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This is a benign neoplasm arising from liver cells or hepatocytes. They are most common in young women and are associated with a history of oral contraceptive use. These tumors are important to recognize since they can clinically mimic a hepatocellular carcinoma, indeed, rare cases have harbored this cancer. These adenomas may also arise in the setting of glycogen storage disorders. Large subcapsular tumors do have a tendency to rupture, particularly during pregnancy.

On gross examination, these tumors are pale, yellow-tan, and may contain bile stained nodules. They are most commonly found beneath the capsule and may be multinodular. Occasional tumors may reach 30 cm.

Under the microscope, these tumors are similar to normal liver but are usually two to three cells thick. No bile ductules or portal triads are present in these lesions but central veins and large muscular arteries are present. There is minimal cytologic atypia. No mitoses or vascular invasion is present. Distinction of these tumors from other nodular lesions may be difficult. The following tables may provide a guide in microscopic distinction.

In addition to the differential diagnosis listed above, in children, there is additional diagnostic concern regarding hepatoblastoma, the fetal variant. The following table may be helpful.


Disease Associations  
Laboratory/Radiologic/Other Diagnostic Testing  
Gross Appearance and Clinical Variants  
Histopathological Features and Variants  
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Fibrolamellar hepatocellular carcinoma occurring 5 years after hepatocellular adenoma in a 14-year-old girl: a case report with comparative genomic hybridization analysis.

Terracciano LM, Tornillo L, Avoledo P, Von Schweinitz D, Kuhne T, Bruder E.

Institute of Pathology, University of Basel, Basel, Switzerland.
Arch Pathol Lab Med. 2004 Feb;128(2):222-6. Abstract quote  

An unusual case of fibrolamellar carcinoma of the liver developed 5 years after removal of a hepatocellular adenoma in a 14-year-old girl belonging to a family with Carney syndrome. Both tumors were studied by light and electron microscopy, flow cytometry, and comparative genomic hybridization.

The first tumor, removed at the age of 9, was a bulky well-circumscribed liver mass composed of large eosinophilic cells with a focal pseudoglandular pattern but without cytologic atypia or sclerosis. A diagnosis of hepatocellular adenoma was rendered. Five years later, another hepatic tumor was removed from the right lobe. Microscopic examination revealed polygonal cells, each with a large amount of eosinophilic cytoplasm and a round nucleus with a conspicuous nucleolus. These cells were arranged in nests and strands and separated by bands of dense fibrous tissue, leading to a diagnosis of fibrolamellar carcinoma. Comparative genomic hybridization analysis revealed no genetic alteration in the adenoma; however, several chromosomal aberrations (loss of chromosome regions 1p and 4p and gains of chromosome regions 6q, 13q, and Xq) were detected in the fibrolamellar carcinoma.

To our knowledge, this is the first report of an association between hepatocellular adenoma and fibrolamellar carcinoma.


Hepatic adenomas: analysis of sex steroid receptor status and the wnt signaling pathway.

Torbenson M, Lee JH, Choti M, Gage W, Abraham SC, Montgomery E, Boitnott J, Wu TT.

Division of Gastrointestinal/Liver Pathology, Department of Pathology (MT, J-HL, SCA, EM, JB, T-TW).


Mod Pathol 2002 Mar;15(3):189-96 Abstract quote

Hepatic adenomas are strongly linked to excess hormonal exposure, but little else is known about their pathogenesis. The Wnt signaling pathway, which is activated in both hepatocellular carcinomas and hepatoblastomas, has not been studied in hepatic adenomas.

Fifteen hepatic adenomas were studied by immunohistochemistry for estrogen, progesterone, and androgen receptors (ER, PR, AR, respectively) and correlated with the results of immunostaining for beta-catenin. Direct sequencing was performed to look for mutations in key genes involved in the Wnt signaling pathway: Exon 3 of beta-catenin encompassing the glycogen synthase kinase 3beta (GSK-3beta) phosphorylation region and the mutational cluster region of the adenomatosis polyposis coli protein (APC). Analysis for loss of heterozygosity (LOH) at chromosome 5q was also performed. Immunostaining for both ER and PR was present in 11/15 (73%) adenomas, and staining with one hormone receptor was positively associated with staining for the other receptor. AR positivity was present in 3/15 cases.

