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Cystic liver lesions: a pictorial review
Insights into Imaging volume 13, Article number: 116 (2022)
Hepatic cysts (HC) are sac-like structures mainly filled with liquid and showing a distinct membrane. They are usually found incidentally through imaging. A wide spectrum of imaging patterns may be observed for common and uncommon, neoplastic and non-neoplastic diseases. While simple hepatic cysts occur frequently and do not require any treatment or follow-up, non-typical cysts should be carefully analysed to avoid misdiagnosing a lesion that would require appropriate management. Therefore, adequate knowledge of all the relevant imaging patterns is critical to secure an accurate diagnosis. The aim of this review is to describe the imaging features of the different types of hepatic cysts.
Cystic liver lesions are common lesions dominated by simple hepatic cysts.
Aetiologies of hepatic cysts are varied: developmental, infectious, neoplastic.
Atypical characteristics of hepatic cysts should always be searched for.
Atypical features are: thick wall, septa or solid portion, enhancement, non-fluid signal.
The clinical context must always be considered.
Hepatic cysts are frequent (2.5% to 18% in the general population), mostly incidental and asymptomatic lesions [1,2,3]. They are well-defined fluid-filled lesions, with or without epithelial lining. Depending on the lesion, the cystic component may be composed of different types of fluid, including bilious, serous, mucinous, necrotic, haemorrhagic, proteinaceous or mixed fluid [4, 5]. Some of them may be diagnosed non-invasively on the basis of specific imaging features . Radiologists should both know and recognise non-typical benign features—i.e. wall thickness, presence of septa, tissular component, enhancement, and signal intensity on MRI [7, 9]—and systematically take the clinical context into consideration.
The aim of this article is to describe and illustrate some of the most frequent cystic hepatic lesions, with a special emphasis on typical radiological features, which allow a non-invasive diagnosis. Even though the extra-hepatic bile ducts abnormalities, rare tumours sometimes cystic (hepatocellular carcinoma, mucinous cholangiocarcinoma, etc.) and post-traumatic lesions will not be addressed in this review, they are listed in Table 1.
Ductal plate malformations correspond to a group of congenital cystic liver lesions, which can affect both the intra- and/or the extrahepatic biliary ducts. They result from insufficient remodelling and resorption of cylindrical ductal plates . Figure 2 emphasises the stage of ductal plate malformation according to the development of the bile duct, from the centre to the periphery.
Simple hepatic cyst
Simple hepatic cysts (SHC) (also known as bile duct cysts or biliary cysts) are congenital parts of the ductal tree detached from the main biliary system, which dilated to become cystic lesion . There is no consensus on their actual origin. They are thought by some authors to result from the dilatation of the bile duct hamartoma (cf. section) , and they do not communicate with the biliary tract. In the literature, their prevalence is reported to range from 2.5 to 18%, occurring more frequently in women, with an incidence that increases with age [5, 10, 11].
SHCs are benign lesions, which are usually asymptomatic. Cystic serous fluid is continually produced by the cuboidal biliary epithelium . A very large cyst can cause abdominal pain or early satiety by compression. Complications, which may include haemorrhage or infection, are rare and may result in the lesion becoming a “complex cyst”.
A SHC is a well-circumscribed unilocular lesion with a thin imperceptible wall, which may be lobulated; it is anechoic on ultrasonography (US) with increased through-transmission. A SHC is hypoattenuating on computed tomography (CT) images (0–20 HU) and appears as hypointense on T1 and strongly hyperintense on T2 images with magnetic resonance imaging (MRI). It does not have internal nodule and does not show enhancement after the administration of intra-venous contrast agents (whether with US, CT or MRI) (Figs. 3 and 4). It can be bi- or multi-lobar (fused cysts) (Fig. 6). The typical features on each imaging modality are sufficient findings allowing a confident diagnosis.
Complications of SHCs are rare. However, they need to be recognised, since they change the features of the cyst and could therefore lead to misdiagnosis. This is especially the case of tumoural cysts .
