eMedicine - Hepatic Adenoma : Article by Karen Kodsi Garfield, MD

You are in: eMedicine Specialties > Radiology > Gastrointestinal

Hepatic Adenoma

Last Updated: February 1, 2007

Synonyms and related keywords: hepatocellular adenoma, HA

AUTHOR INFORMATION Section 1 of 12

Author Information Introduction Differentials Radiograph CT Scan MRI Ultrasound Nuclear Medicine Angiography Intervention Pictures Bibliography

Author: Karen Kodsi Garfield, MD, Consulting Staff, Department of Radiology, St Luke's Hospital
Coauthor(s): Sandor Joffe, MD, Section Chief of Abdominal Imaging, Department of Radiology, Beth Israel Medical Center; Stephen A Okon, MD, Consulting Staff, Assistant Professor of Radiology, Department of Radiology, Beth Israel Medical Center

Karen Kodsi Garfield, MD, is a member of the following medical societies: American Association for Women Radiologists, American Medical Association, and Radiological Society of North America

Editor(s): Neela Lamki, MD, Professor, Department of Radiology, Sultan Qaboos University, Oman; Adjunct Professor, Department of Radiology, Baylor College of Medicine; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; Paul M Silverman, MD, Chief of Body Imaging, Chair in Diagnostic Imaging, Professor, Department of Radiology, University of Texas MD Anderson Cancer Center; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; and John Karani, MBBS, FRCR, Consulting Staff, Department of Radiology, King's College Hospital, London

Disclosure

INTRODUCTION

Section 2 of 12

Author Information Introduction Differentials Radiograph CT Scan MRI Ultrasound Nuclear Medicine Angiography Intervention Pictures Bibliography

Background: Hepatic adenoma (HA) is a rare benign tumor of the liver. Two types of HAs have been identified, including tumors of bile duct origin and tumors of liver cell origin. HAs of bile duct origin usually are smaller than 1 cm and not of clinical interest; typically, they are found incidentally on postmortem examinations. HAs of liver origin are larger and often are clinically significant. On average, they measure 8-15 cm.

Pathophysiology: Histologically, sheets of well-differentiated hepatocytes characterize HAs. The hepatocytes contain fat and glycogen and can produce bile; however, no bile ducts are present. A characteristic lack of portal vein tracts and terminal hepatic veins is noted. Approximately 80% of adenomas are solitary and 20% are multiple. Most HAs do not contain Kupffer cells.

Frequency:

In the US: Although HAs may be idiopathic, the lesions most often are seen in young women using oral contraceptives. The incidence among long-term users of oral contraceptives is approximately 4 cases per 100,000. In women who do not use oral contraceptives or have used them for less than 2 years, the incidence is 1 case per million. In addition, incidence of HAs is increased in patients with glycogen storage disease, diabetes mellitus, hemochromatosis, acromegaly, and in males using anabolic steroids. Case reports by DeMenis et al in 1997 indicate that HA is a complication of pregnancy.

Mortality/Morbidity: HAs may rupture and bleed, causing right upper quadrant pain. Rarely, rupture may lead to hemorrhagic shock. Although they are benign lesions, HAs can undergo malignant transformation to hepatocellular carcinoma (HCC). Although malignant transformation is rare, for this reason, surgical resection is advocated in most patients with presumed HAs.

The primary reason for advocating surgical resection is the risk of hemorrhage.

Race: No known racial predilection exists.

Sex: In a retrospective analysis of 44 patients with HA, Weinmann et al reported a male-to-female ratio of 1:3.9 (9 men and 35 women).

Age: In a study by Weinmann et al (in 44 patients with HA), the mean age was 34 years with an age range of 15-64 years.

Anatomy: HAs typically measure 8-15 cm. Sheets of well-differentiated hepatocytes characterize the lesions. The hepatocytes can produce bile but no bile ducts are present. Portal vein tracts and terminal hepatic veins are lacking. Almost no HAs contain Kupffer cells.

Clinical Details: Although benign, HA can present a diagnostic challenge since lesions can be difficult to distinguish from other benign or malignant hepatic tumors. Clinically, patients with HA may be asymptomatic and lesions may be found incidentally during laparotomy or when radiologic studies are performed. As a result of their largeness, often 8-15 cm, the patient or physician may notice a right upper quadrant mass or hepatomegaly, resulting in a referral for imaging. HAs can rupture and bleed, causing right upper quadrant pain, which may be mistaken clinically for acute cholecystitis. On rare occasions, rupture may lead to hemorrhagic shock.

HAs often are seen in young women on oral contraceptives. The lesions occasionally can regress after cessation of oral contraceptives; however, less commonly, enlargement also has been observed after cessation.