Nuclear accumulation of beta-catenin was present in 7/15 (46%) of adenomas, indicating activation of the Wnt signaling pathway. However, no beta-catenin mutations, no APC mutations in the mutational cluster region, and no 5q LOH were detected. Two APC polymorphisms of unknown significance were seen. No clear association between beta-catenin nuclear accumulation and hormone receptor positivity was discerned.

Activation of the Wnt signaling pathway appears to be important in a subset of hepatic adenomas but does not result from common beta-catenin or APC mutations and does not appear to be directly linked to hormonal receptor status.

Two case reports of childhood liver cell adenomas harboring beta-catenin abnormalities.

Takayasu H, Motoi T, Kanamori Y, Kitano Y, Nakanishi H, Tange T, Nakagawara A, Hashizume K.

Department of Pediatric Surgery, Tokyo University, Tokyo, Japan; Department of Pathology, The University of Tokyo Hospital, Tokyo, Japan; and Division of Biochemistry, Chiba Cancer Center Research Institute, Chiba, Japan.

Hum Pathol 2002 Aug;33(8):852-5 Abstract quote

The benign epithelial neoplasm liver cell adenoma is rare, especially in childhood. We report 2 such cases, 1 of which was associated with Prader-Willi syndrome. Differential diagnosis of the liver cell adenomas on the basis of histopathologic findings proved difficult and was based on the absence of cellular and nuclear atypia, mitotic activity, and invasive growth. In both cases, immunohistochemical staining demonstrated the nuclear accumulation of beta-catenin, and in 1 case, the tumor cells carried a mutation of the beta-catenin gene.

Recently, disregulation of the Wnt/beta-catenin pathway, attributable to abnormalities of the beta-catenin gene, has been reported to be a major event in the development of hepatocellular carcinomas and hepatoblastomas.

Our report may be the first to describe the beta-catenin abnormalities in childhood liver cell adenoma. These findings imply that abnormalities of beta-catenin can be an early initiating event in human liver tumorigenesis.


Hepatic Progenitor Cells in Hepatocellular Adenomas

Louis Libbrecht, M.D. ; Rita De Vos, Ph.D. ; David Cassiman, M.D. ; Valeer Desmet, M.D. , Ph.D. ; Raymond Aerts, M.D. ; Tania Roskams, M.D. , Ph.D.

From the Department of Pathology (L.L., R.D.V., V.D., T.R.), the Laboratory of Cell Pharmacology (D.C.), and the Department of Abdominal Surgery (R.A.), University Hospitals, University of Leuven, Leuven, Belgium.

Am J Surg Pathol 2001;25:1388-1396 Abstract quote

Hepatocellular adenoma is a benign tumor of the liver that has a small but not negligible risk of malignant transformation into hepatocellular carcinoma. In analogy with the established role of oval cells in hepatocarcinogenesis in rodent models, human hepatic progenitor cells may have a function in the development of liver tumors.

To investigate this issue, we performed immunohistochemistry on biopsies of 10 consecutively resected hepatocellular adenomas using markers for hepatic progenitor cells. Sections of paraffin-embedded and frozen biopsies were stained using antibodies against cytokeratins 7, 8, 18, and 19, chromogranin-A, OV-6, and neural cell adhesion molecule. Hepatic progenitor cells were observed in five of 10 hepatocellular adenomas. These five tumors also contained cells with an immunohistochemical phenotype intermediate between hepatic progenitor cells and hepatocytes. Hepatic progenitor cells and intermediate hepatocyte-like cells were scattered throughout the tumors with a density that varied from area to area. Ultrastructural examination confirmed the presence of hepatic progenitor cells.

