Hepatic cysts and benign liver lesions

• Simple hepatic cysts, haemangiomas, focal nodular hyperplasia (FNH) and hepatic adenomas are four common benign masses of the liver, most often found incidentally on imaging done for another reason. ^[1]
• The commonest solid benign liver lesion is the hepatic haemangioma; simple cysts are the commonest cystic ones. ^[1]
• Haemangioma and FNH rarely need treatment: neither ruptures nor becomes cancer in ordinary practice, and neither requires follow-up once the diagnosis is secure. ^[1][2]
• Hepatic adenomas are the lesion that matters clinically. They are driven by oestrogen and metabolic disease, they can bleed (risk over 20% once over 5 cm) and they can become hepatocellular carcinoma (above all the beta-catenin-activated subtype, in men and lesions over 5 cm). ^[1][2]
• The whole task is to distinguish these harmless lesions from hepatocellular carcinoma, which is the commonest primary cancer of the liver and is treated very differently.

By the end of this page you should be able to:

1. Name the four common benign liver lesions and say which are truly harmless.
2. Explain why a haemangioma looks the way it does on imaging and why no biopsy or follow-up is needed.
3. Describe the structure of FNH and why hepatobiliary-contrast magnetic resonance imaging (MRI) is the gold standard for it.
4. Classify hepatocellular adenomas by molecular subtype and link each to its risk of bleeding and cancer.
5. State when an adenoma in a woman should be resected and why any adenoma in a man is resected regardless of size.
6. Manage simple cysts, including giant, infected or bleeding cysts.
7. Tell a benign liver mass from hepatocellular carcinoma in a patient with and without cirrhosis, and know when to biopsy.

A useful way to group them is by tissue of origin and behaviour.

• Simple hepatic cysts are fluid-filled cavities lined by a single layer of epithelium, derived from ductal plate malformations in fetal life. They are disconnected from the bile ducts and contain thin isotonic fluid that resembles bile but contains no bile acids and no bilirubin. ^[3]
• Hepatic haemangiomas are vascular tumours made of cavernous blood spaces lined by endothelium, fed by the hepatic artery. They are the most common solid benign lesion of the liver. ^[1]
• Focal nodular hyperplasia (FNH) is a hyperplastic response of hepatocytes (with Kupffer cells) to an abnormal small artery, producing a nodule of otherwise normal liver with a central fibrous scar. ^[1]
• Hepatocellular adenomas are clonal, benign tumours of hepatocytes. They are grouped by molecular subtype, because each subtype has a different risk of bleeding and cancer. ^[1][2]

Hepatocellular adenomas are classified by mutation:

• Inflammatory adenoma (reported as 30% to 35% in one review, 40% to 55% in a 2021 scoping review and 40% to 50% in a 2020 review of molecular subtypes, a real disagreement between sources) with mutations in IL6ST, STAT3 or GNAS. Associated with obesity, alcohol and steatotic liver disease. Most likely to bleed after the beta-catenin subtype. ^[1][2][4]
• HNF1A-inactivated adenoma (30% to 40% in the older series, HNF1A mutations). Shows diffuse fat on MRI and is the subtype least likely to bleed or become cancer. ^[1][2]
• Beta-catenin-activated adenoma (about 10% of all adenomas in clinical series; molecular series identify exon 3 mutations in 10% to 15% and exon 7/8 mutations in a further 7% to 10%). Mutation in CTNNB1, exon 3 or exons 7/8. Exon 3 lesions have the highest risk of malignant transformation and are more common in men. Half of beta-catenin lesions are mixed inflammatory/beta-catenin adenomas. ^[1][2][4]
• Sonic hedgehog adenoma, a rare recently described subtype, strongly associated with oral contraceptives and obesity, highly vascular and prone to bleeding. ^[1]
• Unclassified adenoma (about 7%): none of the above. ^[1]

