Low-dose aspirin is widely prescribed in the UK for cardiovascular protection, whilst fatty liver disease affects up to 30% of the population. Many patients with metabolic conditions requiring aspirin also have non-alcoholic fatty liver disease (NAFLD), raising important questions about safety and drug interactions. Understanding how aspirin interacts with liver conditions is essential for informed decision-making. This article examines the use of low-dose aspirin in patients with fatty liver, explores safety considerations, and outlines evidence-based management strategies aligned with NHS and NICE guidance.
Summary: Low-dose aspirin is not contraindicated in uncomplicated fatty liver disease or early-stage NAFLD without significant fibrosis, but requires careful assessment in advanced liver disease or cirrhosis due to increased bleeding risk.
- Low-dose aspirin (75 mg daily) works by irreversibly inhibiting platelet aggregation to prevent cardiovascular events.
- Severe hepatic impairment is a contraindication to aspirin; caution is advised in moderate liver disease.
- Patients with cirrhosis, varices, or thrombocytopenia require specialist assessment before continuing aspirin.
- Aspirin is not hepatotoxic and does not directly worsen fatty liver disease at standard doses.
- Lifestyle modification—particularly weight loss of 7–10%—remains the cornerstone of NAFLD treatment.
- Decisions about aspirin in liver disease should involve GP and specialist input to balance cardiovascular benefits against bleeding risks.
Table of Contents
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What Is Low-Dose Aspirin and How Does It Work?
Low-dose aspirin, typically prescribed at 75 mg daily in the UK, is a widely used antiplatelet medication employed for the secondary prevention of cardiovascular and cerebrovascular events. According to the British National Formulary (BNF), it is indicated for patients with established cardiovascular disease—for example, following myocardial infarction or ischaemic stroke—and after coronary artery stenting or bypass surgery. Low-dose aspirin is not routinely recommended for primary prevention in individuals without established disease, due to the risk of bleeding outweighing potential benefits in most cases.
Unlike higher doses used for pain relief, low-dose aspirin works by irreversibly inhibiting the enzyme cyclooxygenase-1 (COX-1) in platelets. This mechanism prevents the formation of thromboxane A2, a substance that promotes platelet aggregation and blood clot formation. By reducing the blood's clotting ability, aspirin helps maintain blood flow through narrowed arteries, thereby lowering the risk of thrombotic events. The antiplatelet effect persists for the lifespan of the platelet (approximately 7–10 days), which is why even a single daily dose provides continuous protection.
Common indications for low-dose aspirin include:
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Secondary prevention following myocardial infarction or ischaemic stroke
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Management of stable angina
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Following coronary artery stenting or bypass surgery
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Acute coronary syndrome
Whilst low-dose aspirin is generally well-tolerated, it is not without risks. The most significant adverse effects relate to gastrointestinal irritation and bleeding, as COX-1 inhibition also affects the protective prostaglandin production in the stomach lining. Patients may experience dyspepsia, gastric ulceration, or in rare cases, serious gastrointestinal haemorrhage.
Important contraindications and cautions include:
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Active peptic ulceration or history of gastrointestinal bleeding
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Haemophilia or other bleeding disorders
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Hypersensitivity to aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs)
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Children under 16 years (risk of Reye's syndrome)
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Third trimester of pregnancy
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Severe hepatic impairment
According to the Summary of Product Characteristics (SmPC) and NHS advice, aspirin should be taken with or after food to minimise gastric irritation. Patients at increased risk of gastrointestinal bleeding—such as those aged over 65 years, with a history of peptic ulcer disease, or taking corticosteroids or selective serotonin reuptake inhibitors (SSRIs)—may benefit from co-prescription of a proton pump inhibitor (PPI) for gastroprotection, as recommended by NICE guidance.
Key drug interactions to be aware of:
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Anticoagulants (warfarin, direct oral anticoagulants) and other antiplatelet agents—significantly increase bleeding risk
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Other NSAIDs—avoid concomitant use due to additive gastrointestinal and bleeding risks
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SSRIs and serotonin-noradrenaline reuptake inhibitors (SNRIs)—increase bleeding risk
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Systemic corticosteroids—increase risk of gastrointestinal ulceration and bleeding
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Heavy alcohol consumption—increases bleeding and gastric irritation
Patients should be counselled about recognising signs of bleeding, such as black or tarry stools (melaena), vomiting blood (haematemesis), or unexplained bruising. If you experience melaena, haematemesis, or signs of severe bleeding, call 999 or go to A&E immediately. For less urgent concerns, such as persistent indigestion or minor bruising, contact your GP.
