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Abstract
1. Introduction
Hepatic adenoma (HA) is a rare, benign tumor of epithelial origin (2% of all
liver tumors [1]) that develops usually in healthy liver [2] and is known to occur
mainly in young female patients, having been linked to the prolonged use of oral
contraceptives [3]. In Europe and North America, it has an incidence of 3/100,000/
year [4]. Even though multiple hepatic adenomas have been described in the litera-
ture, this is a rare occurrence, most of the adenomas being solitary (70–80%), and
thus, often asymptomatic unless they become complicated (voluminous adenomas
causing upper quadrant pain and/or rupture of the tumor with hemoperitoneum
and malignant transformation) [5]. Hepatocellular adenoma is a term sometimes
used instead of hepatic adenoma, being correct in contradiction to liver adenoma
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Liver Disease and Surgery
or liver cell adenoma, which are less desirable because these two can also include
the bile duct adenoma [6]. Even though the prognosis of this type of tumor is
not well established, it is important to differentiate it from other hepatic tumors
since the hepatic adenoma has a particular therapeutic management. Differential
diagnosis however can be challenging, but can be achieved preoperatively by imag-
ing techniques. Positive diagnosis is a histopathological one and is often obtained
postoperatively [7].
2. Epidemiology
The incidence of HA has increased in recent years, but at the same time, imaging
techniques have improved, and therefore, this higher incidence might be explained
by the better diagnostic techniques nowadays available. Also, in recent years, it
seems to be a change in epidemiology, as more cases of HA in male patients are
described, particularly in Europe and Asia. This may be caused by an increased inci-
dence of obesity, another recognized risk factor of HA. Moreover, in recent years,
more and more cases of malignant transformation of HA have been reported, and
this also might be a result of improved histopathological diagnosis.
Although the link between HA and use or oral contraceptive in women of child-
bearing age is maintained, recent studies have shown other emerging important risk
factors such as metabolic syndrome [8].
3. Risk factors
The most important risk factor seems to be the use of oral contraceptives.
Hepatic adenoma used to be exceptionally rare before the age of oral contraceptives,
but after these became popular as a contraceptive solution, more and more cases
of HA were reported. In women who were long-time users of oral contraceptives,
the incidence was 1 in 30–40,000, whereas in women who have never used oral
contraceptives, the incidence was 1 in 1 million, which proves a strong link between
these two. Hepatic adenomas in women with prolonged use of oral contraceptives
tend to be more numerous, more voluminous, and with a higher risk of spontaneous
rupture and bleeding [9–12].
Another important risk factor that became even more important than other
known risk factors, such as glycogen storage diseases and diabetes mellitus type 2
alone, is the metabolic syndrome. Obesity is more and more prevalent in the general
population, and thus, it became a more important risk factor in this pathology.
Weight loss should be considered as the first therapeutic option in the management
of HA in obese patients [13]. A recent study has proved that bariatric-induced
weight loss results in significant regression of HA in severely obese women, which
emphasizes the role of overweight in HA pathophysiology [14]. Even more so,
patients with metabolic syndrome and hepatic adenomas seem to be associated
with a higher rate of malignization [8]. The association between oral contraceptive
use and metabolic syndrome on one hand and HA on the other tends to prove an
important hormonal sensitivity of the tumor (obesity is associated with higher
estrogen levels), and this is supported by the fact that adenomas may stop their evo-
lution or even regress as a result of oral contraceptive cessation [15]. In spite of this,
immunohistological studies failed to prove the direct effect of these hormones via
steroid receptors in normal and adenomatous hepatic tissue, and so the mechanism
by which high estrogen levels may cause an adenomatous transformation is still
incompletely understood [16]. As a hyperestrogenic state, pregnancy has also been
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incriminated as a risk factor, and there have been many reports of ruptured HAs in
pregnant patients with a very high mortality for both mother and child [16–19].
Apart from estrogen, use of anabolic androgens has also been linked to a higher
incidence in HAs, which is being proved not only in body builders but also in
patients treated with steroids for Fanconi syndrome, aplastic anemia, etc. Cessation
of steroid use has also been linked to regression in size of HAs [15].