Our study shows that hepatic progenitor cells are present in a considerable proportion of hepatocellular adenomas, supporting the hypothesis that human hepatic progenitor cells can play a role in the development of hepatocellular tumors.



Pigmented Liver Cell Adenoma in Two Male Patients

Nadir Hasan, M.B., M.R.C.Path.; Michael Coutts, M.A., M.R.C.Path.; Bernard Portmann, M.D., F.R.C.Path.

From the Institute of Liver Studies (N.H., M.C., B.P.) and the Department of Histopathology (N.H.), Guy's, King's and St. Thomas' School of Medicine, London, U.K. Dr. Hasan's current affiliation is the Department of Pathology, Waikato Hospital, Hamilton, New Zealand.

Am J Surg Pathol 2000;24:1429-1432 Abstract quote

We report two cases of hepatocyte neoplasia with extensive deposition of Dubin-Johnson-like pigment in men without Dubin-Johnson syndrome.

This pigment has previously been described in hepatocellular carcinoma but not in liver cell adenoma. The tumors of both patients showed some atypical cytologic features, but no frank histologic evidence of malignancy. Long-term follow up for several years showed no evidence of recurrence after limited surgical excision.

We conclude that tumors with this structure may be cured by limited surgical excision and should be considered as pigmented liver cell adenomas.

Glypican-3 Expression Distinguishes Small Hepatocellular Carcinomas From Cirrhosis, Dysplastic Nodules, and Focal Nodular Hyperplasia-like Nodules.

*Departments and Laboratories of Pathology daggerDepartments and Laboratories of Hepatology double daggerDepartment of Abdominal Transplant Surgery, University and University Hospitals of Leuven, Leuven, Belgium.


Am J Surg Pathol. 2006 Nov;30(11):1405-1411. Abstract quote

Distinguishing small hepatocellular carcinoma (HCC) from other types of small focal lesions that occur in a cirrhotic liver can be difficult on the basis of morphologic features alone.

We investigated whether the expression of glypican-3 (GPC3) could be an ancillary tool in the histopathologic diagnostic process. We performed immunohistochemistry for GPC3 on 16 low-grade dysplastic nodules, 33 high-grade dysplastic nodules, 13 focal nodular hyperplasia-like nodules, and 59 HCCs with a diameter less or equal to 3 cm present in the cirrhotic liver of 66 patients. Both resected lesions and lesions biopsied by needle were included and nonlesional cirrhotic parenchyma was also stained. In a subset of cases (23 samples of cirrhosis, 4 low-grade dysplastic nodules, 5 high-grade dysplastic nodules, 2 focal nodular hyperplasia-like nodules, and 18 HCCs), real time reverse transcriptase-polymerase chain reaction for GPC3 was performed. GPC3 expression was, both on immunohistochemistry and by real time reverse transcriptase-polymerase chain reaction, much higher in small HCCs than in cirrhosis and other types of small focal lesions, indicating that the transition from premalignant lesions to small HCC is associated with a sharp increase of GPC3 expression in a majority of cases.

The sensitivity and specificity of a positive GPC3-staining for the diagnosis of HCC in small focal lesions was 0.77 and 0.96, respectively, in resected cases, and 0.83 and 1, respectively, for needle biopsies. Because the result of the staining was easily interpretable, immunohistochemistry for GPC3 is valuable ancillary tool in the histopathologic diagnosis of small focal lesions in cirrhosis.


TUMOR Liver Cells Bile Ducts Large Vessels Connective Tissue Mitoses Reticulin stain
Adenoma Normal or slightly larger or smaller, may have glycogen and fat Not present Present May be present None Normal or slightly decreased, sinusoidal staining, may show double cell plates
Focal nodular hyperplasia Normal, no small or large cell change Present in scar Present Scar None Normal pattern, sinusoidal staining, may show double cell plates
Nodular regenerative hyperplasia Normal or slightly compressed, suggesting foci of small cell change Present in portal zones Not present Not present None Normal with regenerative foic (thicker cell plates) compressing single cell plates
Fibrolamellar HCC Larger than normal polygonal to spindle shapes, pale bodies, enlarged nuclei, abundant eosinophilic granular cytoplasm Not present Not typical, variable Lamellar fibrosis Rare Not used for diagnosis, variable pattern


