Fat-Containing Lesions of the Liver : a Pictorial Essay

Home , Hepatocellular adenoma

Diagnostic and Interventional Imaging (2015) 96, 201—211

ICONOGRAPHIC REVIEW / Gastrointestinal imaging

Fat-containing lesions of the liver : A

pictorial essay

a a a

M. Tekath , T. Klotz , P.F. Montoriol ,

c a a,∗,b

J. Joubert-Zakeyh , J.-M. Garcier , D. Da Ines

Department of Radiology and Medical Imaging, Clermont-Ferrand University Hospital,

Estaing University Hospital, 1, place Luci-Aubrac, 63003 Clermont-Ferrand cedex 1, France

Clermont University, University of Auvergne, ISIT, CNRS, UMR6284, BP 10448, 63000

Clermont-Ferrand, France

Anatomical and Cytological Pathology, Clermont-Ferrand University Hospital, Estaing

University Hospital, Estaing University Hospital, 1, place Lucie-Aubrac, 63003

Clermont-Ferrand cedex 1, France

KEYWORDS Abstract The presence of fat within a hepatic lesion is unusual and can help to direct the

Liver tumor; radiologist’s diagnosis. The aim of this iconographic review is to specify the various hepatic

Hepatic steatosis; lesions that may contain fat and their appearance particularly on MRI. A histological correlation

Magnetic resonance is also suggested for the most commonly found tumors. The identiﬁcation of fat within a hepatic

imaging tumor, along with other radiological signs and reﬂection on the clinical and epidemiological

context, can lead to a diagnosis being reached or suggested, with conﬁrmation if necessary, by

a pathological examination.

The presence of fat in a liver lesion is not a standard ﬁnding and it can help to guide

the radiologist towards a diagnosis. Fat may be macroscopic or microscopic. MRI is the

modality of choice for detecting a fatty component in a hepatic tumor: fat-saturation

sequence detects extracellular fat while chemical shift imaging identiﬁes microscopic or

intracellular lipids [1].

Once intracellular lipids are demonstrated, this allows a range of diagnoses to be consid-

ered, including multifocal hepatic steatosis, focal nodular hyperplasia (FNH), adenomas,

hepatocellular carcinoma, and some hepatic metastases.

By contrast, the presence of fat in a tumor that is not within the hepatocytes is sug-

gestive of angiomyolipoma, pseudolipoma of the Glisson capsule, fat deposits around the

intrahepatic wall of the inferior vena cava or ‘‘pericaval fat’’, hydatid cyst, teratoma,

liposarcoma and some metastases [2,3].

∗

Corresponding author.

E-mail address: [email protected] (D. Da Ines).

202 M. Tekath et al.

falciform ligament or the gall bladder. This positioning is due

Liver lesions containing intracellular fat

to variations in venous ﬂow within the hepatic parenchyma,

When steatosis is demonstrated within a focal hepatic lesion resulting from the links to the vascular networks of the pan-

through signal drop on the out-of-phase sequence, the fol- creas and duodenum, gall bladder, and digestive system [5].

lowing diagnoses should be the ﬁrst to come to mind: focal Insulin has also been suggested to play a role due to steatosis

steatosis, focal nodular hyperplasia, HNF1␣ mutated ade- being demonstrated in contact with insulinoma metastases

noma, inﬂammatory hepatic adenoma, and hepatocellular [6].

carcinoma. Chemical shift imaging shows fat present in the hepato-

The next stage in the diagnostic process for the radiolo- cytes with a signal drop on the out-of-phase sequence. This

gist is to determine whether the steatosis within the tumor ﬁnding, when seen together with a characteristic location,

is homogeneous and diffuse or focal, and whether or not the a lack of mass effect, geographic borders, and a parallel

lesion is hypervascularised, and, if relevant, whether there enhancement gradient to that of the adjacent parenchyma,

is contrast washout. These features, taken together with allows the diagnosis to be made with certainty [6].

a study of the adjacent parenchyma and the context, will

usually allow a diagnosis to be made or strongly suspected. Focal nodular hyperplasia