Haemorrhage: these cysts can increase in size. They have a heterogeneous content with septations seen as echoic intralesional materials (Fig. 5) (pain can occur during ultrasound examination). On CT, their attenuation is higher than that of simple fluid and, on MRI, the signal produced is that generated by blood flow according to the stage of the bleeding (Figs. 6 and 7). A fluid–fluid level can be observed (Fig. 6). The inner septa are mobile but do not enhance. A pseudo-capsule in the form of a thin peripheral rim enhancement is depicted and should not be mistaken for tumoural tissue.
Infections: they are exceptional, except in the case of polycystic disease. A thick wall with heterogeneous enhancement, a fluid–fluid level and some gas bubbles inside the cyst can be seen. It can be difficult to differentiate these cysts from abscesses, unless a prior examination demonstrated the presence of SHCs.
Rupture: rupture also occurs very rarely and a typical sign suggesting rupture is a “floating wall” inside the cyst. In case of a subcapsular cyst, a rupture can be associated with perihepatic fluid (Fig. 8).
Large symptomatic SHC: even though very large SHCs are usually asymptomatic, they could cause pain or duodenogastric compression. The treatment may be surgical (cyst fenestration) or radiological by sclerotherapy. Due to the difficulty in attributing symptoms to the cyst, a diagnostic test can be carried out through a simple aspiration.
Bile duct hamartoma
Bile duct hamartomas (BH) (also known as von Meyenburg complexes) are benign lesions caused by failure of the small interlobular bile ducts to involute at the late phase of embryogenesis [12–14]. BHs are asymptomatic and disconnected bile duct lesions with only limited dilation, lined by biliary epithelium. The prevalence based on autopsy series is around 5.6% in adults . BHs can be observed in healthy livers or in association with other ductal plate abnormalities . As of 2016, 35 cases of cholangiocarcinoma associated with BH have been reported in the literature, without other associated ductal plate malformation .
BHs are commonly subcapsular or located at the periphery of portal tracts . US images show multiple small (< 1.5 cm) intra-hepatic cysts, which are mostly hyperechoic due to their small size and to a fibrous stroma (Fig. 9a), with comet-tail artefacts [4, 13]. The pattern they produce has been described as a “snowstorm” . They are poorly visible on CT, round or irregular in shape, with strict fluid attenuation and no enhancement (Fig. 9c). MRI allows a better detection with a strongly T2-weighted sequence  resulting in a “starry sky” appearance  (Fig. 9d). Magnetic resonance cholangiopancreatography (MRCP) sequences confirm the lack of communication with the biliary tract (Fig. 9b). In some cases, a thin regular persistent enhanced rim can be seen due to the compressed surrounding liver parenchyma . The typical features on each imaging modality are sufficient to reach a conclusive diagnosis. It may be difficult to discriminate between bile duct hamartomas and simple hepatic cysts when there are only few bile duct hamartomas in the liver parenchyma. The main differentiating patterns include the size of the lesion (small) and their disposition (mostly peripheral). However, from a clinical standpoint, setting them apart is not critical, because both are benign lesions.
Caroli syndrome and disease
These are both extremely rare congenital ductal plate development abnormalities (prevalence of less than one in 1,000,000 inhabitants) . Caroli disease (CD) occurs less frequently than Caroli syndrome (CS). CS must be differentiated from CD. Their pathophysiology is different. CD results from the abnormal development of large bile ducts, whereas CS affects both the central and smaller peripheral bile ducts. CS combines cystic biliary dilatation (congenital intrahepatic ductal dilatation) and the features of congenital hepatic fibrosis, whereas CD is characterised solely by biliary dilatation. The origin of CD is unclear: it is thought to be usually nonhereditary, and it is rarely transmitted in an autosomal dominant mode. CS is transmitted in an autosomal recessive mode. While CD is assumed to result from a partial or complete interruption at an early phase of ductal plate remodelling, in CS, the abnormalities occur both at an early and at a late phase and involve peripheral bile ducts [8, 15]. Follow-up is mandatory for CS and CD due to the increased risk of cholangiocarcinoma . In addition, the cysts and biliary tract can contain stones, resulting from the stagnation of bile.
