciplinary review before bariatric surgery in well-compensated cirrhosis and treats decompensated cirrhosis as a contraindication unless surgery accompanies transplantation. It also supports integrated multidisciplinary care before and after transplant [6].
10Clinical case
A 58-year-old woman with diabetes and a low platelet count
- Presentation
- Seen in a Jeddah diabetes clinic. Type 2 diabetes for 12 years on metformin and gliclazide; hypertension. Weight 88 kg, height 161 cm (BMI 34 kg/m²), eGFR 78 mL/min. No alcohol; hepatitis B and C negative. AST 56 U/L, ALT 40 U/L, platelets 128 ×10⁹/L, albumin 38 g/L, normal bilirubin and INR. Ultrasound: coarse liver, poor views because of body habitus, no ascites.
- Step 1: is this cACLD?
- FIB-4 = (58 × 56) ÷ (128 × √40) = 3,248 ÷ 809.5 = 4.01, well above 2.67. TE with the XL probe after fasting: 22.4 kPa, IQR/median 20%. Stiffness above 15 kPa backed by FIB-4 above 2.67 makes cACLD highly likely. She is Child-Pugh A (score 5) and is referred to hepatology.
- Step 2: portal hypertension
- CSPH cannot be ruled out (stiffness over 15 kPa, platelets under 150). The 25 kPa rule-in threshold cannot be used because her BMI is 30 or more. Stiffness of 20 kPa or more and platelets below 150 mean she needs a screening endoscopy. It shows small oesophageal varices; the hepatologist judges that she has CSPH and starts carvedilol.
- Decision: the care plan
- Continue metformin (compensated, eGFR 78). Replace gliclazide with a GLP-1 receptor agonist for diabetes and obesity (allowed in Child-Pugh A). Start a statin according to cardiovascular risk. Stop any alcohol. HCC surveillance: ultrasound plus AFP every 6 months; MRI if views stay poor. Check hepatitis A and B immunity and vaccinate if needed. Protein is calculated on adjusted body weight: reference weight at BMI 25 = 25 × 1.61² = 64.8 kg; adjusted weight = 64.8 + 0.33 × (88 − 64.8) = 72.5 kg; target 1.2–1.5 g/kg = 87–109 g per day, with a late-evening snack and resistance exercise during moderate weight loss [1].
- Teaching points
- A near-normal ALT hid cirrhosis; the platelet count and FIB-4 were the clues. Obesity made the 25 kPa rule-in invalid, so endoscopy was still needed. Cirrhosis did not mean stopping metformin or statins; it meant adapting them to stage, adding surveillance and protecting muscle. She is not a candidate for resmetirom or for semaglutide as a MASH treatment.
11Test yourself
Choose an answer to see the explanation. Nothing is recorded.
1. A man with MASLD and BMI 36 kg/m² has a TE stiffness of 27 kPa and platelets of 170 ×10⁹/L. What is the best interpretation?
The 25 kPa rule-in threshold applies only when BMI is below 30 kg/m². Ruling out needs both ≤15 kPa and normal platelets.
2. Which combination allows CSPH to be ruled out in MASLD?
EASL accepts stiffness of 15 kPa or less plus platelets of 150 ×10⁹/L or more to rule out CSPH in MASLD (weak recommendation).
3. A patient with obese MASLD cirrhosis has repeatedly poor ultrasound views. What does EASL suggest for HCC surveillance?
Ultrasound alone has about 45% sensitivity for early HCC; AFP raises it, and MRI is reserved for high-risk patients with persistently poor views.
4. Which drug should be stopped when a patient with MASLD cirrhosis decompensates and develops renal impairment?
Metformin should not be used in decompensated cirrhosis, especially with renal impairment, because of lactic acidosis. Insulin is the preferred glucose-lowering option at this stage.
5. What is the current place of MASH-targeted drugs in cirrhosis?
EASL does not recommend any MASH-targeted therapy at the cirrhotic stage. GLP-1 receptor agonists remain usable in Child-Pugh A for diabetes or obesity.
12Key messages
- Stiffness above 15 kPa makes cACLD highly likely; below 10 kPa rules it out if there are no other signs. Refer cACLD to hepatology.
- ≤15 kPa with platelets ≥150 rules out CSPH; ≥25 kPa rules it in only if BMI is below 30. Carvedilol is the preferred beta-blocker when CSPH is present.
- Enrol every patient with cirrhosis in 6-monthly HCC surveillance; add AFP, and MRI if ultrasound views are poor. Saudi 2026 extends surveillance to F3.
- Keep statins, metformin, GLP-1 RAs and SGLT2 inhibitors in compensated disease; adapt or stop them with decompensation. Stop all alcohol.
- Protect muscle with 1.2–1.5 g/kg protein and a late-evening snack. No MASH drug is recommended in cirrhosis; consider transplant once decompensation occurs.
References
- EASL–EASD–EASO Clinical Practice Guidelines on the management of MASLD. J Hepatol 2024;81:492–542. doi:10.1016/j.jhep.2024.04.031
- Rinella ME, et al. AASLD Practice Guidance on the clinical assessment and management of NAFLD. Hepatology 2023;77:1797–835. doi:10.1097/HEP.0000000000000323
- de Franchis R, et al. Baveno VII – Renewing consensus in portal hypertension. J Hepatol 2022;76:959–74. doi:10.1016/j.jhep.2021.12.022
- Younossi ZM, et al. Global consensus recommendations for MASLD and MASH. Gastroenterology 2025;169(5):1017–32. doi:10.1053/j.gastro.2025.02.044
- Bansal MB, et al. Semaglutide therapy for metabolic dysfunction-associated steatohepatitis: November 2025 updates to AASLD Practice Guidance. Hepatology 2026;83(5):1326–40. doi:10.1097/HEP.0000000000001608
- Abaalkhail F, et al. MASLD management in Saudi Arabia: a modified Delphi-based adaptation of international standards. Saudi J Gastroenterol 2026;32(2):104–20. doi:10.4103/sjg.sjg_199_25
How to cite this module
Desoky M. Caring for MASLD cirrhosis. Metabolic Liver Academy, version 1.0. Updated 2026-10-03. Available from: https://drmahmouddesoky.github.io/metabolic-liver-academy/modules/cirrhosis-care.html
For education only. This module summarises published evidence and guidelines; it does not replace clinical judgement, full guidelines or local drug labels. It is not accredited for CME credit. Disclaimer.