RCGP SCA Algorithm — UK Primary Care
Fatty liver is extremely common (25% UK adults have MASLD). Most is benign. The task is identifying the minority who have advanced fibrosis or cirrhosis — they require specialist management.
MASLD (formerly NAFLD) affects 25% of UK adults but progresses to significant fibrosis in only ~5% of patients. The priority is identifying this 5%. Decompensation (jaundice, ascites, encephalopathy, variceal bleed) represents a major turning point — median survival after first decompensation is 1–2 years without transplant. The AST:ALT ratio >2 in a drinker strongly suggests alcoholic hepatitis (AST elevated disproportionately due to pyridoxine deficiency). Acute liver failure (ALT >10× ULN + INR >1.5 + encephalopathy) is a medical emergency requiring same-day specialist assessment.
Both present with raised ALT/GGT and fatty infiltration on USS. Distinction determines treatment pathway — critical clinical step.
The 2023 nomenclature change from NAFLD to MASLD (metabolic dysfunction-associated steatotic liver disease) is clinically important — it explicitly links fatty liver to metabolic syndrome and removes the stigmatising "non-alcoholic" label. MASLD and ALD frequently co-exist (dual aetiology SLD — MetALD). ALD requires alcohol cessation as the primary treatment; MASLD requires metabolic risk factor reduction. GGT is the most sensitive marker of alcohol use but has low specificity — it is elevated by many drugs, obesity, and DM. MCV >100 fl with raised GGT strongly suggests significant alcohol use.
Fibrosis stage determines prognosis and guides referral. FIB-4 is a validated, blood-test-based fibrosis score — calculate for all patients with confirmed MASLD/fatty liver.
Units: Age in years, AST and ALT in U/L, Platelets in 10⁹/L
FIB-4 was validated in large MASLD/ALD cohorts and has excellent negative predictive value for advanced fibrosis (F3-F4) when <1.30 — most patients will be in this low-risk category and can be safely managed in primary care. The indeterminate range (1.30–2.67) requires secondary care assessment — most will be referred for ELF test or FibroScan (transient elastography). Liver stiffness >8 kPa on FibroScan = significant fibrosis; >12 kPa = probable cirrhosis. Liver biopsy remains the gold standard but carries 0.3% risk of significant bleeding — it is reserved for cases where non-invasive tests are inconclusive.
Hepatitis C screening is now universally recommended by NHS England — many patients with hepatitis C acquired it from IVDU in the 1980s-90s and are unaware. Treat-all HCV policy with direct-acting antivirals (DAAs) is highly effective (95%+ cure) and reverses liver fibrosis. Autoimmune hepatitis (AIH) is commonly missed in primary care — it typically presents in young women with elevated ALT, elevated IgG, and positive ANA/ASMA. Missing AIH risks progression to cirrhosis without immunosuppressive treatment. Always check autoimmune markers if LFTs unexpectedly elevated, especially in women of reproductive age.
Patients with MASLD are more likely to die from cardiovascular disease than liver disease. CV risk assessment is a core part of MASLD management — not an afterthought.
The most important clinical message about MASLD: patients die from heart attacks, not liver failure (in the majority). This changes the priority — treating metabolic risk factors (hypertension, dyslipidaemia, DM, obesity) is the primary intervention. The fear of statin-induced liver damage in MASLD is evidence-based myth — statins are safe in MASLD and beneficial for CV risk. GLP-1 agonists (semaglutide) have RCT evidence for significant fibrosis regression in MASH (NASH) — the LEAN and SUSTAIN trials showed histological improvement — making them a priority choice for DM patients with MASLD. Pioglitazone is the only drug with NICE-approved evidence for liver-specific benefit in MASH.
The NICE NG49 pathway establishes FIB-4 as the primary care gatekeeper test — most patients with low FIB-4 never need hepatology referral. This is deliberate: hepatology services are overwhelmed by MASLD referrals because of the high prevalence. The community FibroScan pathway in many ICBs allows primary care to directly access elastography for indeterminate-risk patients without specialist review — check local referral pathways. HCC surveillance (USS 6-monthly + AFP) is only indicated for patients with confirmed cirrhosis — not for all MASLD patients — this distinction avoids over-investigation.
Weight loss of ≥10% is the only intervention consistently shown to reverse significant hepatic fibrosis in MASLD — this is the treatment target. For context: losing 10 kg in a 100 kg patient. GLP-1 agonists (semaglutide) show 59% resolution of MASH and 43% improvement in fibrosis stage in the ESSENCE trial (NEJM 2024) — making them the most promising pharmacological option. Resmetirom received FDA approval in March 2024 (first ever MASH-specific drug) — UK NICE approval pending. HCC risk increases exponentially with fibrosis stage: cirrhosis carries 2–4% annual HCC risk, making 6-monthly surveillance cost-effective.
The fructose reduction message is highly practical and evidence-based: fructose is metabolised almost exclusively in the liver (unlike glucose which is utilised systemically), promoting hepatic de novo lipogenesis. Cutting sugary drinks alone can reduce liver fat by 5–10% in months. Coffee is one of the most surprising evidence-based interventions for liver disease — multiple large studies show dose-dependent protection against cirrhosis and HCC. The OSA-MASLD link is important: untreated OSA causes intermittent hypoxia which independently activates hepatic stellate cells and drives fibrosis. CPAP treatment shows histological improvement in some studies.
HCC surveillance (6-monthly USS + AFP) is highly cost-effective for cirrhotic patients — it doubles the chance of detecting HCC at a curative stage. The AFP threshold for concern is rising levels rather than a single absolute value — a doubling in AFP over 3 months in a cirrhotic patient is highly suspicious. NSAIDs in cirrhosis are particularly dangerous: they inhibit prostaglandin synthesis which maintains renal perfusion in the vasodilated cirrhotic patient — even a short course can precipitate acute hepatorenal syndrome. The "maximum 2 g paracetamol in cirrhosis" rule is often not communicated — patients assume paracetamol is safer than NSAIDs in liver disease, which is partially true at lower doses but not at standard OTC doses (1g × 4).