La radiologia medica

https://doi.org/10.1007/s11547-020-01221-y

ABDOMINAL RADIOLOGY

Sclerotic changes of cavernous hemangioma in the cirrhotic liver:

long‑term follow‑up using dynamic contrast‑enhanced computed
tomography
Nari Shin1 · Ji Ae Choi1 · Jeong Min Choi1 · Eun‑Suk Cho1 · Joo Hee Kim1 · Jae‑Joon Chung1 · Jeong‑Sik Yu1 

Received: 16 December 2019 / Accepted: 27 April 2020

© Italian Society of Medical Radiology 2020

Abstract
Purpose  To determine the intra- and extralesional factors that predict sclerotic degeneration of hepatic hemangiomas in the
cirrhotic liver on long-term follow-up computed tomography (CT) examinations.
Materials and methods  Fifty-seven hepatic hemangiomas (> 5 mm in diameter) in 41 cirrhotic patients, recruited over a
5-year period (January 2005–December 2009), were subjected to CT to determine which factors predict sclerotic contrac-
tion or degeneration in hemangiomas. Prior and follow-up CT examinations (from 2000 to 2018) were included to observe
time-related changes. The patients’ gender, age, cause of cirrhosis, progression of background liver cirrhosis, lesion size/
location/contrast enhancement pattern, and serum aspartate transaminase to platelet ratio index were correlated with sclerotic
changes of each lesion.
Results  According to the dynamic CT features, 36 of 57 (63%) hemangiomas were determined to have sclerotic changes
during the follow-up period (1.1–14.4 years, median: 7.8 years), including 28 lesions (49%) reduced by ≥ 20% in diameter.
In univariate analysis, age (p = 0.047) and morphological progression of background cirrhosis (p = 0.013) were significantly
related to sclerotic change of hemangiomas. In the logistic regression analysis, only morphological progression of back-
ground liver cirrhosis independently predicted sclerotic change (odds ratio: 4.88, p = 0.007). With the exception of exophytic
location free from size reduction (p = 0.023 in multivariate analysis), no other analyzed factors were significantly correlated
with sclerotic changes.
Conclusion  Overall, sclerotic changes of hepatic cavernous hemangioma followed the morphological progression of back-
ground liver cirrhosis, while exophytic lesions tended to be free of size reduction.

Keywords  Liver · Hemangioma · Cirrhosis · Computed tomography

Introduction in high-risk patients, imaging studies are used to exclude

Other than benign cyst, hemangioma is the most common
hepatic tumor that has not been shown to undergo malignant
transformation [1, 2]. In rare cases, large hepatic heman-
gioma lesions can rupture, leading to major complications.
However, in daily practice, the main clinical concern with
this tumor is differential diagnosis from other focal liver
lesions. During surveillance for hepatocellular carcinomas
* Jeong‑Sik Yu
yjsrad97@yuhs.ac
1 in patients with cirrhotic liver was much lower than that
Department of Radiology, Gangnam Severance Hospital,
Yonsei University College of Medicine, 211 Eonju‑ro,
Gangnam‑gu, Seoul 06273, South Korea
hemangioma [3].
Hemangiomas can be classified as hamartomas, so most
do not change in size or appearance over time [4]. However,
some studies have reported that many hepatic hemangio-
mas undergo size change during long-term serial follow-up
[5, 6]. For instance, in a recent study involving > 5 years of
follow-up, cirrhotic changes of the liver parenchyma and
the aging process were identified as significant factors pre-
dicting size reduction in hemangiomas [7]. These examples
notwithstanding, few investigations have focused on hepatic
hemangiomas in the cirrhotic liver [8–10]. One autopsy
series showed that the incidence of hepatic hemangiomas
in the general population [8, 11]. In another study, due to
sclerotic changes, hemangiomas found in explanted cirrhotic