The lack of periportal biliary epithelium regression during embryogenesis creates the aneurysmal dilatation of the large intra-hepatic bile ducts [8, 15]. The liver parenchyma is normal. Frequent symptoms include abdominal pain, jaundice, and/or cholangitis.
The biliary tract is abnormal and there are focal dilated bile ducts, without stenosis (Fig. 10). The cystic dilatations are connected to the biliary tract and have thin walls with a “central dot sign,” corresponding to a residual portal vein and arterial branch . The Doppler or contrast-enhanced CT/MRI images confirm its vascular origin .
MRCP is the modality of choice for assessing these lesions. Cystic hepatic lesions communicate with the biliary tract (Fig. 10). The use of hepatobiliary MRI contrast agents can be useful to confirm the communication between the biliary tracts and cysts . There is no liver atrophy (Fig. 10).
This syndrome combines bile duct dilatations and congenital hepatic fibrosis. CS could be associated with the autosomal recessive polycystic kidney disease (PKHD1 mutation) . The symptoms are due to the consequences of liver fibrosis. Follow-up is required not only to prevent the complications induced by hepatic fibrosis but also because of the increased risk of cholangiocarcinoma (about 7%) .
The features are similar to those of CD, with cysts communicating with the dilated bile ducts, and with the specific “central dot sign” (Fig. 11). They are usually smaller in CS than in CD (< 3 cm), with diffuse fusiform dilatation of the biliary tract .
The associated hepatic fibrosis may lead to specific dysmorphia (hypertrophy of the left and caudate lobes, normal size or hypertrophy of segment IV and hypotrophy of the right lobe ) and to features of portal hypertension (portosystemic collateral vessels, splenomegaly and ascites) (Fig. 12).
Polycystic liver disease
Polycystic liver disease (PLD) may involve the liver only (autosomal dominant polycystic liver disease (ADPLD): ≈ 1:100,000), or the liver and the kidney, in a dominant (autosomal dominant polycystic kidney disease (ADPKD): ≈ 1:600–1,000) or recessive form (autosomal recessive polycystic kidney disease (ARPKD)) ≈ 1:20,000) . The number of cysts required for diagnosis has not been clearly defined. The international PLD registry steering committee suggests that at least 10 simple hepatic cysts should be present for a diagnosis to be made . As with SHCs, complications include organ compression (including biliary and hepatic vessels), haemorrhage, infection (Fig. 13) or rupture. The detection of an infected cyst among multiple ones might be difficult, but 18-Fluorine-fluorodeoxyglucose positron emission tomography (18-F-FDG PET) imaging may provide helpful guidance (Fig. 14).
Cysts, which are similar to SHCs, are spread diffusely throughout the liver (Fig. 15). They may coalesce then showing a linear calcification between them. They frequently lead to hepatomegaly and to vascular compression with venous collaterals .
Other cystic lesions
Peribiliary cysts, which are small serous cysts caused by obstructed extramural hilum peribiliary glands, must not be confused with biliary dilatations. The aetiopathogenesis of these cysts and their exact prevalence are unknown. They are mostly found in cirrhotic liver (50% in autopsy studies ), in ADPKD or ADPLD  and can be solitary (10%). They can sometimes cause compression and cholangitis. A classification of the cysts has been proposed according to their location: type I including intrahepatic biliary tract, type II extrahepatic biliary tract and type III intrahepatic and extrahepatic biliary tract (25).