Rarely, HAs may undergo malignant transformation to HCC. Alpha-fetoprotein (AFP) levels are helpful in differentiating HA from HCC. A high AFP level indicates the presence of HCC, although not all patients with HCC have elevated AFP levels. Several cases have been reported in which highly differentiated HCC was diagnosed within an adenoma, although preoperative AFP results were negative (Casillas et al, 2000).

In a patient who presents with hepatic hemorrhage without antecedent trauma and that is not attributable to anticoagulant therapy, consider the possibility of an underlying liver lesion. The 2 most common liver lesions causing hepatic hemorrhage are HA and HCC. Other neoplasms that can cause hepatic hemorrhage include liver tumors, such as focal nodular hyperplasia (FNH), hemangiomas, and metastases. Other rare causes of nontraumatic hepatic hemorrhage exist, such as amyloidosis and HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome, which is seen in a small subset of women with preeclampsia.

In patients with HA, abnormal liver function enzyme levels have been observed including elevated alkaline phosphatase and elevated gamma glutamyl transpeptidase levels. Although patients with FNH often have normal liver function test results, elevated gamma glutamyl transpeptidase levels also may be seen. Therefore, distinguishing HA from FNH based on laboratory data usually is not possible.

Preferred Examination: A combination of multiphasic CT scans and gadolinium-enhanced MRI is best to identify and characterize most hepatic lesions. Certain characteristics, such as arterial enhancement and the presence of fat and hemorrhage, suggest that the lesion represents an HA. If an enhancing central scar is seen, the diagnosis of FNH can be made. Nuclear medicine studies also can be helpful. Most HAs do not demonstrate uptake on sulfur-colloid and gallium scans.

Limitations of Techniques: Although CT, MRI, and nuclear medicine tests may help characterize lesions as adenomas, findings frequently are nonspecific and biopsy and/or resection may be necessary.

DIFFERENTIALS Section 3 of 12

Author Information Introduction Differentials Radiograph CT Scan MRI Ultrasound Nuclear Medicine Angiography Intervention Pictures Bibliography

Focal Nodular Hyperplasia
Hepatocellular Carcinoma
Hepatocellular Carcinoma, Fibrolamellar
Liver, Metastases
Liver, Trauma

RADIOGRAPH Section 4 of 12

Author Information Introduction Differentials Radiograph CT Scan MRI Ultrasound Nuclear Medicine Angiography Intervention Pictures Bibliography

Findings: Usually, plain radiographs of the abdomen provide no findings to suggest the diagnosis of HA. The liver usually is normal in size. Rarely, coarse calcifications may be present in adenomas; calcifications may be seen in the right upper quadrant on radiographs, but this finding is nonspecific.

Quick Find

Author Information
Introduction
Differentials
Radiograph
CT Scan
MRI
Ultrasound
Nuclear Medicine
Angiography
Intervention
Pictures
Bibliography

Click for related images.

Related Articles

Focal Nodular Hyperplasia

Hepatocellular Carcinoma

Hepatocellular Carcinoma, Fibrolamellar

Liver, Metastases

Liver, Trauma

Patient Education

Click here for patient education.

CT SCAN

Section 5 of 12

Author Information Introduction Differentials Radiograph CT Scan MRI Ultrasound Nuclear Medicine Angiography Intervention Pictures Bibliography

Findings: HAs often are discovered incidentally on CT scans performed for other reasons. Once identified, a multiphasic CT scan should be performed to better characterize most hepatic tumors. Protocols differ from institution to institution.

Typically, helical CT scans are obtained, first of the nonenhanced liver. Then, images are obtained in the hepatic arterial phase using intravenous injection of approximately 120-150 mL of nonionic contrast at a rate of 3-5 mL/s with a 25- to 30-second delay. Images then are acquired in the portal venous phase after a scanning delay of 60-80 seconds.

On CT, the most consistent finding in HAs is the enhancement pattern. Most lesions (90% according to Ichikawa et al) show homogeneous enhancement in the hepatic arterial phase. Unfortunately, this feature is not specific to HAs, since HCC, hypervascular metastases, and FNH can demonstrate similar enhancement in the hepatic arterial phase.
Since HAs are composed histologically of uniform hepatocytes, most are isoattenuating to healthy liver tissue on nonenhanced scans in the portal venous phase.
In a fatty liver, HAs usually are hyperattenuating.
The finding of hemorrhage as an area of high attenuation can be seen in as many as 40% of patients.
Fat deposition within adenomas is identified on CT in only approximately 7% of patients.
Typically, HAs have well-defined borders and do not have lobulated contours.
A low-attenuation pseudocapsule can be seen in as many as 25% of patients.
Coarse calcifications are seen in only 5% of patients.