Hepatic adenoma has also been linked to glycogen storage disease and hepato-
cyte nuclear factor 1A maturity onset diabetes of the young (HNF1A MODY). The
incidence is 51% in patients with type I glycogen storage disease and 25% in those
with type III glycogen storage disease (GSD) [8]. Hepatic adenoma in GSD occurs
before the age of 20 years, is more common in males, and is typically multiple.
Dietary therapy and correction of insulin, glucose, and glucagon levels have been
proved to lead to regression of adenomas [15]. The mechanism by which GSD is
involved in the development of HA is also unknown.
Finally, there seems to be a genetic predisposition, and nowadays, HAs are
believed to result from specific genetic mutations involving TCF1 (transcription
factor 1 gene), IL6ST (interleukin 6 signal transducer gene), and CTNNB1
(β catenin-1 gene) [20].
4. Pathology
Figure 1.
Resected specimen after mesohepatectomy for a large IHA.
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Liver Disease and Surgery
Figure 2.
Normal liver (left) and hepatocellular adenoma (right), HE ×40.
Figure 3.
Hepatocellular adenoma—benign hepatocytes (large, clear, and pale due to accumulation of glycogen)
arranged in plates, cords, and sheets, HE ×200.
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liver tissue, but in H-HA its downregulation results in impaired fatty acid traf-
ficking in hepatocytes, which causes intracellular fat deposition [22]. H-HA is
sometimes associated with maturity-onset diabetes of the young (MODY), type 3,
and familial hepatic adenomatosis. Half of these patients have multiple HAs. More
than 90% have a history of oral contraceptive use. The tumors are characterized
by marked steatosis (Figures 4–7), a very low risk of complications, and a low
risk of malignant transformation. On immunohistochemistry staining, H-HA is
LFABP (liver fatty acid binding protein) negative, which is in contrast with normal
expression in the surrounding nontumoral liver [21]. The sharp contrast between
tumor and adjacent parenchyma in terms of steatosis and LFABP expression enables
delineation of tumor borders which are often irregular and lobulated with often
small HA foci in vicinity.
The second group comprises 10–15% of all patients, includes mainly men, and
is characterized by the presence of mutations that activate β-catenin and cellular
abnormalities. β-Catenin is encoded by catenin β 1 gene (CTNNB1) on chromo-
some 3p21 and represents an important downstream effector of the Wnt/β-catenin
pathway. This pathway is important in liver embryogenesis, cell adhesion, growth,
zonation, and regeneration [22]. An activating β-catenin mutation is also associated
with specific conditions such as glycogen storage disorders or androgen administra-
tion. The phenotype is represented by cellular atypia with high nuclear-cytoplasmic
ratio, nuclear atypia, and pseudoglandular growth pattern. It is identified by
immunohistochemistry due to a strong expression of glutamine synthetase with or
without aberrant cytoplasmic and nuclear expression of β-catenin. β-HA has the
highest risk of malignant transformation than other HA subtypes, and it is very
difficult to be distinguished from the well-differentiated hepatocellular carcinoma
(HCC). Some risk factors are related to β-HA, such as male hormone administra-
tion, glycogenosis, and familial polyposis.
The third group (IHA) includes 50% of all patients and is most common in
overweight women who suffer from metabolic syndrome or have had prolonged
estrogen exposure. Patients with IHA demonstrate both serum and lesional indi-
cators of an active inflammatory response. IHA is characterized histological by
inflammation, marked sinusoidal dilatation or congestion, numerous thick-walled
arteries, and ductular reaction (Figures 8 and 9). This subgroup was previously
named ‘telangiectatic focal nodular hyperplasia.’ The extent of congestion, peliosis,
and hemorrhage is different from case to case. Steatosis may be present in IHA but
is not as extensive as in H-HA. In case of multiple tumors, the amount of steatosis
Figure 4.
Hepatocellular adenoma—HNF1 alpha mutated subtype—steatosis within the tumor, HE ×200.
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Liver Disease and Surgery
Figure 5.
Hepatocellular adenoma—HNF1 alpha mutated subtype—steatosis and pseudoglandular formations,
HE ×200.
