Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 881 - файл
.pdf
23 Benign andMalignant Lesions oftheLiver
337
[10] consisting in a semiannual abdominal ultrasound (US) all at-risk populations
(cirrhotic patients, Child-Pugh stage A and B; cirrhotic patients, Child-Pugh stage
C awaiting liver transplantation; non-cirrhotic HBV carriers with active hepatitis or
family history of HCC; non-cirrhotic patients with chronic hepatitis C and advanced
liver brosis). Paraneoplastic manifestations are rarely associated with HCC and
include hypoglycemia (type A and B), polycythemia, hypercalcemia, and pityriasis
rotunda.
The diagnosis of HCC in cirrhotic patients is made according to the “recall policy,” which is based on the diameter of the nodule.
In cirrhotic patients, nodules <1cm in diameter detected by ultrasound should be
followed every 4months in the rst year and with regular checking every 6months
thereafter.
In cirrhotic patients, diagnosis of HCC for nodules of 1–2cm in diameter should
be based on imaging (computed tomography (CT) or magnetic resonance imaging)
or biopsy-proven pathological conrmation.
In cirrhotic patients, nodules more than 2cm in diameter can be diagnosed for
HCC on one imaging technique or on the combination of CT scan and MRI techniques and/or liver biopsy as needed.
HCC diagnosis is therefore based on imaging or pathology. However, in the
elderly, this may raise some concerns, especially regarding the risks associated
with liver biopsy [1] and to the presence of contraindications to second-level
radiologic imaging, due to chronic kidney disease with reduced creatinine clearance below 30mL/min [14]. This is even truer in non-cirrhotic patients with HCC,
because liver biopsy is recommended to ascertain the nature of the liver lesion
independently of imaging behavior [15, 16]. Although great efforts of studies
focused on molecular pathways and on the classication of HCC according to
gene signatures or molecular abnormalities, they are not currently used for clinical application [17, 18].
The BCLC staging system has been recently recommended for prognostic prediction and treatment allocation of patients with HCC (Fig.23.1) [19]. The severity
of liver function impairment represents one of the most important prognostic parameters included in the BCLC algorithm, together with tumor stage and cancer-related
symptoms. Based on these characteristics, in the BCLC system, patients are stratied in ve categories (0, A–D), each one corresponding to specic therapeutic
approaches and the patients’ outcome.
Resection is the rst-line treatment option for patients with a solitary tumor and
very well-preserved liver function, dened as normal bilirubin with either hepatic
venous pressure gradient ≤10 mmHg or platelet count ≥100,000. Perioperative
mortality is expected to be 2–3% [20, 21]. Neoadjuvant or adjuvant therapies do not
improve the outcome of patients treated with resection [22, 23].
Liver transplantation is considered to be the rst-line treatment option for
patients with single tumors less than 5cm in size or with ≤3 nodules ≤3cm in size
(Milan criteria) who are not suitable for resection [24, 25]. A modest expansion of
Milan criteria applying the “up-to-seven” criteria in patients without microvascular
invasion undergoing liver transplantation seems also to achieve competitive
338
PST 0, Child Pugh
Po
pr
PST > 2, Child Pugh C
Median OS > 60 mo; 5-year survival 40-70%
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
F.R. Ponziani et al.
HCC
STAGE 0
Very early stage (0)
Single < 2 cm
Carcinoma in situ
Single
rtal
essure/bilirubin
Normal
Resection
Curative treatment 30-40%
A
Early stage (A)
Single or 3 nodules ≤ 3 cm
PS 0
3 nodules ≤ 3
cm
Associated diseases
No
Liver transplantation
(CLT/LDLT)
Yes
RF/PEI
STAGE A-C
PST 0-2, Child Pugh A-B
Intermediate stage (B)
Multinodular,
PS 0
TACE
Target 20%
OS 20 mo (45-14)
Advanced stage (C)
Portal invasion,
N1, M1, PS 1-2
SorafenibBest supportive
Target 40%
OS 11 mo (6-14)
STAGE D
Terminal stage (D)
care
Target 10%
OS < 3 mo
Fig. 23.1 Adapted from EASL- EORTC guidelines (2012)
outcomes [26]. However, most of the liver transplant centers have settled a cutoff for
the age of liver transplant candidates, which usually does not exceed 65years.