Do not stop taking aspirin suddenly without medical advice, particularly if you have had a coronary stent, as this may increase the risk of a heart attack or stroke. If you experience side effects or have concerns, speak to your GP or pharmacist. Suspected side effects can be reported via the MHRA Yellow Card scheme at yellowcard.mhra.gov.uk or through the Yellow Card app.
Understanding Fatty Liver Disease: Causes and Symptoms
Fatty liver disease, medically termed hepatic steatosis, occurs when excess fat accumulates in liver cells. It is defined as the presence of steatosis in more than 5% of hepatocytes on histology, or equivalent thresholds on imaging such as MRI-derived proton density fat fraction (MRI-PDFF >5%). In the UK, non-alcoholic fatty liver disease (NAFLD)—also increasingly referred to as metabolic dysfunction-associated steatotic liver disease (MASLD)—is common, affecting an estimated 20–30% of the general population, with higher prevalence in those with obesity, type 2 diabetes, or other metabolic risk factors.
NAFLD exists on a spectrum, ranging from simple steatosis (fat accumulation without significant inflammation) to non-alcoholic steatohepatitis (NASH), which involves inflammation and liver cell injury and may progress to fibrosis, cirrhosis, or hepatocellular carcinoma. The primary causes of NAFLD are closely linked to metabolic syndrome and include obesity, type 2 diabetes mellitus, insulin resistance, dyslipidaemia (particularly elevated triglycerides and low HDL cholesterol), and hypertension. Excessive caloric intake, particularly from refined carbohydrates and saturated fats, combined with a sedentary lifestyle, drives fat deposition in hepatocytes. Less commonly, certain medications, rapid weight loss, or genetic factors may contribute to hepatic steatosis.
Most individuals with early-stage fatty liver disease remain asymptomatic, with the condition often discovered incidentally during routine blood tests or abdominal imaging for unrelated reasons. It is important to note that liver enzymes (ALT, AST) may be normal in many people with NAFLD, so normal blood tests do not exclude the condition. When symptoms do occur, they tend to be non-specific and may include:
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Persistent fatigue and general malaise
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Vague right upper quadrant discomfort or fullness
As the disease progresses to NASH or advanced fibrosis, patients may develop more concerning features such as jaundice, ascites (fluid in the abdomen), peripheral oedema, or signs of portal hypertension. Red-flag symptoms warranting urgent assessment include jaundice with systemic illness, significant abdominal swelling, confusion, or vomiting blood.
According to NICE guideline NG49, there is no recommendation for population screening for NAFLD. However, clinicians should consider the possibility of NAFLD in individuals with abnormal liver function tests or incidental findings of hepatic steatosis on imaging, particularly if metabolic risk factors are present. Once NAFLD is suspected or confirmed, risk stratification for advanced fibrosis should be undertaken using non-invasive tests.
The recommended approach includes:
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First-line: Calculate the FIB-4 score (using age, ALT, AST, and platelet count). A FIB-4 score <1.3 suggests low risk of advanced fibrosis in adults under 65 years; a score >2.67 suggests higher risk. In adults aged 65 years and over, thresholds are adjusted (low risk <2.0; higher risk >2.67).
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Second-line: If FIB-4 is indeterminate or elevated, perform an enhanced liver fibrosis (ELF) blood test. An ELF score ≥10.51 suggests advanced fibrosis and warrants referral to hepatology.
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Imaging: Transient elastography (a non-invasive ultrasound-based technique) may be used to assess liver stiffness and degree of steatosis, supporting fibrosis staging.
Patients with evidence of advanced fibrosis, persistently elevated liver enzymes despite lifestyle modification, or uncertainty about the underlying cause of liver disease should be referred to specialist hepatology services for further assessment and management.
Safety Considerations: Taking Aspirin with Liver Conditions
The relationship between low-dose aspirin and fatty liver disease is complex and requires careful clinical consideration. According to the Summary of Product Characteristics (SmPC) for aspirin, severe hepatic impairment is a contraindication, and caution is advised in patients with hepatic impairment. However, there is no contraindication to using low-dose aspirin in patients with uncomplicated fatty liver disease or early-stage NAFLD without significant fibrosis. The primary concern relates to aspirin's effects on bleeding risk rather than direct hepatotoxicity, as aspirin is not typically considered a hepatotoxic medication at standard doses and does not usually cause elevation of liver enzymes.