Figure 6.
Hepatocellular adenoma—HNF1 alpha mutated subtype—pseudoglandular formations and steatosis within
the tumor, HE ×200.
Figure 7.
Hepatocellular adenoma—steatosis within the tumor, HE ×200.
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Figure 8.
Hepatocellular adenoma—inflammatory subtype, HE ×200.
Figure 9.
Hepatocellular adenoma—inflammatory subtype, HE ×40, with sinusoidal dilatation and hemorrhage within
the tumor.
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Liver Disease and Surgery
Figure 10.
Hepatocellular adenoma—CD34 immunohistochemical stain for endothelial cells, few sinusoids are seen in the
tumor, ×200.
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Figure 11.
Hepatocellular adenoma—reticulin stain—left normal liver and right hepatocellular adenoma—there is no
loss of reticulin network, Gomori ×200.
Figure 12.
Hepatocellular adenoma—HNF1 alpha mutated subtype—mild lipofuscin deposits revealed by glypican 3
immunohistochemical stain, ×200.
4.1 Adenomatosis
Adenomatosis is a distinct clinical entity and was first described in 1985 [27] and
since then has been defined by the presence of more than 10 adenomas, involving
both hepatic lobes, in the absence of glycogen storage diseases, prolonged use of
steroids, or resolution with steroid cessation [28]. It is estimated that adenomatosis
affects both men and women, and, unlike HA, is correlated with a higher risk of
impaired liver function, manifested as an increase in serum alkaline phosphatase
and GGT levels [27] and also with a higher risk of bleeding. Instead, the malignant
degeneration does not correlate with the number of lesions. There are two dif-
ferent patterns of adenomatosis: (1) the massive pattern, which is defined by the
existence of larger lesions, up to 10 cm, that often result in gross hepatomegaly with
deformed contour of the liver and (2) the multifocal pattern, which is character-
ized by smaller lesions, with diameter less than 4 cm, that rarely deform the liver,
but has a tendency to progress fast and become symptomatic [29]. The etiology of
hepatic adenomatosis is suspected to be linked to congenital or acquired abnor-
malities of hepatic vasculature. In a study of 15 patients with adenomatosis, 5 had
abnormalities in hepatic vasculature: congenital absence of portal vein, portal
venous thrombosis with cavernous modification, and intrahepatic portosystemic
shunts [1, 30].
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Liver Disease and Surgery
Most commonly, HA goes unnoticed due to its lack of signs and symptoms,
but when it does become symptomatic, it is either due to its increase in volume,
tumor necrosis, or complications such as life-threatening intra-abdominal bleed-
ing due to spontaneous rupture of the highly vascularized tumor. Sudden, severe
pain with hypotension in a patient with HA indicates rupture into the perito-
neum, an event associated with a mortality of up to 20 percent if not identified
and/or treated accordingly [9, 31, 32]. The risk of bleeding is difficult to estimate
overall, but it is quite high in patients with symptomatic HAs (25–64%). Tumor
size that exceeds 35 mm has been associated with an increased risk of bleeding
[33]. The risk of bleeding depends on the localization of the tumor. Exophytic
lesions (protruding from liver) had the highest risk of bleeding (67%), followed
by subcapsular ones (19%) and at last intrahepatic HA (11%). Lesions in seg-
ments II and III had more bleeds than those in the right liver (34% versus 19%).
The visualization on imaging of peripheral or central arteries represents a risk
of bleeding comparative with no visible vascularization in the lesion [33]. Also
a long history of contraceptive use and recent hormonal use are risk factors for
bleeding from HA. Young age seems to be associated with an increased incidence
of HA rupture, independent of hormonal treatment duration, suggesting a
need for careful surveillance or prophylactic treatment in this population [34].
Bleeding is graded as intratumoral (grade I), intrahepatic (grade II), or extra-
hepatic (grade III) and represents a potentially life-threatening complication in
patients with HAs.
Hepatic adenomas are diagnosed when they cause epigastric or upper quadrant
pain or during an imaging study done for unrelated ailments, and less commonly
when an abdominal mass is palpated on clinical examination. When HA is suffi-
ciently large and compresses bile ducts, jaundice may become another sign.