Local ablation with radiofrequency or percutaneous ethanol injection is considered the standard of care for patients with BCLC 0–A tumors not suitable for surgery. Studies reporting outcomes after radiofrequency ablation (RFA) in elderly
patients showed that old age is not an independent predictor of reduced survival
after RFA.However, the good safety prole of RFA is maintained in the elderly, and
the rate of major complications was found to be similar in elderly and in younger
cirrhotic patients [27–29].
Transarterial chemoembolization (TACE) is recommended for BCLC stage B
patients, with multinodular asymptomatic tumors in the absence of vascular invasion or extrahepatic spread. It is instead discouraged in patients with decompensated liver disease, advanced liver dysfunction, macroscopic vascular invasion, or
extrahepatic spread. There are only few studies addressing the use of TACE in the
elderly, and its use in this setting is still debated. A prospective cohort study performed on 102 patients with HCC who underwent TACE showed similar survival
and safety prole irrespective of age [30, 31]. In a large retrospective study from
Korea, the authors found that TACE was associated with even better results in
elderly than in younger patients, with respect to median OS and disease-specic
survival; moreover, there was no signicant difference in terms of TACE-related
mortality [32]. These data suggest that in the elderly, TACE is an effective therapeutic option for HCC with a satisfactory safety prole.
Sorafenib is the only approved systemic therapy for HCC.It is indicated for
patients with well-preserved liver function (Child-Pugh A) and with advanced
tumors (BCLC C) or those tumors progressing upon locoregional therapies. The
23 Benign andMalignant Lesions oftheLiver
339
efcacy of sorafenib in elderly patients is supported by several studies, showing
similar, or even a trend to longer, overall survival and time to progression in elderly
patients compared with younger subjects [33, 34]. Overall, evidence collected to
date shows that the efcacy and safety prole of sorafenib is not inuenced by age.
However, a stricter monitoring should be considered in the elderly because of the
potential risk of developing and the reduced tolerability of adverse events.
23.2.2 Intrahepatic Cholangiocarcinoma
Intrahepatic cholangiocarcinoma (ICC) is a malignant tumor arising from the intrahepatic biliary tract. It is responsible for 10–20% of primary liver cancers worldwide and is the second most common primary liver malignancy [35]. ICC can be
classied anatomically as perihilar or peripheral [36].
The incidence of ICC varies worldwide, with the highest rates in northeast
Thailand (>80 per 100,000 population) and lower rates in the Western world (0.3–
2.1 per 100,000 population) [37]. Hispanic females, American Indian/Alaskan
Native, and Asian Pacic groups seem the most affected ethnic groups. Despite the
signicant geographical and ethnic variations, recent studies have reported a global
increase in incidence of ICC over the last few decades [38] as well as an increasing
mortality. Similar trends are observed in both sexes with an overall slight male predominance (M: F 1.2–1.5:1) [39].
Cholangiocarcinogenesis is a complex multistep process. It may occur in a
healthy liver or in patients with underlying liver disease. Several risk factors for
chronic inammatory damage and increased cellular turnover have been established, such as hepatobiliary ukes (Opisthorchis viverrini and Clonorchis sinensis,
classied as group 1 carcinogens in WHO classication 2009), primary sclerosing
cholangitis (PSC), cysts of the biliary tract, hepatolithiasis, and toxins [40].
Cirrhosis, chronic hepatitis B and C, obesity, diabetes, and alcoholic liver disease,
although recognized as risk factors for HCC, are also emerging as warning conditions for ICC.Mixed histotypes of hepatocellular-cholangiocarcinoma rather than
the traditional adenocarcinoma can be also observed [41].
ICC early diagnosis is still a major clinical challenge, because patients with
early-stage disease are often asymptomatic [42]. Weight loss, abdominal discomfort, biliary tract obstruction with jaundice, and hepatomegaly or palpable abdominal mass are usually observed at more advanced stages. The only potentially curative
treatment option for patients who have resectable disease is surgery. Unfortunately,
even the clinical outcomes of patients undergoing liver resection are disappointing,
with a 5-year survival rate of 20–35% [43]. Furthermore, the role of adjuvant therapies, including systemic chemotherapy and radiotherapy, remains poorly dened
and of scarce effect.