Patients with advanced liver disease, particularly those with cirrhosis, require more cautious assessment. Chronic liver disease can impair the synthesis of clotting factors and cause thrombocytopenia (low platelet count), and the addition of an antiplatelet agent may compound bleeding risk. According to guidance from the British Society of Gastroenterology (BSG) and European Association for the Study of the Liver (EASL), in patients with cirrhosis—especially those with oesophageal varices, portal hypertension, or significant thrombocytopenia—the benefits of aspirin for cardiovascular protection must be carefully weighed against the increased risk of gastrointestinal haemorrhage. Decisions should be made on an individual basis, ideally involving both hepatology and cardiology input.
Key safety considerations include:
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Hepatic function: Aspirin is contraindicated in severe hepatic impairment. In patients with compensated cirrhosis or moderate hepatic impairment, aspirin may be used cautiously if the cardiovascular indication is strong, but specialist advice is recommended.
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Platelet count and coagulation: Advanced liver disease may cause thrombocytopenia and coagulopathy. Platelet count and clotting function should be assessed before initiating or continuing aspirin.
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Variceal bleeding risk: Patients with known or suspected oesophageal varices are at higher risk of life-threatening bleeding; aspirin should be used only after careful risk–benefit assessment and, where appropriate, variceal screening or prophylaxis.
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Concomitant medications: Avoid combining aspirin with other NSAIDs, anticoagulants, or antiplatelet agents without specialist guidance, as this significantly increases bleeding risk. Caution is also needed with SSRIs, SNRIs, systemic corticosteroids, and heavy alcohol use, all of which increase bleeding risk. Be aware of herbal products (e.g., ginkgo biloba) that may affect bleeding.
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Gastric protection: Consider co-prescribing a proton pump inhibitor (PPI) in patients with additional risk factors for gastrointestinal bleeding, as recommended by NICE guidance on antiplatelet treatment.
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Monitoring: Liver function tests should be monitored as part of routine NAFLD management (as per NICE NG49), not specifically due to aspirin. However, any new or worsening liver enzyme abnormalities should prompt clinical review.
Do not stop taking aspirin suddenly without medical advice, particularly if you have had a heart attack, stroke, or coronary stent, as stopping may increase the risk of a further cardiovascular event. If you have concerns about continuing aspirin, discuss them with your GP or specialist.
Patients should be advised to call 999 or go to A&E immediately if they experience signs of serious bleeding, such as:
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Black or tarry stools (melaena)
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Vomiting blood or material that looks like coffee grounds (haematemesis)
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Severe or persistent abdominal pain
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Jaundice (yellowing of the skin or eyes) with feeling unwell, confusion, or fever
For less urgent concerns—such as persistent indigestion, minor bruising, or questions about your medication—contact your GP.
Any decision to continue, modify, or discontinue aspirin therapy in patients with liver disease should involve discussion between the patient, their GP, and where appropriate, a hepatologist or cardiologist, to ensure the cardiovascular benefits outweigh potential hepatic and bleeding risks.
Alternative Treatments and Lifestyle Changes for Fatty Liver
Management of fatty liver disease centres primarily on addressing underlying metabolic risk factors through lifestyle modification, which remains the cornerstone of treatment according to NICE guideline NG49. Weight loss is the most effective intervention: a reduction of at least 5% of body weight can improve hepatic steatosis, whilst weight loss of 7–10% or more is associated with improvement in steatohepatitis and may even reverse early fibrosis in many patients. Weight loss should be achieved gradually (approximately 0.5–1 kg per week) through sustainable dietary changes and increased physical activity, rather than rapid weight loss programmes, which may paradoxically worsen liver inflammation.
Dietary recommendations include:
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Adopting a Mediterranean-style diet rich in vegetables, fruits, whole grains, legumes, nuts, and healthy fats (particularly olive oil)
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Reducing intake of refined carbohydrates, added sugars, and sugar-sweetened beverages
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Limiting saturated fats and avoiding trans fats
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Moderating portion sizes to create a modest caloric deficit for gradual weight loss
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Reducing or eliminating alcohol consumption: the UK Chief Medical Officers advise that to keep health risks from alcohol low, it is safest not to drink more than 14 units per week on a regular basis, spread over 3 or more days, and to avoid binge drinking. In patients with steatohepatitis, advanced fibrosis, or cirrhosis, abstinence from alcohol is strongly recommended.
Physical activity plays an equally important role, with current NHS recommendations suggesting at least 150 minutes of moderate-intensity aerobic exercise weekly (such as brisk walking or cycling), combined with muscle-strengthening activities on two or more days per week. Exercise improves insulin sensitivity and promotes fat mobilisation from the liver, even in the absence of significant weight loss.