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livers were difficult to detect in preoperative images [8].
Some imaging follow-up studies have reported that hepatic
hemangiomas in the cirrhotic liver tend to contract, probably
because of surrounding hepatic fibrosis [7–9].
During our own clinical practice, we have noticed that
hepatic hemangiomas in the cirrhotic liver show non-uni-
form volume contraction or sclerotic changes which cannot
be easily distinguished from hepatocellular carcinomas at
a certain time point during serial follow-up imaging stud-
ies. For better understanding of the time-related imaging
characteristics of hepatic hemangiomas in the cirrhotic liver,
the present study sought to determine the intra- and extral-
esional factors that predict sclerotic degeneration of hepatic
hemangiomas in the cirrhotic liver on long-term follow-up
computed tomography (CT) examinations.
Materials and methods
Patients
Research approval was obtained from the institutional review
board of our hospital, and the requirement for informed con-
sent was waived in this retrospective study. In the abdominal
CT reports over a 5-year period (January 2005–December
2009) in our hospital’s medical record archive, a total of
93 patients were suggested to have hemangiomas in the
cirrhotic liver. For these patients, all available CT data in
the picture archiving and communication system (PACS)
captured before and after the patient selection period were
extensively reviewed by a study coordinator with a 27 years’
experience of abdominal imaging, and the reviewed images
were taken over 19 years (from January 2000 to Decem-
ber 2018). To be recruited as subjects, the patients were
required to have two or more comparable dynamic CTs
captured at least 1 year apart. Hemangioma was diagnosed
based on the following pre-established imaging features
[12]: (1) gradual centripetal globular enhancement dur-
ing multiphasic dynamic imaging until the delayed phase
(DP); (2) arterial phase (AP) homogeneous enhancement,
with or without arterioportal shunt, followed by sustained
enhancement until DP, with an attenuation density similar
to that of intra-/extrahepatic large vessels. For patients who
had more than two dynamic CTs taken during the follow-up
period, all available CTs were first preliminary reviewed,
and then, initial and last CTs were selected for future image
analysis. When a hemangioma disappeared during serial
CT follow-up, the last CT of the lesion was considered the
end point of observation. When a hemangioma showed no
more globular or early homogeneous enhancement during
serial CT follow-up, it was regarded as completely sclerosed
[13], representing another end point of the observation. The
initial or final size of the lesion, defined as the transverse
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La radiologia medica
diameter on portal venous phase (PVP) images, was required
to be > 5 mm, with no remarkable size increase (> 50% size
increase in 6 months or less) to suggest malignant vascular
or solid tumor during the follow-up period depending on
the recent LI-RADS criteria [14]. In patients with multiple
hemangiomas, up to five lesions were included for analysis;
for the patients with six or more lesions, top five lesions of
the largest transverse diameter were selected. Radiological
confirmation of liver cirrhosis was based on either morpho-
logical features of the segmental atrophy–hypertrophy com-
plex or internal/surface nodules of the fibrosis and regen-
eration process. If patients had neither of these, they were
excluded from the study, even if clinical signs suggested
cirrhosis [8, 15].
Patients with lipiodol accumulation in and around the
hemangioma due to chemoembolization to treat hepatocellu-
lar carcinoma during serial follow-up were also excluded; in
these patients, the last CT before the procedure was regarded
as the end point of CT examination. Patients were excluded
if they had early, homogeneously enhancing lesions on
their initial CT that were indistinguishable from arteriopor-
tal shunt due to similar contrast enhancement in the PVP
and DP images [16, 17]. Ultimately, the study recruited
57 hemangiomas in 41 patients with cirrhosis (26 men, 15
women; mean age: 56.1 years; range: 39–72 years) due to
chronic viral hepatitis B (n = 28), chronic viral hepatitis C
(n = 8), or other causes (alcohol abuse, n = 2; biliary dys-
function, n = 1; unknown, n = 2) (Fig. 1).
CT protocol
CT examinations were performed using either a 16-slice
or 64-slice multidetector CT scanner (Somatom Sensa-
tion 16 or Somatom Sensation 64; Siemens Medical Solu-
tions, Erlangen, Germany). To perform contrast-enhanced
dynamic CT, 120–150 mL of nonionic iodinated contrast
medium was administered intravenously using an automatic
injector at a rate of 2.5–3 mL/s. Acquisition of arterial phase
scans was initiated 15 s after enhancement of the thoracic
aorta, until 100 Hounsfield unit was reached as measured
with a bolus-tracking technique after injection of the contrast
material. The average start times of the AP and PVP scans
were 34 s (30–38 s) and 70 s, respectively, after the initiation
of contrast medium injection. The DP scan was acquired
3 min after injection of the contrast material. All CT images
were acquired in the craniocaudal direction.
Data analysis
Two radiologists (one with 20 years’ experience of abdomi-
nal imaging and the other a second-year radiology resident)
determined various imaging features, as well as the sclerotic
change in the hemangiomas over time, as indicated by the
La radiologia medica
Fig. 1  Patients’ selection dia-
gram. PACS, picture archiving
and communication system
study coordinator using an arrow. They then compared the
initial and final CT images side by side on PACS monitors
in conference. In the axial PVP images, in which both the
enhanced and unenhanced portions are well distinguished
from the surrounding liver, lesion size was measured using
electronic calipers to determine the longest dimension. If
the longest dimension of the hemangioma in the final CT
was ≤ 80% of that in the initial CT image, the lesion was
regarded as shrunken.
Each lesion was ascribed a segmental location (S1, S2/3,
S4, or right hepatic lobe), and when more than a half of
a lesion’s outer border was exposed on the liver surface,
not surrounded by hepatic parenchyma on axial and coro-
nal reconstructed images, it was considered an exophytic
lesion. The enhancement patterns were categorized into
three groups according to the speed of intralesional contrast
enhancement: “rapid” for lesions in which more than 75%
of the area was enhanced on AP images and those that were
almost fully enhanced on PVP images; “slow” for the lesions
in which more than half of the area was not enhanced until
the DP; and “intermediate” for other lesions.
Sclerotic change was determined based on the known
imaging criteria for “sclerosing” or “sclerosed” heman-
giomas including geographic outline, capsular retraction,
decrease in size over time, and loss of previously present
regions of enhancement (Figs. 2, 3) [18]. Additionally, for
the lesions initially showing homogeneous arterial phase
hypervascularity with sustaining contrast enhancement
similar degree to the adjacent vasculature, if the lesion was
changed to show only arterial phase enhancement and not
distinguishable from surrounding liver on PVP or DP on the
final CT images with or without size reduction, it was also
considered to become sclerotic (Fig. 4).
Progression of liver cirrhosis between the initial and
final CT examinations was determined by two other radi-
ologists, with 3 and 5 years’ experience of abdominal
imaging, respectively, and with no knowledge of heman-
gioma status. They compared the final with the initial CT
images side by side on PACS monitors, focusing on previ-
ously established gross morphological changes of cirrho-
sis including atrophy of segment 4/right hepatic lobe and
hypertrophy of caudate lobe/lateral segment, progression
of surface nodularity, or intraparenchymal reticulations/
nodularity [19, 20]. These radiologists independently
determined the presence or absence of liver cirrhosis
progression. Interobserver variation was calculated, and
when the two initial observers differed, a third radiologist
with 10 years’ experience in abdominal imaging reviewed
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Fig. 2  A 61-year-old man with