Many studies have investigated the mechanisms involved in the carcinogenetic
process in ICC at different levels of cell biology, from single gene mutations to
protein aberrations. In this perspective, there are many candidates for targeted therapies such as MET, EGFR and ERBB2, FGFR2, JAK/STAT, RAS/RAF/MAPK, and
340
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
F.R. Ponziani et al.
PI3K/AKT/mTOR pathways and even IDH mutations, although no therapeutic
approach has been currently introduced in clinical practice [44].
23.2.3 Hemangiosarcoma, Epithelioid Hemangioendothelioma,
andOther Primary Malignant Tumors
Although rare, angiosarcoma is the most common malignant mesenchymal tumor of
the liver [45]. It occurs almost exclusively in adults and is most prevalent in the sixth
and seventh decades of life. Men are affected four times as often as women. The most
common presenting symptom is upper abdominal pain. Other frequent complaints are
abdominal swelling, rapidly progressing liver failure, malaise, weight loss, poor appetite, and nausea [46]. The duration of symptoms generally ranges from 1week to
6months, but a few patients have had symptoms for as long as 2years before seeking
medical attention. A rising serum bilirubin level and other evidence of progressive
hepatic dysfunction may be present, especially in case of the later stages of the tumor.
Hepatic arteriography reveals a characteristic appearance. The hepatic arteries
are displaced by the tumor, which shows a blush and “puddling” in the middle of the
arterial phase that persist for many seconds, except in the central area, which may
be hypovascular.
Hepatic angiosarcomas grow rapidly, and the prognosis is poor; death ensues
within 6months. Patients may have thrombocytopenia resulting from entrapment of
platelets within the tumor (Kasabach-Merritt syndrome), disseminated intravascular
coagulation with secondary brinolysis, or microangiopathic hemolytic anemia as a
result of fragmentation of erythrocytes within the tumor circulation. Operative treatment is usually precluded by the advanced stage of the tumor, while chemo- and
radiotherapy showed poor results [47].
Epithelioid hemangioendothelioma is a rare tumor, described in females at all
ages in adulthood [48]. No specic symptoms are usually referred, and imaging
studies show a characteristically highly vascular mass, which may inltrate throughout the liver. Case reports indicate that the tumor can be visualized on PET.Correct
diagnosis requires histologic examination of tissue obtained by biopsy. It is important to distinguish this tumor with low-grade malignant potential from hemangiosarcoma, as a better prognosis can be reached, if treated appropriately and
aggressively. The rst treatment modality for epithelioid hemangioendothelioma is
surgery, including resection or liver transplantation [
Other rare sarcomas arising in the liver include liposarcoma, lymphoma, and
rhabdomyosarcoma.
49].
23.3 Benign Tumors
Benign liver tumors are frequently found incidentally, as a consequence of the widespread use of imaging tests, and often have a favorable course. Several types of
benign liver tumors have been identied (Table 23.1); EASL guidelines [50]
23 Benign andMalignant Lesions oftheLiver
341
Table 23.1 Histological
classication of benign liver
tumors, adapted from Coelho
etal. indication and treatment
of benign hepatic tumors
Epithelial origin Type of tumor
Hepatocyte Hepatocellular carcinoma
Multiple adenomatosis
Focal nodular hyperplasia
Nodular rigenerative hyperplasia
Bile cells Bile duct adenoma
Biliary hamartomas (von
Meyenburg complex)
Non-epithelial origin Type of tumor
Mesenchymal Hemangioma
Angiomyolipoma
Lipoma, myelolipoma
Others Inammatory pseudotumors
provide a contemporary aid for the practical diagnosis and management of the more
common ones: hemangiomas, focal nodular hyperplasia (FNH), and hepatocellular
adenoma (HCA). In association with an unremarkable baseline history, physical
examination, blood tests, and imaging are usually sufcient to establish a diagnosis
of a benign liver tumor and informed decisions on patients’ management [50].