Peribiliary cysts are characterised by multiple, usually small (from 1 to 55 mm ), simple cystic lesions, appearing as a “string of pearls” around the hilar portal veins (Fig. 16). They are predominantly located in the left lobe due to the preponderance of the peribiliary gland . While they do not communicate with the biliary tract, they can communicate with one another, thereby mimicking biliary dilatations. MRCP is helpful to differentiate them from biliary dilatations (Fig. 16) and hepatobiliary MRI contrast agent can be used to prove the absence of biliary communication . On rare occasions, peribiliary cysts can be confused with dilated lymphatic vessels .
Hepatic lymphatic malformation
Hepatic lymphatic malformations (HLM) are extremely rare (8 cases reported in the literature up to 2010 ). They consist of benign cystic dilatations of the liver’s lymphatic spaces, commonly associated with systemic lymphangiomatosis [6, 27]. These cysts are lined with endothelial cells and filled with lymph . Three subtypes of HLM are described in the literature: capillary (super-microcystic), cavernous (microcystic), or cystic (macrocystic) [6, 27]. Through immunohistochemistry, D2-40 has been reported to be a highly specific antibody for the identification of the lymphatic endothelium when making a diagnosis during histological analysis [
They can be unilocular, but are more often multilocular, with septa and wall, which may enhance inconsistently. Confusion can occur with cystadenomas, cystadenocarcinomas or sclerosing haemangiomas [26, 29], but MRI can be usefully relied upon to avoid such a likelihood. The hepatic lymphatic malformations produce varying signals in T1- and T2-weighted sequences, depending on the quantity of fat and fluid components . Lympho-MR sequences can show dilated lymph duct surrounding the lesion, thereby supporting the diagnosis of HLM [25, 28]. Finally, hepatic lymphatic malformations can spontaneously disappear (Fig. 17).
Ciliated hepatic foregut duplication cyst
Ciliated hepatic foregut duplication cyst (CHFC) is a very rare (about 100 cases reported in the literature up to 2012 ) and usually incidental finding. It seems to be caused by a congenital malformation from the embryonic foregut . It comprises four layers: an inner pseudo-stratified columnar epithelial lining, a subepithelial loose connective tissue, smooth muscle and a fibrous capsule . Abdominal discomfort may be due to its subcapsular localisation .
The diagnosis can only be made by histology or through fine needle aspiration showing ciliated pseudostratified tall columnar epithelial cells suspended in a mucoid background with immunohistochemical stains . Complete surgical excision is recommended  due to the risk of malignancy, especially if the cyst is larger than 5 cm [35, 36].
A small (< 4 cm) solitary subcapsular cyst in segment IV is very suggestive of CHFC. However, it has also been described in segment V or VIII [32, 33, 36]. Cysts are non-enhancing, without septa, partition or internal nodule.
Its contents are usually fatty or protein-rich, which may lead to the creation of a fluid–fluid layer . On US, CHFC are hypoechoic, but usually not completely anechoic; on CT, they can be spontaneously hyperattenuating. On MRI, cysts are hyperintense on T2-weighted images, but the signal intensity is nonetheless not as high as that of simple hepatic cysts. On T1 images, the signal is usually spontaneously hyperintense. CHFCs do not demonstrate any contrast enhancement (Fig. 18) .
However, classical signs can be missed when the component of the cyst varies.
The differential diagnosis includes: haemorrhagic cyst, mucinous cystic neoplasm of the liver, metastasis of melanoma, dysplastic nodule (on cirrhosis liver), epidermoid and endometrial cyst. Some imaging patterns can help to accurately identify the different lesions. The haemorrhagic cyst is frequently larger, more heterogeneous and may show a peripheral hypointense T2 wall. The mucinous cystic neoplasm may show enhanced inner septa and a thick enhanced wall. The metastases of melanoma are most of the time less hyperintense on T2 and may show a slight enhancement. The dysplastic nodule is not hyperintense on T2. The epidermoid cyst is very rare and may be differentiated by fine needle aspiration. The endometrial cyst usually has sub-capsular topography.