alcoholic liver cirrhosis with
sclerotic change of heman-
gioma in the morphologically
progressed cirrhosis. a, b In
the arterial phase of initial CT
(a) shows peripheral globular
enhancement (arrowheads) with
subsequent filling (arrow) of
contrast material in a 1.6-cm
hemangioma in the portal
venous phase (b). Asterisk
indicates a benign cyst. c, d
Four-year follow-up CT shows
markedly shrunken heman-
gioma (arrows) with remaining
minimal contrast enhancement
on arterial (c) and portal venous
phase (d) images. Progressed
cirrhosis was suggested by the
newly noted surface nodularity
of background liver

Fig. 3  A 62-year-old man with

cirrhotic liver from chronic C
viral hepatitis with an exophytic
hemangioma. a, b Portal venous
phase (a) and delayed phase (b)
images of initial CT show grad-
ual contrast filling-in enhance-
ment (arrowheads) in a 4.8-cm
exophytic hemangioma. c, d
The lesion is not shrunken on
9.5-year follow-up CT, but the
previously enhancing area in the
posterior portion of the lesion
(arrowheads) shows no visible
contrast enhancement on portal
venous (c) and delayed phase
(d) images. Overall background
cirrhosis was morphologically
progressed (not shown)

the images in the same manner in a later analysis with a Statistics

unified dataset. From the patients’ medical records, the
aspartate transaminase–platelet ratio index (APRI) values
within 1 week of the initial and final CT were calculated
using the following equation: APRI = [(serum aspartate
transaminase/upper normal value of aspartate transami-
nase)/platelet count] × 100.
Kappa statistics were calculated to establish interobserver
variation (0.00–0.20, slight agreement; 0.21–0.40, fair
agreement; 0.41–0.60, moderate agreement; 0.61–0.80, good
agreement; 0.81–1.00, excellent agreement) to determine the
morphological progression of background liver cirrhosis. All