23.3.1 Hepatic Hemangiomas
Hepatic hemangiomas are the most common benign primary liver tumors, belonging to the group of non-epithelial lesions. Hemangiomas are present in 0.4–20% of
the general population and are typically discovered incidentally during evaluation
for non-specic abdominal complaints, most frequently diagnosed in women
between 30 and 50years [51]. Lesions measuring 10cm are called “giant hemangiomas” and may be symptomatic, including pain and the Kasabach-Merritt syndrome [52].
Hemangiomas are most often asymptomatic as they are incidentally discovered
and may change in size during long-term follow-up. There is no relationship
between the size of hemangiomas and complications, while there is little relationship between symptoms and characteristics of the lesion. When observed at abdominal ultrasound (US), hemangiomas have a classic appearance as a homogeneous
hypoechoic mass usually measuring less than 3 cm in diameter with acoustic
enhancement and sharp margins [53]. Contrast enhancement (CE) study allows the
denition of peripheral and globular enhancement of the lesion followed by a central enhancement on delayed phases [53]. MRI is the key imaging modality for the
diagnosis of these lesions [54].
Surgical management is still debated in terms of advantages even in large
lesions or lesions with mild symptoms. Symptomatic or giant hemangiomas are
not common, and surgical resection is rarely indicated, except in the presence of
KMS [52].
342
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
F.R. Ponziani et al.
23.3.2 Focal Nodular Hyperplasia (FNH)
Focal nodular hyperplasia is the second most frequent benign tumor of the liver. The
average age at presentation ranges between 35 and 50years [55]. In most cases, it is
solitary and smaller than 5cm. It is widely thought that this lesion arises as a proliferative cell response to an aberrant dystrophic artery and may be associated with
other conditions characterized by arterial damage [56].
On US, FNH is usually slightly hypo- or isoechoic and very rarely hyperechoic.
Typically, Doppler US reveals central arteries with a spoke-wheel pattern.
MRI has the highest diagnostic performance for the diagnosis of FNH.CEUS
achieves a high accuracy in FNH less than 3cm.
Regardless of the specic imaging technique used, typical general ndings are
(1) homogeneity of the lesion except for the central scar, (2) slight difference from
the adjacent liver on pre-contrast imaging, (3) strong and homogeneous enhancement on the arterial phase with a central vascular supply, (4) the lesion becomes
similar to the adjacent liver on portal and delayed phases, (5) the central scar can be
best seen on MRI, and (6) a lack of capsule and often lobulated contours [57].
In the absence of symptoms and given the rarity of complications, a conservative
approach is recommended. For a lesion typical for FNH, the follow-up is unnecessary unless in the presence of an underlying vascular disease [58].
23.3.3 Hepatocellular Adenoma (HCA)
Hepatocellular adenoma is approximately ten times less common than FNH and is
typically diagnosed in women 30–40years old. Several studies have supported the
potential role of sex hormones in the development of HCA.In particular, the link
between oral contraceptive pills and increased risk of HCA in women was strengthened by the demonstration of occasional tumor regression upon drug withdrawal.
Notably, the incidence of HCA has increased in males due to the increased use of
anabolic-androgen steroids in body builders and gym activities. The recent increase
in the HCA prevalence has been also associated with obesity and metabolic
syndrome.
A molecular classication of HCA has been proposed showing two main types,
respectively, observed in women and men. Indeed, the course of HCA diagnosed in
women is more often benign, the content of fat is increased, and the hallmark is the
absence of expression in tumor hepatocytes of genes controlled by HNF-1a, among
them, liver fatty acid binding protein (LFABP), which is in contrast highly expressed
in non-tumor hepatocyte.
The second subtype “inammatory HCA” is characterized by the activation of
the JACK/STAT pathway, a molecular key present in several malignancies. “Betacatenin- activated HCA” is another subtype, highly associated with risk of malignant
transformation [59].
MRI is superior to all other imaging modalities in the diagnosis of HCA and is
useful to distinguish the different subtypes. Biopsy should be considered within a
23 Benign andMalignant Lesions oftheLiver
343
benign liver tumor to exclude malignancy. In the case of tissue availability obtained
for diagnostic purpose, curative intervention is advised for the activated b-cateninmutated HCA, irrespective of size [60].