Mucinous cystic neoplasm of the liver
Mucinous cystic neoplasms of the liver (MCN-L), previously known as biliary cystadenoma and cystadenocarcinoma, are rare cystic neoplasms (3–5% of hepatic cysts ) without biliary communication. MCN-L are composed of cuboidal to columnar epithelial cells, which variably produce mucin and which are associated with ovarian-type subepithelial stroma. They are subdivided into non-invasive and invasive types  and frequently occur in women. The diagnosis can be hinted at by the intralesional assay of specific tumour markers (TAG-72) .
Treatment requires surgery, since imaging cannot differentiate non-invasive from invasive types with certainty .
They are frequently large (1.5–35 cm) solitary multilocular cystic lesions, mostly located close to the hepatic hilum in segment IV, with well-circumscribed irregular margins and septations. Internal septa can be calcified . Septations arising from the internal cyst wall without external indentation seem to be a specific sign that can be relied upon to differentiate MCN-L from SHC .
On US, they appear as large unilocular anechoic lesions, with thickened and irregular walls and internal septations . Contrast-enhanced ultrasonography (CEUS) can confirm the enhancement of inner septa.
On CT, they appear as a solitary hypoattenuating lesion with septations, a thick wall, rarely with calcification . The attenuation of the cyst varies, depending on the nature of the component.
On MRI, the signal intensity of the lesion may vary depending on the fluid content within each stall (e.g. protein rich), which is very specific . A fluid–fluid level can be seen when there is haemorrhagic content. The capsule and the septa are enhanced with contrast administration (Fig. 19).
It is difficult to carry out a differential diagnosis with mucinous metastases. Of course, the existence of older imaging is crucial, and the context and history of primary mucinous tumour are important elements to consider. The appearance and evolution under treatment are part of the diagnosis in this case. The presence of septa and mural nodule is atypical for mucinous metastases.
MCN should not be confused with an abscess. Unlike the abscess, the solid part of the lesion and the parietal thickening are asymmetric, with thin-walled and thickened parts. The fluid content of the cystic portion is pure fluid (frank hyperintensity on T2-weighted MRI), and no peripheral oedema is observed (hypoattenuated on CT, hyperintense on MRI).
Intraductal papillary neoplasm of the bile duct
Intraductal papillary neoplasm of the bile duct (IPNB) is a rare premalignant neoplasm of the bile duct (10% of all bile duct tumours ). However, 40% can contain malignant component  and the risk of malignant transformation is high. Lesions must be treated by surgical resection whenever possible [41,42,43].
The appearance of the lesions depends on the quantity of mucin produced by the tumours . They mainly appear as an intraluminal cystic mass within the bile duct, with upstream duct dilatation (Fig. 21). If there is an increase in the production of mucin, lesions can appear only as focal or diffuse bile duct dilatations, without any visible solid part. The aneurysmal dilatation of a branch of the biliary tree is considered a characteristic sign of IPNB by some authors . An obvious intracystic solid mass is suggestive of a malignant transformation . An intra-luminal mass may appear hypo- or hyperechoic on US, and highly enhanced on CEUS, CT and MRI during the arterial phase (Fig. 21). CEUS is very sensitive for the detection of cystic walls or nodule enhancement . In contrast to intraductal cholangiocarcinoma, enhancement does not increase in the portal and delayed phases . Diffusion may be restricted, but it is not indistinguishable from that of cholangiocarcinoma.
Secondary cystic lesion: cystic metastasis
Cystic metastases occur less frequently than solid metastases and purely cystic metastatic tumours without prior treatment are extremely rare. The cystic part of the metastases can be due to spontaneous necrosis, especially in the case of hyperenhancing metastases (neuroendocrine tumours, malignant melanomas, sarcomas or gastrointestinal stromal tumours (GIST)), or it can arise secondary to a systemic or locoregional treatment . There are exceptional cases of cystic liver metastases from squamous cell carcinoma . Mucin production (mucinous colorectal or ovarian adenocarcinoma) can also lead to cystic features.