• Overall. Focal liver lesions are common because ultrasound, computed tomography (CT) and MRI are used more often. About 15% of people in general have a hepatic incidentaloma, rising to up to 30% of those over 40. Most are benign in a healthy person; the same imaging finding in a person with cirrhosis or known cancer is more likely to be malignant. ^[2]
• Simple cysts. Found in 2.5% to 18% of adults. Most are under 3 cm and asymptomatic. Cysts over 10 cm are called giant. The cyst is more common in women and in older people. ^{[3] [1]}
• Haemangioma. The commonest solid benign liver lesion. Prevalence 3% to 20%, peak incidence in adults aged 30 to 50 years, women more than men with a ratio of 4.5:1 to 5:1. Most are under 5 cm and remain stable. ^[1]
• FNH. The second commonest solid benign lesion, 8% of all primary liver tumours, prevalence 0.3% to 3% of the general population. Peak age 30 to 50 years, women 6 to 8 times more often than men. Between 2 cm and 20 cm in size, but up to 85% are under 5 cm. ^[1]
• Hepatocellular adenoma. Rare and strongly female (9:1). Annual incidence 30 to 40 cases per million among oral contraceptive users, against 1 case per million among non-users. Increasingly described in people with obesity and metabolic syndrome even without oral contraceptive use. ^[1][2]

• Simple cysts are congenital. They arise from ductal plate malformations, are present from fetal life, and are not acquired. They are not pre-malignant. ^[3]
• Haemangioma has no clear modifiable cause; a genetic subset is described. Hormonal exposure (pregnancy, oral contraceptives, anabolic steroids) has been associated with growth and with bleeding, but haemangiomas do not express oestrogen or progesterone receptors, so contraception and pregnancy are not contraindicated in a patient with a haemangioma. ^[1]
• FNH is believed to develop in response to a vascular abnormality: a small dysplastic artery produces a local hyperplastic response. Contraceptives and pregnancy do not clearly change the size, number or prognosis of FNH: the association is weaker than for adenoma and may partly reflect the fact that more imaging is done in young women. ^[1]
• Adenoma is the lesion with real risk factors. Prolonged androgen exposure (oral contraceptives, anabolic steroids, obesity) is the major driver of formation and growth, and stopping the pill or losing weight can make an adenoma regress. Adenomatosis (10 or more adenomas) is associated with metabolic disorders such as HNF1A maturity-onset diabetes of the young and glycogen storage disease. Rare associations include familial adenomatous polyposis and McCune-Albright syndrome. Size matters: an adenoma over 5 cm carries a bleeding risk of over 20%; across cohorts haemorrhage is reported in up to 25% of adenomas and potentially lethal haemorrhage in around 10%. ^[1][2][4]

The liver receives most of its blood from the portal vein and a minority from the hepatic artery. Benign lesions create their own characteristic vascular patterns, and this is why their imaging differs. ^[1]

• Haemangioma is a slow-flowing vascular tangle. Contrast pools in the periphery first and fills in centrally over minutes, which is why the delayed "fill-in" on CT or MRI is characteristic. ^[1]
• FNH is normal liver tissue rearranged around one abnormal artery, so it takes up hepatocyte-specific contrast; a hepatobiliary phase scan is the key test. ^[1]
• Adenoma is a clonal growth of hepatocytes with abnormal arteries but no portal tracts; it shows hypervascularity with less organised perfusion and uptake. Molecular subtype determines behaviour: beta-catenin activation turns on Wnt signalling and raises the risk of cancer; inflammatory activation (IL-6/STAT3) drives sinusoidal dilatation and raises the risk of bleeding. ^[1][2]
• Cysts are static fluid collections under pressure. They do not become cancer. Symptoms arise from size (compression), infection, bleeding into the cyst or rupture, not from the cyst itself. ^[3]

• Simple cyst: a thin-walled, unilocular, anechoic cavity filled with clear fluid; no septations or solid elements. Multiplicity and calcified or thick walls point to something else. ^[3]
• Haemangioma: cavernous spaces lined by a single layer of endothelium, with fibrous septa; often in the right lobe. ^[1]
• FNH: nodules of hyperplastic hepatocytes around a central artery, with bile duct proliferation in fibrous septa; no capsule. The central scar is a fibrous band containing abnormal arteries and veins, not a true tumour. ^[1]
• Adenoma: sheets of hepatocytes with arteries but no portal tracts or bile ducts; no capsule. Fat in HNF1A type; inflammatory cell infiltration and sinusoidal dilatation in the inflammatory type; nuclear beta-catenin expression and aberrant glutamine synthetase staining in the beta-catenin type. ^[1][2]