Treatment decisions are usually based on gender, size, and patterns of progression. Upon HCA diagnosis, lifestyle changes such as weight loss and discontinuation of contraceptives should be recommended. HCA resection is recommended
irrespective of size in men and in any instance of proven beta-catenin mutation; in
women, a period of 6 months observation after lifestyle change is advised, and
resection is indicated in the case of nodules ≥5cm and for those continuing to grow.
In case of lesions <5cm in women, a reassessment at 1year and annual imaging
thereafter are recommended. A sure indication for embolization and subsequent
resection is a bleeding HCA with hemodynamic instability [61].
References
1. Stewart BW, Kleihues P, editors. World cancer report. Lyon: IARC Press; 2003.
2. Borzio M, Dionigi E, Parisi G, Raguzzi I, Sacco R.Management of hepatocellular carcinoma
in the elderly. World J Hepatol. 2015;7(11):1521–9.
3. Asahina Y, Tsuchiya K, Tamaki N, Hirayama I, Tanaka T, Sato M, Yasui Y, Hosokawa T, Ueda
K, Kuzuya T, Nakanishi H, Itakura J, Takahashi Y, Kurosaki M, Enomoto N, Izumi N.Effect of
aging on risk for hepatocellular carcinoma in chronic hepatitis C virus infection. Hepatology.
2010;52:518–27. https://doi.org/10.1002/hep.23691.
4. Borzio M, Fornari F, De Sio I, Andriulli A, Terracciano F, Parisi G, Francica G, Salvagnini M,
Marignani M, Salmi A, Farinati F, Carella A, Pedicino C, Dionigi E, Fanigliulo L, Cazzaniga
M, Ginanni B, Sacco R.Adherence to American Association for the Study of Liver Diseases
guidelines for the management of hepatocellular carcinoma: results of an Italian eld practice
multicenter study. Future Oncol. 2013;9:283–94.
5. Nordenstedt H, White DL, El-Serag H.The changing pattern of epidemiology in hepatocel-
lular carcinoma. Dig Liver Dis. 2010;42(Suppl):S206–14.
6. Kim YJ, Jang BK, Kim ES, Chung WJ, Park KS, Cho KB, Hwang JS.Hepatocellular carcinoma
in the elderly: clinical characteristics, treatment, survival analysis in Korean patients older than
70 years. J Korean Med Sci. 2012;27:1147–54. https://doi.org/10.3346/jkms.2012.27.10.1147.
7. Pignata S, Gallo C, Daniele B, Elba S, Giorgio A, Capuano G, Adinol LE, De Sio I, Izzo F,
Farinati F, Del Naja C, Stanzione M, Castiglione F, Marone G, Cuomo O, Felder M, Gaeta
GB, De Maio E, Di Maio M, Signoriello G, Perrone F. Characteristics at presentation and
outcome of hepatocellular carcinoma (HCC) in the elderly. A study of the Cancer of the Liver
Italian Program (CLIP). Crit Rev Oncol Hematol. 2006;59:243–9. https://doi.org/10.1016/j.
critrevonc.2006.01.002.
8. Sia D, Villanueva A, Friedman S, Llovet MJ.Liver cancer cell of origin, molecular class, and
effects on patient prognosis. Gastroenterology. 2017;152:745–61.
9. Parkin DM, Bray F, Ferlay J, Pisani P.Global cancer statistics, 2002. CA Cancer J Clin.
2005;55:74–108.
10. European Association for the Study of the Liver. EASL-EORTC clinical practice guidelines:
management of hepatocellular carcinoma. J Hepatol. 2012;56:908–43.
11. Nguyen VT, Law MG, Dore GJ.Hepatitis B-related hepatocellular carcinoma: epidemiologi-
cal characteristics and disease burden. J Viral Hepat. 2009;16(7):453–63.
12. Bosetti C, Boffetta P, Lucchini F, Negri E, La Vecchia C.Trends in mortality from hepatocel-
lular carcinoma in Europe 1980–2004. Hepatology. 2008;48:137–45.
13. Donato F, Tagger A, Gelatti U, etal. Alcohol and hepatocellular carcinoma: the effect of lifetime
intake and hepatitis virus infection in men and women. Am J Epidemiol. 2002;155(4):323–31.