TUMOR Patient Age Serum AFP Cell Size Reticulin Stain Light/Dark cells Nodularity
Hepatoblastoma, fetal type <2-3 yrs + < or normal Focally absent + +
Adenoma >10 yrs - normal or > Intact - +/-


Angiotensin I-converting Enzyme (CD143) Is Down-regulated in Focal Nodular Hyperplasia of the Liver.

Grantzdorffer I, Lendeckel U, Carl-McGrath S, Roessner A, Rocken C.

Department of Pathology and dagger Institute of Experimental Internal Medicine, Otto-von-Guericke-University, Magdeburg, Germany.


Am J Surg Pathol. 2004 Jan; 28(1): 84-8. Abstract quote  

SUMMARY: In surgical pathology, focal nodular hyperplasia (FNH) is sometimes difficult to diagnose, and liver cirrhosis (LC) and hepatocellular adenoma (HA) are often among the differential diagnoses. Recently, we found a reduced expression of angiotensin I-converting enzyme (CD143) in FNH compared with cirrhotic and noncirrhotic liver. Intrigued by this observation, we investigated the expression pattern of CD143 in FNH, LC, and HA and its possible diagnostic value.

The expression of CD143 was studied by immunohistochemistry in 20 FNHs, 13 corresponding extralesional noncirrhotic liver parenchyma, 20 patients with LC, and four HAs. Endothelial cells were identified with antibodies directed against CD31 and CD34. CD31+, CD34+, and CD143+ sinusoidal endothelial cells were found in extralesional liver, LC, HA, and FNH. However, the number of CD143+ sinusoidal endothelial cells and the intensity of immunostaining were significantly reduced in FNH compared with extralesional liver, LC, and HA. The expression of CD143 was further assessed using a numerical scoring system ranging from 0 to 6. The mean immunoreactivity score for CD143 was 2.4 +/- 1.7 for sinusoidal endothelial cells in FNH, 5.7 +/- 0.6 in extralesional liver, 4.8 +/- 1.1 in LC, and 5.8 +/- 0.5 in HA. The differences between the mean immunoreactivity scores for CD143 were highly significant. The difference between FNH and extralesional liver was confirmed on transcriptional level by fluorescence-mediated real-time RT-PCR, which also showed a significantly decreased level of CD143 mRNA in FNH.

Our study provides evidence that CD143 is down-regulated in FNHs and that the phenotype of endothelial cells lining the sinusoids in FNH differs from those in non-neoplastic liver, LC, and HA. The observed variations in expression patterns for CD143 might be of diagnostic use in surgical pathology.

Identification of a unique gene expression signature that differentiates hepatocellular adenoma from well-differentiated hepatocellular carcinoma.

Chen ZM, Crone KG, Watson MA, Pfeifer JD, Wang HL.

From Lauren V. Ackerman Laboratory of Surgical Pathology and Division of Laboratory Medicine, Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO.

Am J Surg Pathol. 2005 Dec;29(12):1600-8. Abstract quote  

It is often difficult to distinguish hepatocellular adenoma (HCA) from well-differentiated hepatocellular carcinoma (WDHCC) when limited tissue from a needle biopsy is evaluated.

The aim of this study was to identify gene expression patterns that can distinguish HCA from WDHCC, with the ultimate goal of discovering novel diagnostic markers. Gene expression profile analysis was performed using Affymetrix U133Plus2 GeneChip microarrays on RNA isolated from frozen tissue of 6 HCA and 8 WDHCC specimens. Statistical analysis of microarray data identified 63 genes whose expression levels were significantly different between HCA and WDHCC. These included 57 genes overexpressed by HCA and 6 overexpressed by WDHCC. Eight genes were chosen for further analysis by quantitative RT-PCR on RNA derived from archived, paraffin-embedded tissue blocks of an independent validation set comprising 9 HCAs and 9 HCCs. Seven of the 8 genes demonstrated average expression differences between HCA and HCC that were concordant with the microarray findings, and their expression pattern correctly classified the 18 tumors into HCA and HCC using unsupervised clustering analysis. Furthermore, immunohistochemical staining performed on a third, independent set of 27 HCAs and 33 HCCs confirmed the expression differences at protein levels for 5 of the genes.