Regarding pharmacological interventions, there is currently no medication licensed specifically for the treatment of NAFLD or NASH in the UK. However, optimising treatment of associated metabolic conditions is essential and may have additional hepatic benefits:
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Diabetes management: Achieving good glycaemic control is important. Metformin is safe in NAFLD but does not directly treat liver disease. GLP-1 receptor agonists (e.g., semaglutide, liraglutide) promote weight loss and may improve liver histology in some patients, though they are not licensed for NASH and should be considered only under specialist guidance.
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Dyslipidaemia: Statins are safe and effective in patients with NAFLD and should not be withheld or stopped due to mildly abnormal liver enzymes. Statins reduce cardiovascular risk, which is a leading cause of morbidity and mortality in people with NAFLD. Liver function should be monitored as per standard practice.
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Hypertension: Blood pressure should be controlled according to NICE guidance, using standard antihypertensive agents as appropriate.
Off-label pharmacological options (specialist use only):
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Vitamin E: High-dose vitamin E (800 IU daily) has shown benefit in some patients with biopsy-proven NASH without diabetes or cirrhosis, but it is not licensed for this indication. Potential risks include an increased risk of haemorrhagic stroke and prostate cancer (in men) with long-term use. Vitamin E should only be initiated and monitored by a specialist.
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Pioglitazone: This thiazolidinedione, used in type 2 diabetes, has shown promise in improving liver histology in patients with NASH, but it is not licensed for this indication. Potential adverse effects include weight gain, fluid retention (which may precipitate or worsen heart failure), increased fracture risk (particularly in women), and a signal for bladder cancer. Pioglitazone should only be initiated by a specialist after careful patient selection and counselling.
Monitoring and follow-up:
According to NICE NG49, adults with NAFLD who do not have advanced fibrosis should be retested for advanced fibrosis every 3 years using non-invasive tests (FIB-4 and, if indicated, ELF). More frequent monitoring may be appropriate in patients with additional risk factors or progressive disease. Liver function tests and metabolic parameters (HbA1c, lipid profile, blood pressure) should be monitored as part of routine care.
Referral to specialist hepatology services is recommended if:
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There is evidence of advanced fibrosis (e.g., ELF score ≥10.51, high liver stiffness on transient elastography)
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Liver enzymes remain persistently elevated despite lifestyle modification
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There is uncertainty about the underlying cause of liver disease
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The patient has decompensated liver disease or complications of cirrhosis
Regular engagement with primary care, adherence to lifestyle changes, and appropriate monitoring help track disease progression and treatment response. Patients should be supported with tailored advice, and where available, referral to dietetic or weight management services may be beneficial.
Frequently Asked Questions
Can I take low-dose aspirin if I have fatty liver disease?
Yes, low-dose aspirin is generally safe in uncomplicated fatty liver disease or early-stage NAFLD without significant fibrosis. However, if you have advanced liver disease, cirrhosis, or low platelet counts, your doctor will need to carefully assess whether the cardiovascular benefits outweigh the increased bleeding risk.
Does aspirin make fatty liver worse or damage the liver?
No, aspirin is not considered hepatotoxic and does not typically worsen fatty liver disease at standard doses. The main concern with aspirin in liver disease relates to bleeding risk rather than direct liver damage, particularly in patients with advanced fibrosis or cirrhosis.
What are the warning signs I should watch for when taking aspirin with liver problems?
Call 999 or go to A&E immediately if you experience black or tarry stools, vomiting blood, severe abdominal pain, or jaundice with confusion or fever. These may indicate serious bleeding or liver complications requiring urgent medical attention.
Should I stop taking aspirin if I've been diagnosed with NAFLD?
Do not stop taking aspirin without medical advice, especially if you have had a heart attack, stroke, or coronary stent, as stopping suddenly may increase your risk of a cardiovascular event. Discuss any concerns with your GP, who can review your individual circumstances and advise whether aspirin remains appropriate.
Can lifestyle changes help my fatty liver if I'm on aspirin for my heart?
Yes, lifestyle modification is the most effective treatment for fatty liver disease and works independently of aspirin therapy. Gradual weight loss of 7–10% through a Mediterranean-style diet and at least 150 minutes of weekly exercise can improve liver inflammation and may even reverse early fibrosis.
When should I see a specialist about taking aspirin with liver disease?
You should be referred to hepatology if you have evidence of advanced fibrosis (such as an ELF score ≥10.51), cirrhosis, persistently elevated liver enzymes despite lifestyle changes, or complications like varices. Specialist input ensures your aspirin therapy is balanced against bleeding risks and that your liver condition is appropriately managed.
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