344
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
F.R. Ponziani et al.
14. Forner A, Vilana R, Ayuso C, Bianchi L, Solé M, Ayuso JR, etal. Diagnosis of hepatic nodules
20mm or smaller in cirrhosis: prospective validation of the noninvasive diagnostic criteria for
hepatocellular carcinoma. Hepatology. 2008;47:97–104.
15. Stigliano R, Marelli L, Yu D, Davies N, Patch D, Burroughs AK.Seeding following percu-
taneous diagnostic and therapeutic approaches for hepatocellular carcinoma. What is the
risk and the outcome? Seeding risk for percutaneous approach of HCC.Cancer Treat Rev.
2007;33:437–47.
16. Sersté T, Barrau V, Ozenne V, Vullierme MP, Bedossa P, Farges O, etal. Accuracy and dis-
agreement of CT and MRI for the diagnosis of small hepatocellular carcinoma and dysplastic
nodules: role of biopsy. Hepatology. 2011;55(3):800–6. https://doi.org/10.1002/hep.24746.
[Epub ahead of print].
17. Boyault S, Rickman DS, de Reyniès A, Balabaud C, Rebouissou S, Jeannot E, et al.
Transcriptome classication of HCC is related to gene alterations and to new therapeutic targets. Hepatology. 2007;45:42–52.
18. Chiang DY, Villanueva A, Hoshida Y, Peix J, Newell P, Minguez B, etal. Focal gains of VEGFA
and molecular classication of hepatocellular carcinoma. Cancer Res. 2008;68:6779–88.
19. Llovet JM, Fuster J, Bruix J, Barcelona-Clinic Liver Cancer Group. The Barcelona approach:
diagnosis, staging, and treatment of hepatocellular carcinoma. Liver Transpl. 2004;10(2, Suppl
1):S115–20.
20. Roayaie S, Llovet JM, Obeidat K, Labow D, Sposito C, Pellegrinelli A, etal. Hepatic resection
for hepatocellular carcinoma <2cm in diameter. Hepatology. 2012;49(44):518–23.
21. Llovet JM, Schwartz M, Mazzaferro V.Resection and liver transplantation for hepatocellular
carcinoma. Semin Liver Dis. 2005;25:181–200.
22. Vitale A, Volk ML, Pastorelli D, Lonardi S, Farinati F, Burra P, etal. Use of sorafenib in
patients with hepatocellular carcinoma before liver transplantation: a cost–benet analysis
while awaiting data on sorafenib safety. Hepatology. 2010;51:165–73.
23. Truesdale AE, Caldwell SH, Shah NL, Argo CK, Al-Osaimi AM, Schmitt TM, etal. Sorafenib
therapy for hepatocellular carcinoma prior to liver transplant is associated with increased complications after transplant. Transpl Int. 2011;24:991–8.
24. Mazzaferro V, Bhoori S, Sposito C, Bongini M, Langer M, Miceli R, etal. Milan criteria in
liver transplantation for HCC: an evidence-based analysis on 15 years of experience. Liver
Transpl. 2011;17:S44–57.
25. Bruix J, Sherman M, AASLD Practice Guideline. Management of hepatocellular carcinoma:
an update. Hepatology. 2011;53(3):1020–2.
26. Clavien PA, Lesurtel M, Bossuyt PM, Gores GJ, Langer B, Perrier A, etal. Recommendations
for liver transplantation for hepatocellular carcinoma: an international consensus conference
report. Lancet Oncol. 2012;13:e11–22.
27. Massarweh NN, Park JO, Farjah F, Yeung RS, Symons RG, Vaughan TL, Baldwin LM, Flum
DR.Trends in the utilization and impact of radiofrequency ablation for hepatocellular carcinoma. J Am Coll Surg. 2010;210:441–8. https://doi.org/10.1016/j.jamcollsurg.2009.12.026.
28. Shiina S, Tateishi R, Arano T, Uchino K, Enooku K, Nakagawa H, Asaoka Y, Sato T, Masuzaki
R, Kondo Y, Goto T, Yoshida H, Omata M, Koike K.Radiofrequency ablation for hepatocellular carcinoma: 10-year outcome and prognostic factors. Am J Gastroenterol. 2012;107:569–
77. https://doi.org/10.1038/ajg.2011.425.