They can be multilocular or unilocular, and present thick walls, irregular contours or mural nodules (Figs. 22, 23, 24, 25). Irregular thick septa are possible (Fig. 25). Since the fluid component results from mucin, necrosis or haemorrhage , the attenuation on CT and the signal on MRI are different from pure fluid. US may be useful to distinguish truly fluid cystic masses from cystic metastases, especially when they are small. CEUS can reveal fine peripheral arterial enhancement with early washout (Fig. 22). The clinical setting has to be considered.
Infectious cystic lesions
Frequent organisms of pyogenic abscesses are Escherichia coli, Klebsiella pneumoniae, Enterococcus, and Streptococcus . Hyper-virulent strains of Klebsiella pneumoniae have been responsible for severe emerging diseases for the past two decades, particularly in Southeast Asia. Some of them are responsible for bacteremia combined with multiple abscesses (monomicrobial liver abscesses, endophthalmitis, brain abscesses) .
The differential diagnosis of pyogenic abscess is the amoebaean abscess.
Abscesses are rarely purely cystic and their appearance varies according to the pathologic stage. Before they turn into cystic abscesses, they display a pre-suppurative phase. Then, they appear as multiple cystic nodules (honeycomb pattern) which coalesce in a unique large irregularly shaped cystic cavity (cluster sign), surrounded by hypoattenuating inflammatory parenchyma (Fig. 26). The cluster sign is a feature indicative of pyogenic abscess . The cystic central part appears on US as a large heterogeneous cystic mass, with mixed anechoic, hypoechoic and hyperechoic parts (Fig. 27). On CT and MRI, a rim and septa enhancement has been reported and the “double target” characteristic sign may be observed. This sign is a hypoattenuating central area of pus surrounded by an inner hyperattenuating ring (granulation tissue) and an outer hypoattenuating zone (inflammatory oedema) . Gas may be present (Fig. 27). The central restriction of diffusion due to pus may be seen in larger abscesses.
The appearance of abscesses can vary due to their pathogenesis: while cholangitic abscesses are mostly multiple small cystic nodules, abscesses by hematogenous dissemination are mostly larger and less numerous, and abscesses by contiguous spread are commonly solitary .
The thrombotic occlusion of the portal vein or of its branches, or the hepatic veins, is an additional feature supporting the diagnosis of pyogenic abscess .
Hydatid cysts are caused by Echinococcus granulosis infection . They consist of three layers: the outer pericyst, which corresponds to compressed and fibrosed liver tissue; the endocyst, an inner germinal layer; and the ectocyst, a thin, translucent interleaved membrane . The cysts are mainly asymptomatic, but they can become complicated (biliary fistula, compression, rupture) (Fig. 28) .
Their characteristic appearance varies, depending on the stage of the disease. On US, both the World Health Organization (WHO) and the Gharbi classification systems are used.
The WHO classification system contains seven categories, which depend on the stage of the disease. The first category is called cystic lesion (CL). These are unilocular anechoic lesions, which appear as simple hepatic cysts. CE1 (cystic echinococcosis 1) corresponds to an active stage: it appears as a uniform anechoic cyst with internal echoes (“hydatid sand”) on US, which may only be seen after patient repositioning. A peripheral hypointense capsule is visible on MRI. CE2 (active stage) (Fig. 29) is as a well-defined multicystic mass with septa. Half of the cases demonstrate calcification of the cyst wall [51, 52], which can be better seen on CT. It displays a multivesicular “honeycomb” appearance due to daughter cysts surrounding a larger “mother” cyst. On CT, the attenuation of the mother cyst is usually higher than that of the daughter cysts due to debris (hydatid sand and detached cysts wall); the signal intensity of the mother cyst is, respectively, higher and lower on T1- and T2-weighted MRI (Fig. 29). T2-weighted MRI sequences are more sensitive than CT to detect and characterise the cystic mass as a typical wheel-spoke pattern (Fig. 29). T2 images show septa and low signal intensity due to the presence of calcifications and to the fibrotic component. They have a different signal on T1-weighed images due to the cyst fluid, which varies according to the amount of proteinaceous debris . Diffusion is not restricted . CE3 is a transitional stage. CE3A is a unique cyst with detached laminated membranes described as the “water lily sign”[51–53]. CE3B shows daughter cysts within a solid matrix. CE4 corresponds to an inactive stage. There are no more daughter cysts. It produces both hypoechoic and hyperechoic signal, whose pattern resembles a ball of wool . (inactive/degenerative stage), is partially or completely calcified.