Taken together, our data demonstrate significant molecular differences between HCA and WDHCC, despite their morphologic similarity. More importantly, we have identified a unique set of genes whose expression pattern can discriminate between these two types of hepatocellular neoplasms, suggesting the possibility of future development of ancillary molecular and immunohistochemical diagnostic methods.


Laparoscopic liver resection of benign liver tumors.

Descottes B, Glineur D, Lachachi F, Valleix D, Paineau J, Hamy A, Morino M, Bismuth H, Castaing D, Savier E, Honore P, Detry O, Legrand M, Azagra JS, Goergen M, Ceuterick M, Marescaux J, Mutter D, de Hemptinne B, Troisi R, Weerts J, Dallemagne B, Jehaes C, Gelin M, Donckier V, Aerts R, Topal B, Bertrand C, Mansvelt B, Van Krunckelsven L, Herman D, Kint M, Totte E, Schockmel R, Gigot JF.

Hopital Universitaire Dupuyten, Limoges, France.
Surg Endosc. 2003 Jan;17(1):23-30. Epub 2002 Oct 08. Abstract quote  

OBJECTIVE: The objective of this study was to assess the feasibility, safety, and outcome of laparoscopic liver resection for benign liver tumors in a multicenter setting.

BACKGROUND: Despite restrictive, tailored indications for resection in benign liver tumors, an increasing number of articles have been published concerning laparoscopic liver resection of these tumors.

METHODS: A retrospective study was performed in 18 surgical centres in Europe regarding their experience with laparoscopic resection of benign liver tumors. Detailed standardized questionnaires were used that focused on patient's characteristics, clinical data, type and characteristics of the tumor, technical details of the operation, and early and late clinical outcome.

RESULTS: From March 1992 to September 2000, 87 patients suffering from benign liver tumor were included in this study: 48 patients with focal nodular hyperplasia (55%), 17 patients with liver cell adenoma (21%), 13 patients with hemangioma (15%), 3 patients with hamartoma (3%), 3 patients with hydatid liver cysts (3%), 2 patients with adult polycystic liver disease (APLD) (2%), and 1 patient with liver cystadenoma (1%). The mean size of the tumor was 6 cm, and 95% of the tumors were located in the left liver lobe or in the anterior segments of the right liver. Liver procedures included 38 wedge resections, 25 segmentectomies, 21 bisegmentectomies (including 20 left lateral segmentectomies), and 3 major hepatectomies. There were 9 conversions to an open approach (10%) due to bleeding in 45% of the patients. Five patients (6%) received autologous blood transfusion. There was no postoperative mortality, and the postoperative complication rate was low (5%). The mean postoperative hospital stay was 5 days (range, 2-13 days). At a mean follow-up of 13 months (median, 10 months; range, 2-58 months), all patients are alive without disease recurrence, except for the 2 patients with APLD.

CONCLUSIONS: Laparoscopic resection of benign liver tumors is feasible and safe for selected patients with small tumors located in the left lateral segments or in the anterior segments of the right liver. Despite the use of a laparoscopic approach, selective indications for resection of benign liver tumors should remain unchanged. When performed by expert liver and laparoscopic surgeons in selected patients and tumors, laparoscopic resection of benign liver tumor is a promising technique.
Surgical outcomes of isolated caudate lobe resection: a single series of 19 patients.

Sarmiento JM, Que FG, Nagorney DM.

Division of Gastroenterologic and General Surgery, Mayo Clinic, Rochester, Minn 55905, USA.