29. Tateishi R, Shiina S, Teratani T, Obi S, Sato S, Koike Y, Fujishima T, Yoshida H, Kawabe T,
Omata M.Percutaneous radiofrequency ablation for hepatocellular carcinoma. An analysis of
1000 cases. Cancer. 2005;103:1201–9. https://doi.org/10.1002/cncr.20892.
30. Cohen MJ, Bloom AI, Barak O, Klimov A, Nesher T, Shouval D, Levi I, Shibolet O.Trans-
arterial chemo-embolization is safe and effective for very elderly patients with hepatocellular carcinoma. World J Gastroenterol. 2013;19:2521–8. https://doi.org/10.3748/wjg.v19.
i16.2521.
31. Cohen MJ, Levy I, Barak O, Bloom AI, Fernández-Ruiz M, Di Maio M, Perrone F, Poon RT,
Shouval D, Yau T, Shibolet O. Trans-arterial chemo-embolization is safe and effective for
23 Benign andMalignant Lesions oftheLiver
elderly advanced hepatocellular carcinoma patients: results from an international database.
Liver Int. 2014;34:1109–17. https://doi.org/10.1111/liv.12486.
32. Yau T, Yao TJ, Chan P, Epstein RJ, Ng KK, Chok SH, Cheung TT, Fan ST, Poon RT.The
outcomes of elderly patients with hepatocellular carcinoma treated with transarterial chemoembolization. Cancer. 2009;115:5507–15. https://doi.org/10.1002/cncr.24636.
33. Cabibbo G, Maida M, Cammà C, Craxì A.Is the efcacy of sorafenib treatment in patients
with hepatocellular carcinoma affected by age? Expert Rev Anticancer Ther. 2013;13:1355–
61. https://doi.org/10.1586/14737140.2013.859989.
34. Dufour JF. Hepatocellular carcinoma: sorafenib: for once age is not an issue. Nat Rev
Gastroenterol Hepatol. 2014;11:273–4. https://doi.org/10.1038/nrgastro.2014.48.
35. Bridgewater J, Galle PR, Khan SA, Llovet JM, Park J, Patel T, Pawlik TM, Gores
GJ. Guidelines for the diagnosis and management of intrahepatic cholangiocarcinoma. J
Hepatol. 2014;60(6):1268–89.
36. Aishima S, Oda Y.Pathogenesis and classication of intrahepatic cholangiocarcinoma: differ-
ent characters of perihilar large duct type versus peripheral small duct type. J Hepatobiliary
Pancreat Sci. 2015;22:94–100.
37. Khan SA, Toledano MB, Taylor-Robinson SD.Epidemiology, risk factors, and pathogenesis of
cholangiocarcinoma. HPB (Oxford). 2008;10:77–82.
38. Shaib Y, El-Serag HB. The epidemiology of cholangiocarcinoma. Semin Liver Dis.
2004;24:115–25.
39. Shaib YH, Davila JA, McGlynn K, El-Serag HB.Rising incidence of intrahepatic cholangio-
carcinoma in the United States: a true increase? J Hepatol. 2004;40:472–7.
40. Khan SA, Thomas HC, Davidson BR, Taylor-Robinson SD. Cholangiocarcinoma. Lancet.
2005;366:1303–14.
41. Palmer WC, Patel T. Are common factors involved in the pathogenesis of primary liver
cancers? A meta-analysis of risk factors for intrahepatic cholangiocarcinoma. J Hepatol.
2012;57:69–76.
42. Blechacz B, Gores GJ.Cholangiocarcinoma: advances in pathogenesis, diagnosis, and treat-
ment. Hepatology. 2008;48:308–21.
43. Ruzzenente A, Conci S, Valdegamberi A, Pedrazzani C, Guglielmi A. Role of sur-
gery in the treatment of intrahepatic cholangiocarcinoma. Eur Rev Med Pharmacol Sci.
2015;19(15):2892–900.