Hepatic alveolar echinococcosis
This is a rare parasitic infection due to Echinococcus multilocularis. In contrast to the hydatid cyst, a fibrous capsule does not usually demarcate the outer margin. It is a chronic and latent disease, which is usually detected incidentally . When it is symptomatic, it causes compression symptoms. The treatment is medical and surgical. The prognosis is usually poor, sometimes leading to liver transplantation.
Hepatic alveolar echinococcosis (HEA) lesions present irregular margins, with a mixed component of solid and cystic parts. Calcifications frequently occur. The lack of enhancement is very helpful to reach a diagnosis.
On US, HEA lesions appear as a large heterogeneous mass, with areas of hyper- and hypoechogenicity (Fig. 30), hyperechoic spots (corresponding to calcifications), and a central cystic anechoic cavity (due to necrosis) . More rarely they appear as multiple hyperechoic nodules with calcification and a cystic part. CT is helpful to identify the calcification. The lesions, which are hypoattenuating, heterogeneous, with irregular margins and calcification, may attract the surrounding parenchyma and distort the hepatic capsule. Usually, no contrast enhancement is observed. In the late phase, the fibrotic component may display mild enhancement. The use of MRI prior to surgery is crucial, because it helps to assess the diagnosis, demonstrating the multivesicular structure of the lesion, and allowing vascular or biliary tree involvement to be assessed . The signal intensity of the cystic part ranges from low to intermediate on T1-weighted images and is high on T2-weighted images; the fibrous part demonstrates low signal intensity both on the T1- and the T2-weighted images (Fig. 30).
Therapeutic efficacy in HAE is essentially evaluated on the basis of repeated 18-F-FDG PET CT .
Cystic liver lesions encompass a wide and varied spectrum of features. To characterise them, a particular attention should be paid to wall thickness, to the presence of enhanced septa or solid components, to the fluid signal on MRI and to the clinical context. Since cystic liver lesions may be malignant, all non-SHCs should be investigated to make a conclusive diagnosis.
- 18-F-FDG PET:
18-Fluorine-fluorodeoxyglucose positron emission tomography
Autosomal dominant polycystic kidney disease
Autosomal dominant polycystic liver disease
Bile duct hamartomas
Carbohydrate antigen 19-9
Cystic echinococcosis 1
Cystic echinococcosis 2
Cystic echinococcosis 3
Cystic echinococcosis 4
Cystic echinococcosis 5
Congenital hepatic fibrosis
Ciliated hepatic foregut duplication cysts
Gastrointestinal stromal tumour
Hepatic alveolar echinococcosis
Hepatic lymphatic malformation
Intraductal papillary neoplasms of the bile duct
Mucinous cystic neoplasms of the liver
Magnetic resonance cholangiopancreatography
Magnetic resonance imaging
Polycystic liver disease
Simple hepatic cysts
Tumour-associated glycoprotein 72
World health organization
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We thank all the radiology team of University Hospital of Angers, who participated in the collection of cases.
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Chenin, M., Paisant, A., Lebigot, J. et al. Cystic liver lesions: a pictorial review. Insights Imaging 13, 116 (2022). https://doi.org/10.1186/s13244-022-01242-3
- Computed tomography
- Magnetic resonance imaging