Most benign lesions are found by chance and produce no symptoms. When they do, the symptom is usually explained by size, site or complication rather than by the lesion itself. ^[1]

• Simple cysts. Usually none. A giant cyst (over 10 cm) can cause upper abdominal discomfort, early satiety, nausea or a palpable mass by compressing the stomach or diaphragm. Acute pain suggests intracystic haemorrhage or rupture. Fever and tenderness suggest cyst infection. ^[1][3]
• Haemangioma. Almost always silent. A large or "giant" haemangioma (definitions vary: over 5 cm to some authors, over 10 cm to others) can cause right upper quadrant discomfort, nausea or early satiety and, very rarely, high-output cardiac failure or Kasabach-Merritt syndrome (consumptive coagulopathy with thrombocytopenia, prolonged prothrombin time and low fibrinogen, more common in children than adults). ^[1]
• FNH. Usually incidental. A third or fewer patients have abdominal discomfort or pain; the lesion itself does not rupture or bleed. Equally it does not become cancer. Size ranges widely, but 10% of FNH grow and 10% regress on follow-up. ^[1]
• Adenoma. Many are incidental. Presenting features are abdominal pain, a palpable mass or, most dangerously, intra-abdominal haemorrhage and shock (risk over 20% if over 5 cm). Raised liver enzymes are described in the inflammatory subtype. ^[1]

The key question is never "what is this lump?" in isolation; it is "is this patient likely to have liver cancer?" Two situations dominate:

1. Healthy liver, incidental finding: usually benign (cyst, haemangioma, FNH, adenoma) or a metastasis from an occult primary.
2. Cirrhosis or chronic hepatitis B: any new nodule is cancer until proven otherwise.

The aim is to make a firm diagnosis non-invasively wherever possible, because a biopsy in a vascular lesion can bleed. Hepatobiliary-contrast MRI has changed practice: a confident labelled scan avoids most biopsies. ^[1][2]

• First-line.
  • Ultrasound is the first test for simple cysts and the usual first scan for an incidental lesion. A simple cyst is anechoic with a thin wall and no enhancement. ^[3]
  • Liver function tests, bilirubin, albumin, prothrombin time/INR and platelets to assess the background liver, because cirrhosis or chronic hepatitis B changes the whole interpretation. Low platelets suggest portal hypertension. ^[1]
• Characterisation.
  • Contrast-enhanced ultrasound shows enhancement in real time and helps distinguish haemangioma fill-in from the enhancement of cancer. ^[1]
  • Multiphasic CT or contrast-enhanced (including hepatobiliary-contrast) MRI is the definitive test. Haemangioma: T2-bright with peripheral, nodular, discontinuous enhancement matching blood pool and centripetal fill-in. FNH: arterial enhancement with a scar in a minority, and uptake of hepatobiliary contrast in almost all. Adenoma: subtype-specific patterns in up to 80% (diffuse fat for HNF1A, atoll sign for inflammatory, iso- to hyperintense on hepatobiliary phase for beta-catenin exon 3), and generally hypointense on hepatobiliary phase. ^[1][2]
  • Sensitivities and specificities quoted: grayscale ultrasound 94% sensitive and 80% specific for distinguishing haemangioma from hyperechoic malignancy under 3 cm; hepatobiliary-contrast MRI 92% to 97% sensitive and 91% to 100% specific for FNH; HNF1A adenoma fat pattern 87% to 95% sensitive and 85% to 100% specific; atoll sign 97% specific (88% to 100% in another series) for inflammatory adenoma. ^[1][4]
• When to biopsy. Biopsy is reserved for genuinely indeterminate lesions, or where subtype or cancer cannot be excluded by imaging, because the management decision depends on it. It is not needed for a classic haemangioma, FNH or simple cyst. In a patient with cirrhosis or chronic hepatitis B, the possibility of cancer is higher and multidisciplinary discussion is needed; hepatobiliary-contrast MRI may still characterise the benign lesion, but the threshold for biopsy is lower. ^[1][2]
• Cyst-specific tests. Infected cysts are diagnosed by fever, right upper quadrant tenderness, leukocytosis, raised C-reactive protein, positive blood culture or gas/wall thickening on imaging. Definite infection needs cyst aspirate showing inflammatory material or organisms (rarely done). 18FDG PET-CT is reserved for suspected infection in polycystic liver and kidney disease when CT or MRI is negative. Haemorrhage into a cyst is suggested by sudden severe pain with ultrasound, CT or MRI showing a complex cyst. ^[3]