44. Andersen JB, Spee B, Blechacz BR, Avital I, Komuta M, Barbour A, Conner EA, Gillen
MC, Roskams T, Roberts LR, Factor VM, Thorgeirsson SS.Genomic and genetic characterization of cholangiocarcinoma identies therapeutic targets for tyrosine kinase inhibitors.
Gastroenterology. 2012;142:1021–31.
45. Wu CH, Chiu NC, Yeh YC, Kuo Y, Yu SS, Weng CY, Liu CA, Chou YH, Chiou YY.Uncommon
liver tumours: case report and literature review. Medicine (Baltimore). 2016;95(39):e4952.
https://doi.org/10.1097/MD.0000000000004952. Review.
46. Lahat G, Dhuka AR, Hallevi H, etal. Angiosarcoma: clinical and molecular insights. Ann
Surg. 2010;251:1098–106.
47. Maluf D, Cotterel A, Clark B, et al. Hepatic angiosarcoma and liver transplantation: case
report and literature review. Transplant Proc. 2005;37:2195–9.
48. Miller WJ, Dodd GD, Federle MP, etal. Epithelioid hemangioendothelioma of the liver: imag-
ing ndings with pathologic correlation. AJR Am J Roentgenol. 1992;159:53–7.
49. Darras T, Moisse R, Colette JM.Epithelioid hemangioendothelioma of the liver. J Belg Radiol.
1988;71:722–33.
50. European Association for the Study of the Liver (EASL). EASL clinical practice guidelines on
the management of benign liver tumours. J Hepatol. 2016;65:386–98.
51. Gandol L, Leo P, Solmi L, Vitelli E, Verros G, Colecchia A.Natural history of hepatic hae-
mangiomas: clinical and ultrasound study. Gut. 1991;32:677–80.
52. O’Rafferty C, O’Regan GM, Irvine AD, Smith OP.Recent advances in the pathobiology and
management of Kasabach-Merritt phenomenon. Br J Haematol. 2015;171:38–51.
345
346
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
F.R. Ponziani et al.
53. Quaia E, Bertolotto M, Dalla Palma L.Characterization of liver hemangiomas with pulse
inversion harmonic imaging. Eur Radiol. 2002;12:537–44.
54. Semelka RC, Brown ED, Ascher SM, Patt RH, Bagley AS, Li W, etal. Hepatic hemangiomas:
a multi-institutional study of appearance on T2-weighted and serial gadolinium-enhanced
gradient-echo MR images. Radiology. 1994;192:401–6.
55. Marrero JA, Ahn J, Rajender Reddy K, Americal College of Gastroenterology. ACG clini-
cal guideline: the diagnosis and management of focal liver lesions. Am J Gastroenterol.
2014;109:1328–47. quiz 1348.
56. D’Halluin V, Vilgrain V, Pelletier G, Rocher L, Belghiti J, Erlinger S, etal. Natural history
of focal nodular hyperplasia. A retrospective study of 44 cases. Gastroenterol Clin Biol.
2001;25:1008–10.
57. Buetow PC, Pantongrag-Brown L, Buck JL, Ros PR, Goodman ZD.Focal nodular hyperplasia
of the liver: radiologic-pathologic correlation. Radiographics. 1996;16:369–88.
58. Birn J, Williams TR, Croteau D, Schwartz S, Sturza S, Getzen T.Transarterial embolization of
symptomatic focal nodular hyperplasia. J Vasc Interv Radiol. 2013;24:1647–55.
59. Zucman-Rossi J, Jeannot E, Nhieu JT, Scoazec JY, Guettier C, Rebouissou S, etal. Genotype-
phenotype correlation in hepatocellular adenoma: new classication and relationship with
HCC.Hepatology. 2006;43:515–24.
60. Laumonier H, Bioulac-Sage P, Laurent C, Zucman-Rossi J, Balabaud C, Trillaud
H.Hepatocellular adenomas: magnetic resonance imaging features as a function of molecular
pathological classication. Hepatology. 2008;48:808–18.
61. Chun YS, Parker RJ, Inampudi S, Ehrenwald E, Batts KP, Burgart LJ, etal. Imaging surveillance
of hypervascular liver lesions in non-cirrhotic patients. J Gastrointest Surg. 2015;20:564–7.
Соседние файлы в папке @xirurgi_2025