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Fig. 4  A 61-year-old man with

cirrhotic liver from chronic B
viral hepatitis having a 1.1-cm
rapid enhancement pattern. a,
b In the arterial phase of initial
CT (a) shows a homogeneously
enhancing hemangioma at
the peripheral portion of right
hepatic lobe combined with
arterioportal shunt (arrow) and
sustaining enhancement of the
lesion (arrow) in portal venous
phase (b). c, d Final CT shows
similar appearance after 8 years
(arrow) on arterial phase image
(c), but there is no distinguish-
able lesion at the corresponding
area on portal venous phase (d)

continuous variables (patients’ age, follow-up interval) were
analyzed using one-way analysis of variance combined with
the Student–Newman–Keuls test for pairwise comparisons
of sclerotic changes or size contraction. All other categorical
variables were analyzed using Chi-squared or Fisher’s exact
tests. The logistic regression test was applied to statistically
significant variables as an independent analysis of factors
predictive in sclerotic changes in hemangioma. All statisti-
cal analyses were performed using SPSS Statistics version
23 (IBM Corp., Armonk, NY, USA), and values of p < 0.05
were considered statistically significant.
Results
During follow-up period (ranged from 1.1 to 14.4 years;
median, 7.8 years), 28 lesions (49%) had shrunken to ≤ 80%
of their initial diameter, while other lesions were not changed
in size or enlarged (Figs. 2, 3, 4). Besides the shrunken
lesions, eight more lesions (14%) among the not shrunken
lesions showed other imaging features to suggest sclerosing
or sclerosed hemangiomas in the final images (Fig. 3), and
a total of 36 out of 57 (63%) lesions were regarded to have
time-related sclerotic changes (Table 1). The lesion-based
initial age of the patients with 36 sclerotic hemangiomas was
higher than that of the patients with 21 non-sclerotic lesions
(mean age: 57.6 vs. 52.5; p = 0.047).
The interobserver agreement regarding the presence of
morphological progression of background cirrhosis was
good (kappa value: 0.613), and 24 patients (59%) with 36
hemangiomas were regarded to have time-related progres-
sion of cirrhosis after the third observer’s decisions were
added. Morphological progression of background liver cir-
rhosis was significantly related to the sclerotic changes of
hemangiomas than other lesions without sclerotic change
(75% vs. 38%; p = 0.013).
In the case of exophytic lesions, only one out of ten
lesions was shrunken compared to other lesions surrounded
by hepatic parenchyma (10% vs. 57%; p = 0.012), while the
incidence of overall sclerotic changes showed no significant

Table 1  Final contrast-enhanced Geo- Capsular Loss of initially Disappearance

dynamic CT findings suggesting graphic retraction enhanced regions on PVP or D­ Pa
sclerotic changes in 36 hepatic outline
hemangiomas compared to
initial CT Shrunken lesions (n = 28) 21 12 14 14
No remarkable size reduction (n = 8) 6 4 7 1
Total (n = 36) 27 16 21 15

Numbers are the number of lesions

a
 Arterial phase enhancement not distinguishable from background liver on PVP (portal venous phase) or
DP (delayed phase)