There are no specific serologic markers or laboratory findings for HA, but cer-
tain findings can lead the diagnosis away from an adenoma and toward a liver cell
carcinoma in case of an increased serum alpha-fetoprotein, or toward a metastasis
in the case of increased serum tumor markers for digestive tract tumors [35].
The definite diagnosis in this pathology is naturally a histological one; however,
obtaining it preoperatively means making a biopsy from a fragile and highly vas-
cular tissue, with significant risk of bleeding. Having to deal with a benign lesion,
and given the fact that the amount of tissue obtained is rarely enough or suitable
for a diagnosis, this risk is not justified. Thus, the diagnosis of this tumor is based
on analyzing a combination of epidemiologic and clinical data and imaging stud-
ies, but often the confirmation of the diagnosis is done by the pathologist, after the
hepatic resection.
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6.1.1 Ultrasound
The most accessible, cost-friendly, and probably responsible for most discover-
ies of asymptomatic HA is the ultrasound, even though it cannot distinguish it from
other liver tumors. On gray scale ultrasound, HA is seen as a well-defined solid,
echogenic mass, but sometimes as complex hyper/hypoechoic, heterogeneous mass
with anechoic areas due to fat, hemorrhage, necrosis, and calcifications; a capsule
may also be seen [36]. Color Doppler US can aid in the distinction from FNH in the
absence of a central arterial signal, FNH having characteristic intratumoral and
peritumoral vessels [37, 38]. Contrast-enhanced ultrasound with sulfur hexafluo-
ride microbubbles (SonoVue or Lumason) greatly improves diagnosis as compared
to US without contrast.
Figure 13.
HA located in segment VII as shown by imaging on NECT (A), CECT—arterial phase (B), portal venous phase
(C), parenchymal phase (D), MRI T1w (E), and T2w (F). Atoll sign characterized by a hyper intense band in
the periphery and isodensity in the center of the lesion with respect of the surrounding liver is relevant on CT in
portal venous phase (C). A hyperintense rim in T2 wi is described in inflammatory adenoma (arrow in F).
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Liver Disease and Surgery
Figure 14.
NECT with large liver mass with central calcifications, small lipomatous inclusions, solid components and
necrosis (A), CECT—arterial phase (B), portal venous phase (C), and parenchymal phase (D).
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Figure 15.
CT evaluation: liver adenoma with central necrotic area and encapsulation (arrow).
Some MRI findings of HAs are similar to CT findings, but MRI is usually more
sensitive in detecting fat from hemorrhage. The appearance of HAs on MRI is highly
variable, especially in T1, but if contrast medium is used, then it may be better
characterized, showing early arterial enhancement and becoming nearly isointense
to liver on delayed images.
On T1-weighted images (T1wi), HA appears as a heterogeneous signal inten-
sity mass. The increased signal of HA is due to fat and recent hemorrhage, and the
decreased signal intensity is due to necrosis, calcification, or old hemorrhage. A
fibrous pseudocapsule may be seen in HA as a hypointense rim. In T2wi, the mass
appears heterogeneous; increased signal intensity corresponds to old hemorrhage
or necrosis, and the decreased signal intensity is due to the fat or recent hemor-
rhage. The peripheral rim (fibrous pseudocapsule) in HA appears hypointense
in liver parenchyma (Figure 16). After contrast injection (T1wi + C) in arte-
rial phase, adenomas are heterogeneous hypervascular masses (inflammatory
HA+++) and in delay phase a pseudocapsule, which is hyperintense comparative
to the normal liver, can be seen. After Gadoxetate-enhanced MR (Gd-EOB-
DTPA), in HA there is no substantial contrast uptake or retention on hepatobili-
ary phase [40].
Figure 16.
MRI evaluation: liver adenoma with central necrotic area and pseudocapsule hyperintense to the surrounding
liver (arrow).