There is no staging system for "benign liver lesion" as a whole. The relevant thresholds are the management cut-offs below. ^[1][2]

• Haemangioma: typical imaging on at least one contrast-enhanced modality is diagnostic. Avoid percutaneous biopsy unless all imaging is inconclusive and cancer remains a realistic possibility: the risk of bleeding exists, but actual complication rates are low when a cuff of normal parenchyma is traversed. MRI is especially useful in fatty liver or cirrhosis, where haemangiomas are rare and harder to recognise. ^[1][2]
• FNH: confident imaging (ideally hepatobiliary-contrast MRI) is diagnostic. Lesions that are atypical, or where adenoma cannot be excluded, need biopsy. A multidisciplinary benign-liver-tumour team (hepatologist, hepatobiliary surgeon, diagnostic and interventional radiologist, pathologist) is recommended by EASL 2016 for this step. ^[1][2]
• Adenoma: MRI with hepatobiliary contrast is the best test, often assigning a subtype. Biopsy is indicated when imaging is indeterminate or a treatment decision depends on subtype. Identification of the beta-catenin subtype and its distinction from unclassified adenoma or cancer on imaging is not currently possible, which is why suspicious beta-catenin lesions are resected rather than watched. ^[1][2]
• Cysts: ultrasound is the first test; further imaging is not indicated for an asymptomatic simple cyst that looks typical. CT or MRI is used when symptoms or complications are suspected. ^[3]

Where sources disagree honestly: EASL, ACG (2014) and the Brazilian Society of Hepatology (2015) disagree on the role of biopsy in haemangioma (ACG discouraged percutaneous biopsy; EASL allowed it when imaging is inconclusive), on follow-up (FNH follow-up anywhere from none to 2 to 3 years depending on contraceptive use; for haemangioma only SBH recommended routine follow-up for lesions over 5 cm and in pregnancy), and on when to operate (ACG considered surgery for haemangiomas over 10 cm; others only for symptoms or complications). They also disagree on beta-catenin MRI features. A modern review (2024) supplies a pragmatic synthesis rather than a single standard. ^[1][2]

• Cyst infection. Ciprofloxacin and/or a third-generation cephalosporin are the recommended first empirical antibiotics (E. coli is the usual organism), used alone or together for about 4 to 6 weeks. Drainage is added if fever stays over 38.5 degrees Celsius after 48 hours of antibiotics, if cultures show resistance, in severe immunocompromise, if intracystic gas is seen on CT or MRI, or if the infected cyst is over 5 cm. ^[3]
• Cyst haemorrhage. Usually conservative; anticoagulants and antiplatelet agents are held for about 1 to 2 weeks, individualised to the balance between bleeding and thrombosis risk. ^[3]
• Adenoma rupture. Resuscitation, transfusion and urgent surgery/embolisation; then definitive resection once the patient is stable. ^[1]
• Adenoma in a man. Resect regardless of size, because most male adenomas are beta-catenin activated. ^[1][2]

Simple cysts.

• Most need nothing: no treatment, no follow-up imaging. ^[3]
• Symptomatic or giant cysts are managed by aspiration with sclerotherapy (ethanol, minocycline or polidocanol), laparoscopic deroofing or resection; no one method has been shown superior, so the centre's expertise should decide. Aspiration alone recurs. ^[3]
• Cysts should never be partially resected for cancer prevention, because there is no cancer risk. ^[1]

Haemangioma.

• Small, asymptomatic, typical lesions: no treatment, no follow-up, reassurance. Pregnancy and contraceptives are not contraindicated. ^[1][2]
• Large or growing lesions that plausibly cause symptoms: non-anatomic resection or enucleation for deep lesions; transarterial embolisation or ablative therapy as less invasive alternatives; transplantation only for unresectable, complicated giant lesions (very rare, under 0.02% of transplants). Always exclude reflux, peptic ulcer, gallstone disease and irritable bowel before attributing pain to the haemangioma. ^[1]

FNH.