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difference between exophytic and other lesions (50% vs.
66%; p = 0.473). Other factors, including patients’ sex, fol-
low-up period, cause of cirrhosis, segmental location, con-
trast enhancement pattern, or APRI, showed no significant
correlation to sclerotic changes of hepatic hemangiomas
(p > 0.05 in all cases) (Table 2).
Logistic regression showed that only morphological pro-
gression of cirrhosis was significantly correlated with scle-
rotic changes of hemangioma (odds ratio: 4.88; p = 0.007).
Exophytic location of the lesion was significantly predictive
of no size reduction (odds ratio: 0.08; p = 0.023) among the
various factors on the logistic regression test.
Discussion
With regard to the mechanism by which cirrhosis affects
hepatic cavernous hemangioma, it may be possible that
fibrotic changes in the surrounding hepatic parenchyma
mechanically compress the lesions, which consist of vari-
ably sized vascular spaces [8]. Alternatively, the cavernous
spaces may be obliterated, causing the stroma to be merged
into the fibrotic background parenchyma. However, even in
the cirrhotic liver, size change in hemangiomas occurred
somewhat sporadically during daily practice. Thus, we
hypothesized that other factors or mechanisms induce
changes of hemangiomas in the cirrhotic liver. Except for
exophytic lesion location, which was associated with sig-
nificantly less time-related size reduction, no intrinsic or
extrinsic factors induced significant contraction of hepatic
hemangioma in the present study, indicating that it is impos-
sible to predict size change in individual hepatic cavernous
hemangiomas, even in patients with cirrhosis. Exophytic
lesions would not be affected by mechanical compression
from surrounding fibrotic liver tissue and would therefore
not be subjected to this rule.
Meanwhile, volume contraction is regarded an indica-
tion of sclerotic changes in hepatic cavernous hemangiomas
[18]. However, in the present study, several cases showed
imaging features to suggest sclerosing or sclerosed heman-
giomas without volume contraction during the follow-up
period. Based on this observation, we could suggest another
mechanism to induce sclerotic changes of hemangiomas.
Hemangiomas are supplied by hepatic arterial flow and
drained through the surrounding hepatic sinusoids and/or
portal venules, and the gross appearance of draining portal
vein often mimics arterioportal shunt for the early enhancing
hyperdynamic lesions during the dynamic imaging [21–23].
Portal venous hypertension is one of the main features of
liver cirrhosis, and it is aggravated as cirrhosis progresses
[24]. Increased portal venous pressure around hemangiomas
may induce intralesional congestion or stasis in the vascular
pool resulting in thrombosis, fibrin deposition, and fibrosis.
This hemodynamic theory could be applied to all hepatic
hemangiomas, even in the case of exophytic lesions.
Among the early, homogeneously enhancing small
hemangiomas with sustained strong enhancement on
PVP and DP, some lesions became indistinguishable from
background parenchyma on PVP and DP; except one tiny
(0.6 cm) lesion, all other lesions showing this feature were
combined with size reduction in the present study (Table 1).
We speculated that during the process of replacing cavern-
ous spaces by thrombosis or fibrosis, remaining small cav-
ernous spaces were early enhanced by arterial flow, but the

Table 2  Analyzed intrinsic and extrinsic factors of hepatic hemangiomas that predict sclerotic changes between the initial and final computed
tomography examinations
Factors Sclerotic change Size reduction
+ (n = 36) − (n = 21) p value  + (n = 28) − (n = 29) p value

Age, years (mean ± SD) 57.6 ± 9.2 52.5 ± 8.6 0.047* 56.8 ± 8.9 54.7 ± 9.6 0.390

Sex (male vs. female) 19 vs. 17 13 vs. 8 0.694 16 vs. 12 16 vs. 13 0.907
Follow-up years (mean ± SD) 6.6 ± 3.8 5.4 ± 2.8 0.230 6.6 ± 3.9 5.7 ± 3.1 0.324
Morphological progression of cirrhosis 27 8 0.013* 20 15 0.209
Cause of cirrhosis, (HBV vs. others) 26 vs. 10 16 vs. 5 0.987 23 vs. 5 19 vs. 10 0.261
Exophytic lesion 5 5 0.473 1 9 0.012*
Segmental location (C1, L23, Q4, Rt) 0, 5, 4, 27 1, 6, 3, 11 0.229 0, 4, 3, 21 1, 7, 4, 17 0.500
Enhancement pattern (R, I, S, N) 16, 12, 8, 0 9, 8, 3, 1 0.524 13, 11, 4, 0 12, 9, 7, 0 0.564
Initial APRI (mean ± SD) 1.5 ± 1.8 2.2 ± 2.4 0.211 1.6 ± 2.0 1.9 ± 2.1 0.508
Worsened APRI during follow-up 21 8 0.230 15 14 0.893

All numbers of data were from lesion-based numbering or measurement

*
 Statistically significant p values
SD standard deviation, vs. versus, HBV hepatitis B virus infection, C1 caudate lobe (segment 1), L23 lateral segment (segments 2 and 3), Q4
quadrate lobe (segment 4), Rt right hemiliver, R rapid, I intermediate, S slow, N not visualized, APRI aspartate transaminase–platelet ratio index