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Liver Disease and Surgery
MRI with hepatobiliary agents is an important tool not only in differential sub-
type definition but even in surveillance with early identification of complications
and discovery of some signs of HA malignant degeneration [41]. Lesion enlarge-
ment and heterogeneity of signal intensity and of contrast enhancement are signs
of malignant transformation [42].
Imaging recommendations: the best imaging tool is represented by Gadoxetate-
enhanced MRI including multiphase and hepato-biliary phase acquisition [43]. The
best sequence to evaluate fat into HA is T1wi with in and opposed TE.
Figure 17.
HNF1A-mutated HA: diffuse lipid deposition within HA best seen using T1 with TE in and out of phase
(arrow).
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Figure 18.
Inflammatory liver adenoma: hyperintensity T2 wi and hypervascularity of the liver mass through the late AP,
and discreetly hyperintense in portal and late phase.
the portal venous and delayed phases (Figure 18). The atoll sign is specific for IHA
and may be due to sinusoidal dilatation. In up to 30% of cases, there is evidence of
hemorrhage, and a 10% likelihood of malignant degeneration is estimated. At mul-
tidetector CT, IHA is depicted as heterogeneously hyperattenuating mass in NECT
and in CECT shows enhancement features similar to those at MRI. At CEUS, it has
arterial vascularity with centripetal filling, a sustained enhanced rim and central
wash-out in the late venous phase.
Unclassified hepatic adenoma (U-HA) does not fit other profiles of HA subtypes.
Most HAs have a decreased uptake of Gallium and colloid, early and retained
uptake of hepatobiliary agents, and no uptake on PET scanning.
If radiological studies cannot distinguish HA from HCC and FNH, a combination
of radionuclide imaging, including technetium (99mTc)-sulfur colloid sulfur-colloid,
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The surgeons must be convinced that HA subtypes are important for the man-
agement of the patients. From now on, a diagnosis of HA cannot be conceived
without group classification. The number and location of HA play a great role
in management, but various clinical conditions such as age, sex, etiology, back-
ground liver, or comorbidities must be taken into consideration. Other aspects
also play a role in decision making, like where the patient lives, the degree of his/
her anxiety, and cost of surveillance. The management of patients with HA must
be planned by a complex team formed by surgeons, hepatologists, pathologists,
radiologists, gastroenterologist, molecular biologists, and geneticists.
There are no clear guidelines for the management of HA, because the treatment
depends on many factors such as HA size, number, localization, gender, age, pres-
ence of symptoms, and complications.
In young women treated with contraceptive pills, asymptomatic lesions under
5 cm in diameter should be kept under close observation with CT/CEUS repeated
every 6 months [51] and repeated alpha-feto-protein, all the while ceasing to use
contraceptive pills [52]. Any modification in imaging suggesting a malignant trans-
formation or an increase in the serum tumor marker should lead to liver resection.
There are some authors who advocate resection of adenomas of any size given their
risk of malignization and bleeding, if the resection can be performed with accept-
able risk. The facts that surgical excision guarantees a definitive diagnosis and
long-term cure favor the universal indication of surgery for HA [53].
The indications for surgery in nonemergent cases are: HA > 5 cm, female patients
taking oral contraceptives with HA > 3 cm [47], HA with growing size, HA with
HCC or dysplastic foci, β-catenin-activated HA, imaging features of malignant
transformation, increased serum alpha fetoprotein, HA in males regardless of the
tumor size, HA in GSD, symptomatic patients, or when malignancy cannot be
excluded [54]. The type of resection depends mainly on number, size, histological
type, and localization of HA. The resection techniques vary from simple enucleation
to liver transplantation [55]. Liver resection for HA can be anatomic or nonanatomic.
Anatomic resections reported in the literature for HA refer to minor hepatectomies
that imply the removal of the tumor with one or two segments of the liver [56], but
also major hepatectomies like left and right hemihepatectomy, mesohepatectomy
[57], and left or right extended hepatectomy [26, 58]. Nonanatomical resections are
wedge resections [59]. Enucleation seems to be a choice for such benign tumor, but
is not advisable due to the risk of remnant tumor that can cause tumor recurrence or,
worse, malignant degeneration, especially for β-catenin HA. It was speculated that
the classical 1 cm oncological safety margin could be lowered to 0.5 cm for HA. The
safety margin at the edge of resection is mandatory, if any suspicion of HCC exists.