• No treatment if the diagnosis is secure and the patient is asymptomatic. Surgical resection or bland transarterial embolisation is reserved for large or progressive lesions with convincing symptoms. ^[1]
• Non-anatomic wedge resection or segmentectomy is used, because FNH is not pre-malignant and functional liver should be spared. ^[1]
• Where imaging suggests FNH but cannot exclude adenoma in a patient still taking oestrogen-containing pills, follow-up cross-sectional imaging at 6 to 12 months to confirm stability is reasonable; once FNH is unequivocally confirmed, no further surveillance is needed. Underlying vascular liver disease is the main exception. ^[1]

Hepatocellular adenoma.

• Remove risk factors first: stop oestrogen-containing contraceptives and anabolic steroids, lose weight, control metabolic syndrome. ^[1][2]
• Resect in all men, regardless of size. ^[1][2]
• Resect in a woman if the lesion is over 5 cm, is beta-catenin activated (on MRI or biopsy), is sonic hedgehog, bleeds, or grows more than 20% over 6 months despite risk-factor modification. ^[1][2]
• Small, stable or regressing adenomas under 5 cm: MRI at 1 year, then annually, spacing out once stability is confirmed. ^[1]
• Because beta-catenin exon 3 lesions have the highest cancer risk, "watch and wait" is not used for them. ^[2]

• Counselling about contraception and metabolic health is the single most effective intervention for adenoma. ^[1]
• Tumour board (benign liver tumour multidisciplinary team) discussion for every lesion with atypical imaging or a management question. ^[2]

• Refer any lesion that is indeterminate on imaging, any adenoma, and any lesion in a patient with cirrhosis or chronic hepatitis B, for multidisciplinary review. ^[1]
• Refer suspected ruptured or infected cyst or adenoma bleeding urgently. ^[1]

• Simple cyst: infection (E. coli most common), intracystic haemorrhage, rupture (rare), and mass effect from giant cysts (compression of stomach, bile ducts or inferior vena cava; portal hypertension reported with very large cysts). ^[3]
• Haemangioma: very rarely rupture (usually after blunt trauma, with high mortality), high-output cardiac failure and Kasabach-Merritt syndrome with giant lesions, biliary or gastric compression. ^[1]
• FNH: none of clinical consequence in ordinary practice. No rupture, no haemorrhage, no malignant change. ^[1]
• Adenoma: intra-abdominal haemorrhage and shock (risk over 20% once over 5 cm, with haemorrhage reported in up to 25% of adenomas overall), malignant transformation to hepatocellular carcinoma (risk factors: beta-catenin exon 3 subtype, over 5 cm, male sex, glycogen storage disease). Most hepatocellular carcinomas arising from adenomas are well differentiated and recur little. ^[1][2][4]

• Simple cysts: benign for life; most never change size. Treatment success is measured by relief of symptoms, not cyst volume. ^[3]
• Haemangioma: benign for life; typical lesions need no follow-up. ^[1]
• FNH: benign for life; usually stable, 10% grow, 10% regress; no cancer. ^[1]
• Adenoma: excellent once the risk factors are removed and high-risk lesions resected; recurrence after resection is uncommon if risk factors are controlled. ^[1]

There is no population screening for benign liver lesions: they are usually harmless and finding them causes anxiety. Prevention instead targets the causes:

• Hepatitis B vaccination and treatment for hepatitis B and C where relevant (these target cancer risk and cirrhosis, not benign lesions).
• Weight control and treatment of metabolic syndrome, both to prevent adenomas and to make existing ones regress.
• Review of oestrogen and anabolic steroid use, especially in women with a known adenoma.

• Pregnancy. Pregnancy is not contraindicated in haemangioma or FNH. Giant haemangiomas in pregnancy may be monitored; definitive treatment is for symptom or growth. Adenoma in pregnancy is higher risk because oestrogen levels rise: an adenoma over 5 cm found before pregnancy should be treated first, and pregnant patients with large adenomas need specialist follow-up. Any treated cyst or adenoma is usually deferred to after delivery unless it is complicated.
• Children. Haemangioma in an infant is a different, often regressing entity; paediatric liver tumours (hepatoblastoma, hemangioendothelioma) have their own pathways. Adenoma in a child is rare and should raise glycogen storage disease.
• Older adults. Cysts and haemangiomas are common and usually incidental; the same disciplined interpretation of a new nodule applies in cirrhosis at any age.
• Immunocompromised and people with polycystic liver and kidney disease. Infected cysts, multiple giant cysts and cystic haemorrhage are more common; 18FDG PET-CT has a specific role in suspected cyst infection in polycystic disease.