This is the most commonly seen benign tumor of the hepato-

Focal pseudo-nodular steatosis

cytes, with an estimated prevalence of 9/1000 and a female

The conditions under which hepatic steatosis is most often to male ratio of 8:1 [7]. FNH is thought to be an abnor-

found are excessive alcohol consumption, insulin resistance, mal proliferation of the hepatic parenchyma in response

obesity, hyperlipidaemia, hepatitis B and C infection, and to a congenital vascular malformation. It is usually discov-

the use of certain medications. Hepatic steatosis is the ered incidentally or further to non-speciﬁc symptoms. It is

result of a build-up of fat vacuoles in the hepatocytes, and essential to identify FNH correctly because no monitoring

it can be diffuse, focal, or multifocal (Fig. 1). Focal pseudo- is needed, and contraception does not need to be discon-

nodular hepatic steatosis can be mistaken for a focal lesion tinued. MRI is the most sensitive modality for diagnosis of

on sonography or CT [4]. Areas of focal hepatic steatosis are this condition [8]. Typically, FNH is a well-circumscribed,

usually found in the periportal region, in contact with the lobulated lesion with no capsule, with iso- or low signal

Figure 1. Focal steatosis mimicking a tumor (*) in the left lobe and segment I in a patient with chronic liver disease with indented contours

and hypertrophy of the caudate lobe (arrow heads). These areas of steatosis appear in iso-signal on in-phase T1 images (a) and T2 images

(c), with a marked signal drop on the out-of-phase sequence (b). With contrast enhancement, these areas have iso-signal intensity in the

arterial phase (d) and slight low signal intensity in the portal (e) and delayed phases (f). There are vessels coursing through these areas,

without displacement.

Fat-containing lesions of the liver: A pictorial essay 203

intensity on T1-weighted sequences, iso- or slight high signal intensity in a late delayed phase (after 1—3 h) follow-

intensity on T2-weighted sequences, that is usually homo- ing administration of gadobenate dimeglumine, while 100%

geneous, but can be non-homogeneous if the lesion is large. of adenomas showed low signal intensity. More recently,

There is a characteristic central scar (or area of ﬁbrosis), the use of gadoxetic acid has been evaluated [12] to

especially in lesions larger than 2 cm. It presents intense study the dynamic contrast enhancement patterns of

arterial phase enhancement and becomes iso-intense to lesions, focusing particularly on an acquisition taken 20 min

the adjacent parenchyma in the portal phase. The central after administration (hepatobiliary phase). In this study,

area of ﬁbrosis shows low signal intensity on T1-weighted 91.2% of FNH showed iso- or slight high signal intensity

sequences, high signal intensity on T2-weighted sequences, compared to the adjacent parenchyma 20 min after admin-

with delayed phase enhancement. istration. In cases with atypical enhancement patterns, a

While intracellular lipids are possible in FNH, this is large central scar or an abundant fatty component was

an atypical ﬁnding. The frequency of this feature varies noted.

enormously between studies, ranging from 22—85% [8—10].

There is probable overestimation due to these being lesions

Hepatocellular adenomas (HCA)

that have undergone biopsy or resection because of their

atypical appearance on imaging.

Hepatocellular adenomas are uncommon benign tumors with

Intratumoral steatosis (Fig. 2) is shown by a signal

an estimated prevalence of 0.03% and a female to male ratio

drop on out-of-phase T1-weighted images. This does not

of 9:1. Adenomas are usually diagnosed in young women

always equate to an atypical appearance on MRI if the

of childbearing age, who are often found to be using oral

other criteria are brought together. It can, however,

contraception. Histologically, this tumor corresponds to a

lead to difﬁculties in diagnosis, especially in making the

benign proliferation of normal hepatocytes without portal

distinction from the differential diagnosis of inﬂamma-

tracts [13]. It is crucial to make or suggest the diagno-

tory hepatic adenoma [9]. The use of hepatocyte-speciﬁc

sis of adenoma on imaging due to its potentially serious

contrast agents can give weight to diagnosis in these

complications [14]: haemorrhage (20% of cases), and trans-

instances. In this respect, Grazioli et al. [11] showed

formation to hepatocellular carcinoma (10%). The latter is

that over 96% of FNH demonstrated iso- or high signal

a particular risk for men, with 47% affected compared to 4%

Figure 2. MRI of FNH with fat content. Well-circumscribed lesion at the junction of segments VI and VII (arrow) showing slight high signal

intensity on T2 (a), iso-signal intensity on in-phase T1 (b) outside the central scar, which shows low signal intensity (*), and marked low

signal intensity on out-of-phase T1 images (c). With gadolinium enhancement, there is contrast uptake in the arterial phase (d) with the

central scar showing low signal intensity (*) and enhancement in the delayed phase (e). On histology (f), H and E stain enlarged 100 times

shows an area of inﬂammatory ﬁbrous septa (*) containing bile ducts in the centre of the lesion, around which are vacuolated and steatotic

hepatocytes (arrows).