Surgery in elective cases is less than 1% and most tumors can be operated
laparoscopically, with significant advantages [59–61]. A better cosmetic result,
a shorter hospitalization (4 days) with early return to normal life, and a lower
incisional rate are the main advantages that laparoscopy has comparative with
open approach. However, laparoscopy should be performed only in specialized
centers with extensive experience in both hepatic and laparoscopic surgery.
The first non-anatomical laparoscopic liver resection for HA reported by Ferzli
et al. [62] in 1995 was followed one year later by the first anatomic laparoscopic
resection for HA performed by Azagra et al. [63]. Pure laparoscopic procedure
can be performed for HA with no mortality and reduced morbidity even in
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Even the resection of only the complicated nodule (i.e., hemorrhagic liver
nodule) seems appropriate as the first step toward enlisting for liver trans-
plantation. Multiple resections are the preferable options in patients with liver
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Figure 19.
Upper left: massive liver adenomatosis that deforms the contour of the left lateral sector. Upper right: a left
lateral sectionectomy is planned and a cotton loop around hepatic pedicle is placed for Pringle maneuver.
Lower left: intraoperative aspect after left lateral sectionectomy. Lower right: sectioned surgical specimen with
evidence of the largest HA.
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Figure 20.
Liver adenomatosis with a voluminous adenoma of the left liver in a 47-year-old male patient who had a liver
transplantation. A-C. CECT of the liver with adenomatosis. D. Total hepatectomy specimen with numerous
adenomas of various sizes, a voluminous adenoma in the left liver, and blood clots due to intratumoral
bleeding.
procedure to be used in both elective and emergency conditions. For small lesions,
TAE can achieve complete resolution and thus avoidance of liver surgery entirely.
TAE may be also used as means to shrink the tumors to a size that renders them
approachable for subsequent surgical resection [76]. TAE can reduce the size of
large adenomas, multiple adenomas, or adenomas that are in a surgical inacces-
sible localization alleviating the symptoms and reducing the risk of perioperative
bleeding. It has a low rate of complications (8%). These complications associated
with TAE include post-embolization syndrome, temporary renal failure, and cyst
formation [77]. One pyogenic abscess after TAE was also reported as a complication
after TAE for a large HA. No sufficient data exist until now to conclude that TAE
reduces the risk of hemorrhage or malignant transformation of residual HA, despite
reports of a reduction in tumor size.
Radiofrequency ablation has its shortcomings, such as the need of many ses-
sions in order to destruct the tumor completely, but it may be a very good option for
tumors that cannot be operated [78].
Medical treatment such as administration of the SRC inhibitor dasatinib or
JAK1/2 inhibitor ruxolitinib could be a new alternative in the future [79].
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Liver Disease and Surgery
Adenomas greater than 5 cm that are discovered during pregnancy need individu-
alized approach. Surgery is recommended during second trimester to minimalize
the risks for both the mother and the fetus. Radiofrequency has been an option
performed during the first and second trimester [18]. Angioembolization poses
the radiation risk to the fetus early in pregnancy and must be avoided in the first
trimester.
Pregnancy induces not only an increased level of endogenous hormones
but also an increased liver vascularity that puts the patient at risk for adenoma
rupture especially in the third trimester [81]. However, a ruptured HA discovered
during pregnancy should be immediately resected by laparotomy or laparoscopy
[28, 82, 83].
8. Conclusions
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Thanks
We thank our mentor Prof. Dr. Irinel Popescu, MD, PhD, FACS, for giving us the
possibility to use data and iconography of patients that he operated on, in order to
complete writing this chapter.
Author details
Mirela Patricia Sîrbu Boeți1,2*, Beatrice Tivadar2, Ioana G. Lupescu1,3, Vlad Herlea4,5,
Mirela Boroș3, Dana Tomescu1,6 and Vladislav Brașoveanu2,5
© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms
of the Creative Commons Attribution License (http://creativecommons.org/licenses/
by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,
provided the original work is properly cited.
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