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volume averaging effect with thrombus or fibrosis in the
same voxel could decrease the attenuation density of the
whole lesion during PVP and DP like hypervascular solid
tumors. In the liver with advanced cirrhosis, such finding
may mimic arterioportal shunt or hepatocellular carcinoma
especially for small lesions [16].
For other intra- and extrahepatic factors analyzed in the
present study with negative results, we assumed that heman-
giomas in the macronodular cirrhosis from chronic B viral
hepatitis might be less affected by rather scanty background
hepatic fibrosis than in other patients with micronodular
cirrhosis with thicker and concentrated fibrotic septa [25].
However, even in patients with chronic viral hepatitis B,
micronodular cirrhosis usually occurs in the advanced stage
of cirrhosis. This may have been the reason for the lack of
significant difference among the different causes of cirrhosis.
Considering the segmental differences of fibrotic change
in the liver especially for the micronodular cirrhosis, we
assumed that the segmental location could affect the preva-
lence of sclerotic changes in hemangiomas; however, no
such significant difference was found, perhaps because only
a limited number of lesions were located in the hypertro-
phied caudate lobe (S1) or lateral segment (S2/3), and the
majority of subjects was cirrhosis from chronic viral hepa-
titis B which usually shows relatively non-segmental homo-
geneous fibrosis throughout the liver [26].
Although gross morphological progression of liver cir-
rhosis was closely related to sclerotic changes in hepatic
hemangiomas, the APRI as a quantitative indicator of liver
cirrhosis showed no significant difference in the present
study. Like the Child classification, which was not analyzed
in the present study due to incomplete laboratory data, the
APRI comprises functional parameters and is not a direct
reflector of degree of hepatic fibrosis [27, 28]. The results
of the present study suggest that sclerotic change of heman-
giomas cannot be predicted based on abnormal increase
in the APRI alone. The follow-up period of each heman-
gioma showed no correlation with size reduction or scle-
rotic changes in the present study, suggesting that sclerotic
change, with or without size reduction, occurred at a certain
time rather than as a gradual event during long-term follow-
up. There may be no correlation between the APRI and
sclerotic change in hemangioma because we did not know
exactly when the causing hemodynamic change or hepatic
dysfunction induced the sclerotic change in the target lesions
during the long-term follow-up.
The present study had several limitations. Firstly, because
hemangioma is benign, cases selection and determination
of sclerotic changes were based on pre-established imag-
ing findings, without pathological verification. Secondly,
because the study had a retrospective design, no histological
or quantitative imaging data were available detailing back-
ground liver fibrosis status at the time of the initial and final
CT examinations. In the present study, after the exclusion
of patients without gross morphological signs of cirrhosis
in the last CT, a temporal change in liver fibrosis was only
considered subjectively in order to determine the progres-
sion of cirrhosis with good agreement between the observ-
ers. Thirdly, although the temporal progression of sclerotic
changes was analyzed in the present study, hemangiomas
likely already had sclerotic components in the cirrhotic
background at the time of initial CT. At least, 15 lesions
in the present study were already associated with adjacent
parenchymal retraction and certain non-enhancing areas
on the DP images. A certain number of lesions might be
excluded from the initial selection of the subjects due to
the atypical imaging features of hemangiomas. Finally, the
follow-up period was not constant across patients, and it was
not possible to determine an exact timing of hemangioma
sclerosis combined with progression of background liver cir-
rhosis to produce any quantitative results. Ideally, the study
subjects would have normal liver at the time of the initial
CT, with gradual progression of cirrhosis enabling stratifi-
cation on serial follow-up CT examinations. However, it is
not feasible to meet such conditions during clinical practice.
In conclusion, the results of the present study suggest that
sclerotic changes of hepatic cavernous hemangioma follow
the morphological progression of background liver cirrhosis
or aging of the patients. Except the exophytic lesions show-
ing no time-related volume reduction which is relatively free
from compression effect by surrounding fibrotic liver, size
change of hemangioma looks rather sporadic and cannot be
predictable by any other intrinsic or extrinsic factors even
in the cirrhotic liver.
Compliance with ethical standards 
Conflict of interest  The authors declare that they have no conflict of
interest.
Ethical standards
All procedures performed in studies involving human participants were
in accordance with the ethical standards of the institutional and/or na-
tional research committee and with the 1964 Helsinki Declaration and
its later amendments or comparable ethical standards. For this type of
study, formal consent is not required.
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