204 M. Tekath et al.

of women [15]. The lesion can be single or multiple. The risk HNF1␣ (hepatocyte nuclear factor 1 alpha)

of progression does not correlate to the number of lesions, mutated adenoma

but to their sub-type. ␣

HNF1 (hepatocyte nuclear factor 1 alpha) mutated ade-

Recent advances in cytogenetics and molecular biol-

noma (Fig. 3) accounts for 30—46% of HCA, depending on

ogy have led to four sub-types of hepatocellular adenoma

the study. Histologically, it is characterised by an absence of

being identiﬁed: HNF1␣ mutated adenoma, inﬂammatory

cytologic atypia and inﬂammatory inﬁltrate, while there is

adenoma, ␤-catenin mutated adenoma, and unclassiﬁed

diffuse and homogeneous steatosis. These features explain

adenomas [16—18]. Each type has a speciﬁc set of features

its appearance on imaging. Thus, MRI will show a lesion with

on MRI [19,20], which means that this modality has increased

high signal intensity on T1-weighted in-phase sequences

speciﬁcity for the diagnosis of HNF1␣ mutated and inﬂam-

with a uniform signal drop on out-of-phase imaging. On T2-

matory adenomas [19,21]. It is essential to identify the

weighted sequences, the tumor will show iso- or slight high

sub-type of HCA because each one has speciﬁc complications

signal intensity. After administration of gadolinium chelates,

and different management is needed as a result. The two

enhancement is moderate or even absent in the arterial

␣

most common sub-types are HNF1 mutated adenoma and

phase, and does not persist into the portal or delayed phase.

inﬂammatory adenoma, both of which can contain intracel-

The main differential diagnosis is hepatocellular carcinoma

lular fat.

with fat content.

Figure 3. Example of a female with steatotic adenomas (arrows) showing slight high signal intensity on T2 (a), iso-signal on T1 (b) and

clear low signal on T1 (*) on the out-of-phase sequence (c). These lesions enhance moderately during the arterial phase (d) with low signal

intensity that persists into the portal (e) and delayed phases (f). Histology, H and E stain, enlarged 12.5 times (g), shows an adenoma (*)

made up of narrow sheets of hepatocytes with cytoplasm occupied by large vacuoles of steatosis. On the left of the image, a displaced band

of healthy liver (arrowheads), and note that none of the hepatocytes here show steatosis.

Fat-containing lesions of the liver: A pictorial essay 205

There is no risk of malignant transformation in HNF1␣ T2-weighted images due to the dilated sinusoids. Arterial

mutated adenomas, and the risk of haemorrhage is low but phase enhancement is intense and persists into the portal

it increases with lesion size. and delayed phases. The atoll sign is seen in 43% of cases

[20], corresponding to a peripheral band of high signal

Inﬂammatory hepatic adenoma intensity on T2-weighted sequences with delayed phase

enhancement, while the lesion centre is iso-intense.

Inﬂammatory hepatic adenoma, previously known as telang-

iectatic FNH, accounts for 40—55% of HCA. It is clinically

B-catenin activated adenomas

associated with obesity, hepatic steatosis, and, in terms of

B-catenin activated adenomas are less common; more often

laboratory study signs, raised inﬂammatory markers. Intra-

found in men [15], and account for 10% of HCA. Cytologic

cellular fat in the tumor is noted in 11% of cases [18]. In

atypia and a pseudoglandular growth pattern may be seen.

contrast to HNF1␣ mutated adenoma, steatosis within the

Although it has a varying appearance on imaging, a fatty

tumor is often focal and heterogeneous. However, Ronot

component within the lesion has never been demonstrated.

et al. [21] report the presence of diffuse steatosis in 21%

This is a heterogeneous lesion on all sequences, showing

of cases of inﬂammatory hepatic adenoma although it was

iso-signal intensity on T1- and T2-weighted sequences, with

still non-homogeneous (while it was homogeneous in HNF1␣

arterial phase enhancement and washout following admin-

mutated adenoma).

istration of gadolinium chelates. A central scar is possible,

In histological terms, inﬂammatory adenoma is char-

being seen in 75% of cases, which will show high signal inten-

acterised by the presence of inﬂammatory inﬁltrates,

sity on T2-weighted sequences, but this is not a speciﬁc sign

dystrophic vessels, and dilated sinusoids. A small num-

since it can also been seen in other adenoma sub-types.

ber (5—10%) can present ␤-catenin activation and progress

␤

-catenin mutated adenoma is associated with an

to hepatocellular carcinoma [17]. There is greater risk of

increased risk of malignant transformation [16].

haemorrhage than in HNF1␣ mutated adenomas.