• Ultrasound alone diagnoses most simple cysts and suggests most haemangiomas in an otherwise healthy person. The same skill is the single most useful test in any setting.
• A typical haemangioma on ultrasound in a healthy person does not need CT or MRI, especially where contrast imaging is unavailable.
• Most benign lesions need no treatment: reassure, document the diagnosis and avoid repeated imaging.
• Where advanced imaging is unavailable, an atypical or growing lesion, any adenoma and any lesion in a cirrhotic patient should be referred to a centre with multiphasic CT or MRI and a multidisciplinary team.
• Haemangioma pain should not be over-attributed: exclude gallstones and peptic disease before offering surgery.

• The four common benign liver lesions are simple cysts, haemangiomas, FNH and hepatocellular adenomas; metastases and cancer are more common in a person with known cancer or cirrhosis. ^[1]
• Simple cysts are common (2.5% to 18% of adults), usually under 3 cm and asymptomatic, with no cancer risk; giant cysts are over 10 cm and can obstruct, bleed or become infected. ^[3]
• Haemangioma is the commonest solid benign liver lesion (3% to 20% prevalence, women 4.5 to 5 times more often, peak 30 to 50 years); it almost never bleeds or becomes cancer and needs no follow-up once typical on imaging. ^[1]
• FNH is the second commonest solid benign liver lesion (0.3% to 3% prevalence, women 6 to 8:1), has no cancer or bleeding risk, is diagnosed best by hepatobiliary-contrast MRI (about 92% to 97% sensitive and 91% to 100% specific), and does not require follow-up once confirmed. ^[1][2]
• Hepatocellular adenomas are rare and oestrogen-driven (30 to 40 cases per million pill users against 1 per million non-users); they can bleed (haemorrhage in up to 25% of cases overall, risk over 20% once over 5 cm, potentially lethal haemorrhage around 10%) and become cancer. ^[1][2][4]
• Adenoma subtypes: inflammatory 30% to 35% (40% to 55% and 40% to 50% in other reports), HNF1A-inactivated 30% to 40%, beta-catenin activated about 10% (10% to 15% exon 3 plus 7% to 10% exon 7/8 in molecular series, highest cancer risk), sonic hedgehog (rare, bleed-prone) and unclassified (about 7%). ^[1][2][4]
• In men, resect any adenoma regardless of size. In women, resect if over 5 cm, beta-catenin (or sonic hedgehog) subtype, growing more than 20% in 6 months, or if bleeding occurs. ^[1][2]
• Stop oestrogen-containing contraceptives and lose weight: both steps can make an adenoma regress. ^[1][2]
• Cysts are treated only for symptoms; infection needs ciprofloxacin and/or a third-generation cephalosporin for 4 to 6 weeks (with drainage if fever persists above 38.5 degrees Celsius for 48 hours, gas is seen, or the cyst is over 5 cm), and haemorrhage is usually managed conservatively with antiplatelet/anticoagulant hold of 1 to 2 weeks. ^[3]
• In cirrhosis or chronic hepatitis B, a new liver nodule is hepatocellular carcinoma until proven otherwise; LI-RADS and hepatobiliary-contrast MRI help, but a biopsy may be needed when imaging is indeterminate. ^[1]
• Sources genuinely disagree: ACG (2014), SBH (2015) and EASL (2016) recommendations differ on haemangioma biopsy and follow-up, on when to operate, on FNH follow-up and on beta-catenin MRI features. A modern review (2024) and a 2025 Korean cyst guideline are the more recent open sources. ^[1][2]

• Hepatocellular carcinoma and other liver masses (comparison lesion table and non-invasive diagnosis in at-risk patients).
• Liver abscess and parasitic liver disease (hydatid cysts, amoebic disease as differential).
• Cirrhosis and its complications, hepatitis B and C, liver transplantation.
• Metabolic syndrome, obesity, and liver disease.