Surgery. 2002 Oct;132(4):697-708; discussion 708-9. Abstract quote

BACKGROUND: Isolated caudate lobe resection is a complex surgical procedure that requires technical expertise and knowledge of the surgical anatomy.

METHODS: All consecutive patients who were operated on for isolated caudate lobe resections by the senior author were studied. En bloc resections with adjacent hepatic parenchyma (as part of extended hepatectomies) or partial resections of the caudate lobe were excluded. Follow-up was completed by outpatient evaluation and mail correspondence.

RESULTS: Nineteen patients met the inclusion criteria (6 male, 13 female). Mean age (+/-SD) was 52 (+/-3) years. Primary diagnoses were colorectal metastases, hemangioma, hepatocellular carcinoma, adenoma, and neuroendocrine metastases. Margins were negative in all but 1 patient. One patient needed inferior vena cava resection. Pringle's maneuver was used in 1 patient (5%). Mean (+/-SD) operative time was 211 (+/-15) minutes, and estimated blood loss was 760 (+/-150) mL. Median blood transfusion was 0 U (range, 0-4). Complications (bile leak) were seen in 1 patient (5%). Median length of stay was 7 days (range, 4-14). There were no perioperative deaths.

CONCLUSIONS: Isolated caudate lobe resection is a feasible procedure that can be done with low morbidity/mortality. Sound surgical judgment and detailed knowledge of the caudate lobe anatomy are keys for a safe performance of this procedure.
Surgical management of benign tumors of the liver.

Kammula US, Buell JF, Labow DM, Rosen S, Millis JM, Posner MC.

Department of Surgery, University of Chicago, Pritzker School of Medicine, Chicago, IL 60637, USA.

Int J Gastrointest Cancer. 2001;30(3):141-6. Abstract quote

INTRODUCTION: Benign tumors of the liver are increasingly being diagnosed and continue to represent a management challenge. These lesions constitute a substantial component of hepatic neoplasms evaluated and resected at a tertiary referral center. We reviewed our experience with resection of benign liver lesions to clarify the safety and effectiveness of this treatment.

METHODS: Between January 1996 and January 2000, 28 patients with benign hepatic lesions were identified from a cohort of 140 hepatic resection patients. Demographic characteristics, operative management, morbidity, mortality and follow-up were retrospectively analyzed.

RESULTS: The mean age in our patients was 35 +/- 14, with 24/28 (86%) patients being female. Seven of the 24 woman (29%) at presentation were either pregnant or immediate postpartum. A history of OCP use was noted in 14/24 (58%) female patients. The most common presenting symptom was abdominal pain in 12/28 (43%). Resection for an undiagnosed mass occurred in 11/28 (39%) patients. The distribution of pathology was hemangioma 10/28 (35.7%), adenoma 8/28 (28.6%), hepatic cyst 5/28 (17.9%), hamartoma 2/28 (7.1%), and FNH 3/28 (10.7%). Average size of the tumor was 7.4 +/- 3.9 (range 2.5-15 cm) with a mean of 1.4 +/- 0.8 lesions (range 1-3) per patient. Tumors were evenly distributed between the right and left side while eight patients (29%) had bilobar tumors. Enucleation rather than anatomic resection was performed in 18/28 (64%) patients, with a mean blood loss of 457 +/- 532 cc (range 50-2200 cc). Blood transfusion was required in only 3/28 (10%) patients, while total vascular isolation was used in only a single patient undergoing an extended left hepatectomy. Mean length of stay was 6.8 +/- 3.2 d (range 3-14 d). Three complications (10.7%) were encountered: pulmonary embolus, ileus and non-operative bile leak. There were no mortalities in this series. Recurrence of tumor occurred in only one patient with a giant hepatic cyst managed laparoscopically.

CONCLUSIONS: In our institution, the management of clinically relevant benign tumors of the liver comprises a significant proportion of our resectional practice (20%). Our data suggests that both enucleation and anatomically based resections can be performed safely with minimal blood loss and transfusion requirements. Resection of symptomatic lesions was highly effective in treating abdominal pain due to these benign tumors. We advocate resection of non-resolving hepatic adenomas, symptomatic lesions, or when malignancy cannot be excluded.
Laparoscopic hepatectomy for benign liver tumors.