MRI most often demonstrates a lesion with iso-signal

Unclassiﬁed adenomas

intensity on T1-weighted sequences, with focal areas of

signal drop on out-of-phase images if there is an intracellu- Unclassiﬁed adenomas (Fig. 4) are a group of lesions that

lar fat component. There is marked high signal intensity on do not present speciﬁc features in terms of morphology or

Figure 4. MRI of a hepatocellular adenoma that is unclassiﬁed on imaging (arrow) of the left liver lobe showing non-homogeneous iso-signal

on T2 fat-sat (a), iso-signal on in-phase T1 (b) with moderate signal drop (*) on the out-of-phase sequence (c). There is a minimally intense

contrast uptake (arrow head) in the arterial phase (d) with homogeneous low signal intensity in the portal phase (e). Histology, H and E

stain, enlarged 12.5 times (f), points to a ␤-catenin mutated adenoma (*) with no steatotic component; the sheets of tumor hepatocytes are

thin, there is no portal tract within the lesion, and dilated sinusoid capillaries can be seen in the central part of the adenoma. Peripherally,

the healthy parenchyma is displaced (arrow heads).

206 M. Tekath et al.

immunophenotype. Steatosis within the lesion has not been the cause of difﬁculties in making the distinction with the

reported in this adenoma sub-type. differential diagnosis of HNF1␣ mutated adenoma.

Extracellular fat-containing liver lesions

Hepatocellular carcinoma (HCC)

Angiomyolipoma

HCC is the most common primary hepatic tumor, developing

in a cirrhotic liver in 80% of cases [22]. This lesion produces More commonly seen in the kidneys, sporadic hepatic

a variable signal on T1- and T2-weighted sequences, with angiomyolipoma is rare, with an increased frequency in

hypervascularisation in the arterial phase and washout in the patients with tuberous sclerosis.

portal and/or delayed phase. In bulky tumors, the presence It is a benign lesion made up of smooth muscle cells, ves-

of a capsule and mosaic perfusion is possible. The diagnostic sels, and adipocytes. There is signiﬁcant variability in the

criteria for HCC in a cirrhotic liver were amended in 2011 proportions of these three components, resulting in equally

[23]: the diagnosis can be conﬁrmed on CT or MRI for any variable appearances on imaging, which makes preopera-

tumor larger than 1 cm if there is arterialisation and visi- tive diagnosis rare. The proportion of fat in particular can

ble contrast washout in the portal and/or delayed phase. range from under 10% to over 90% [25]. Typically, the lesion is

Intracellular fat is not an uncommon ﬁnding (Fig. 5), being non-homogeneous, with variable high signal intensity on T2-

reported in 19.6% of cases [24]. Steatosis within the lesion weighted sequences, high signal intensity on T1-weighted

is mainly seen in small low-grade lesions (particularly those sequences, and a signal drop on fat-suppressed images. With

between 1 and 1.5 cm in diameter). This intracellular fat use of a contrast agent, it demonstrates non-homogeneous

is common and diffuse in well-differentiated HCC (42%). It enhancement that occurs early and persists, showing that

becomes less common and more focal as the grade and tumor vessels are present in and around the tumor [25].

size increase. In one study, Katumi et al. [24] reported that A small series of cases [26] of atypical AML (Fig. 6) with

the presence of a capsule was rare in HCC with intracellu- no fat component brings together the various enhance-

lar fat content (absent in 81% of cases). This feature can be ment characteristics, still showing non-homogeneous

Figure 5. HCC of the dome of the liver (arrow) with a high intracellular fat component. The lesion presents slight high signal intensity

on in-phase T1 (a), with a marked signal drop (*) on the out-of-phase T1 sequence (b) and high signal intensity on T2 fat-sat (c). The

enhancement pattern is also typical of HCC with marked arterialisation (arrowheads) (d), then washout in the portal (e) and delayed phases (f).