Kalil AN, Mastalir ET.

Department of Surgery of Fundacao Faculdade Federal de Ciencias Medicas de Porto Alegre and Hospital Santa Rita, Santa Casa de Porto Alegre, Brazil.
Hepatogastroenterology. 2002 May-Jun;49(45):803-5. Abstract quote  

We describe our initial experience with videolaparoscopic hepatectomies. From November 1997 to May 1999, 6 female patients whose ages ranged from 36 to 71 years with hepatic benign tumors were submitted to laparoscopic hepatectomy. Three patients had hepatic adenomas, 1 non-parasitic cyst, 1 focal nodular hyperplasia and 1 hemangioma.

The laparoscopy was performed under general anesthesia with a pneumoperitoneum of carbonic gas. The following were used: 0 degree and 30 degrees optics, 5, 10 e 12-mm trochars, a ring forceps, dissecting forceps, simple grasping forceps, curved scissors, mono- and bipolar cautery, endoscopic clip and vascular stapler. No ultrasonic scalpel or argonium coagulation were used. The surgical specimens were removed through a Pfannenstiel incision around 4-5 cm long, for a better anatomopathological evaluation. The surgical time ranged from 3 hours to 4 hours and 30 minutes. One patient had a prolonged ileus during the immediate postoperative period. Only a single patient had an abdominal drain. The time of hospitalization ranged from 2 to 7 days. No complications were observed in relation to the pneumoperitoneum. No deaths occurred in this series.

In this way, laparoscopic hepatectomy may be an alternative approach in carefully selected patients.
Indications and long-term outcome of treatment for benign hepatic tumors: a critical appraisal.

Terkivatan T, de Wilt JH, de Man RA, van Rijn RR, Zondervan PE, Tilanus HW, IJzermans JN.

Department of Surgery, University Hospital Rotterdam-Dijkzigt, Dr Molewaterplein 40, 3015 GD Rotterdam, the Netherlands
Arch Surg. 2001 Sep;136(9):1033-8. Abstract quote  

HYPOTHESIS: The natural history and clinical behavior of benign hepatic tumors during long-term follow-up may not justify primary surgical treatment.

DESIGN: Retrospective study.

SETTING: Tertiary referral center.

PATIENTS: Two hundred eight patients diagnosed as having a benign liver tumor between January 1, 1979, and December 31, 1999.

INTERVENTION: Seventy-four patients underwent hepatic surgery and 134 were managed conservatively by radiological follow-up.

MAIN OUTCOME MEASURES: Symptoms and complications were assessed during management and follow-up.

RESULTS: In the surgically treated population, the liver lesion was symptomatic in 47 patients (64%) and an incidental finding in 27 (36%). The operative morbidity and mortality were 27% (20 of 74 patients) and 3% (2 of 74 patients), respectively. Overall, 28 (80%) of 35 patients with complaints were asymptomatic after surgery. During observation of the tumor in the conservatively managed group, 39 (87%) of 45 patients who presented with complaints were asymptomatic during a mean follow-up of 45 months; 6 patients had mild abdominal pain considered to be unrelated to the tumor.

CONCLUSIONS: Conservative management of solid benign liver lesions such as focal nodular hyperplasia and hemangioma can be performed safely, irrespective of their size. We only advise surgery for liver lesions when there is an inability to exclude malignancy or in the case of severe complaints related to the tumor. Resection is always advocated in the case of a large hepatocellular adenoma (>5 cm) to reduce the risk of rupture and malignant degeneration.

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DeMay RM. The Art and Science of Cytopathology. Volume 1 and 2. ASCP Press. 1996.
Weedon D. Weedon's Skin Pathology Second Edition. Churchill Livingstone. 2002
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Hepatocellular Carcinoma-Fibrolamellar Type

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