Fat-containing lesions of the liver: A pictorial essay 207

Figure 6. A well-circumscribed angiomyolipoma with heterogeneous high signal intensity on T2 (a), clear low signal intensity on in-phase

T1 images (b) outside a central zone (*) that shows slight high signal intensity with signal drop (arrowheads) on out-of-phase T1 sequences

(c) and T1 fat-sat (d). After contrast material administration, the tumor shows intense enhancement in the arterial phase (e) with rapid

and heterogeneous washout in the portal (f) and delayed phases (g). Note the visualisation of the vessels in and around the lesion (arrows).

Immunohistochemistry, enlarged 200 times (h), shows that some of the tumor cells express actin with variable intensity (brown staining).

The contrasting stain (pale blue) allows the majority of the smooth muscle cells to be drawn out as epithelioid, as well as showing the

adipocytes, which seem to have empty cytoplasm under the microscope. Enlarged 40 times, HE staining (i) shows the lesion to have tree-like

vasculature (arrowheads).

208 M. Tekath et al.

arterialisation but with washout in the portal phase and frequency in patients with chronic liver disease and it must

delayed phase, no ﬁbrous capsule, and vessels present in not be mistaken for a neoplasm or a thrombus [27].

and around the tumor.

Pericaval fat collection Pseudolipoma of the Glisson capsule

This is an asymptomatic lesion that is an incidental ﬁnding.

This is a rare and benign type of fat formation that develops

It is well-circumscribed, sub-capsular, and presents purely

in contact with the endoluminal side of the inferior vena

fatty density (Fig. 8).

cava wall (Fig. 7). This ‘‘incidentaloma’’ increases in

Figure 7. MRI showing pericaval fat developed in a cirrhotic liver. This lesion (white arrow) is indistinguishable from the adjacent fat on

T2 imaging (a), in-phase (b) and out-of-phase T1 imaging (c). It is visible because of a marked signal drop (*) on the T2 fat-sat sequence (d).

It remains in clear low signal intensity (*) on T1 fat-sat contrast-enhanced sequences in the arterial (e), portal (f), and delayed phases (g)

with enhancement of the inferior vena cava at its periphery (black arrowheads). Note the presence of ascites, recanalisation of the round

ligament due to cirrhosis, and an unremarkable biliary cyst in segment IV. The pericaval fat (arrow) is more easily seen on CT (h): note this

axial view of the same patient.

Fat-containing lesions of the liver: A pictorial essay 209

Figure 8. Pseudolipoma of the Glisson capsule (arrow) adjacent to segment I. It was an incidental ﬁnding on an emergency CT to investigate

a gynaecological haemorrhage. On axial (a—c) and coronal (d—f) reconstructions, this lesion is hypodense with fatty density, homogenous,

sub-capsular, and there is no contrast uptake in either the arterial (b, e) or portal phases (c, f). Note the abundant haemoperitoneum (*).

Hydatid cyst hydatid cyst formation. These can be asymptomatic or they

can cause pain, secondary infection, or rupture. The pres-

Echinococcosis is a zoonotic disease caused by Echinococcus ence of a fat-ﬂuid level within a hydatid cyst is not usual

ganulosis and E. multilocularis infection, affecting mainly (Fig. 9) and is thought to be an indirect sign of commu-

the liver, especially the right lobe. nication with the biliary tree, which may be longstanding

While the parasite E. multilocularis causes alveolar [28].

echinococcosis, it is E. granulosis infection that causes

210 M. Tekath et al.

Figure 9. Hydatid cyst in a patient originating from an endemic area. It is a well-delineated lesion, in which two components can be

distinguished, the ﬁrst being dependent ﬂuid (arrow) with high signal intensity on T2 (a) and T2 fat-sat sequences (b), and low signal

intensity on T1 (c, d). The second component is fatty (arrowheads), showing high signal intensity on T2 (a), in-phase (c) and out-of-phase

T1 sequences (d), with marked signal drop on the T2 fat-sat sequence (b). No uptake after administration of contrast material either in the

arterial (f) or portal phase (g).

Conclusion Disclosure of interest

The presence of fat in a hepatic lesion is not an unusual The authors declare that they have no conﬂicts of interest

ﬁnding. Identifying the fat is a crucial step in the process of concerning this article.

diagnosing aetiology. This ﬁnding, especially when demon-

strated with the input of MRI, points to different groups

of diagnoses depending on whether the fat component is References

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