Degree of Confidence: Since conventional HCC can contain fat and areas of hemorrhage, differentiating HA from HCC is difficult. In the presence of CT signs of portal hypertension and cirrhosis, the diagnosis of HCC is favored. In addition, the presence of an elevated AFP level favors HCC. However, on the basis of imaging alone, HA may be difficult to distinguish from HCC. Even histologic analysis between HA and well-differentiated HCC is challenging.

Since both HAs and hypervascular metastases demonstrate intense enhancement on arterial phase imaging, differentiation between the two also is often difficult. The presence of multiple lesions favors metastatic disease; however, HAs also can be multiple in number, which is an entity termed hepatic adenomatosis. The presence of a primary neoplasm, such as pancreatic islet cell tumor, renal cell carcinoma, breast carcinoma, thyroid carcinoma, melanoma, or carcinoid, favors metastatic disease.

Although HA and FNH have some similarities clinically and on imaging, certain imaging features can distinguish them reliably. Clinically, both tumors appear in young women. On imaging, both tumors usually are hypervascular in the hepatic arterial phase. In addition, both tumors usually are isoattenuating to liver on the portal venous phase and on unenhanced images. The presence of a central scar probably is the most reliable discriminating feature. Most patients with FNH demonstrate a central scar that is hypoattenuating on the hepatic arterial phase images and hyperattenuating on delayed images.

False Positives/Negatives: Significant overlap is noted between the CT appearances of HA, HCC, FNH, and hypervascular metastases, making a definitive diagnosis based on CT imaging criteria alone difficult and often not possible.

MRI Section 6 of 12

Author Information Introduction Differentials Radiograph CT Scan MRI Ultrasound Nuclear Medicine Angiography Intervention Pictures Bibliography

Findings: Some MRI findings are similar to CT findings (see CAT Scan); however, MRI usually is more sensitive in detecting fat and hemorrhage.

HAs tend to be hyperintense or isointense to liver tissue on T1-weighted images (up to 93% in a series by Paulson et al).
High signal on T1-weighted images probably relates to the presence of fat or, less commonly, to hemorrhage within the lesion.
Chemical-shift imaging showing loss of signal on out-of-phase images can confirm the presence of fat. Unfortunately, HCC is known to contain fat in as many as 40% of lesions; therefore, the presence of fat does not help differentiate the lesions.
Other hepatic lesions can be hyperintense on T1-weighted images, such as melanoma metastases and cavities containing proteinaceous material.
On T2-weighted images, HAs most often are slightly hyperintense to liver tissue. This finding is not specific since many hepatic lesions, including HCC and metastases, are hyperintense on T2-weighted images.
Heterogeneity, defined as any difference of signal within a lesion on T1-weighted or T2-weighted images, is seen in approximately one half of patients. Heterogeneity relates to the presence of either hemorrhage or necrosis. This finding is not specific since HCC and metastases can bleed and become necrotic. Although uncommon, FNH also can be hemorrhagic.
A peripheral rim corresponding histologically to a pseudocapsule is seen in 17-31% of patients. Signal characteristics of the rim are variable. Most often, the peripheral rim, when seen, is of low signal intensity on T1-weighted images, variable intensity on T2-weighted images, and usually does not enhance.
After gadolinium administration, the pattern of enhancement is similar to that of CT. Most HAs show intense enhancement in the arterial phase and are isointense to liver tissue on delayed imaging.
HAs, unlike FNH, do not have a central scar. If a low signal intensity scar is seen on T1-weighted images and the scar enhances after gadolinium is administered, the diagnosis of FNH is strongly favored. A central scar has never been reported in an HA.
On routine MRI of the liver consisting of T1-weighted and T2-weighted images, chemical-shift imaging, and dynamic gadolinium-enhanced imaging, distinguishing between HAs, HCC, and hypervascular metastases usually is not possible.
Recently, studies were performed to determine if MRI using ferumoxides (superparamagnetic iron oxides) enhancement may help better distinguish FNH from HA and HCC in indeterminate cases. Ferumoxides are taken up by the reticuloendothelial cells in a healthy liver. Since FNH contains Kupffer cells, the ferumoxides are taken up by healthy liver tissue and by FNH, which results in marked reduction in the signal intensity of healthy liver tissue and FNH on T2-weighted images. Usually, no other lesions show significant signal loss on T2-weighted images. Lesions such as HCC, HA, and metastases usually become conspicuous because they lack a significant number of Kupffer cells. Lesions such as FNH drop out almost as much as healthy liver tissue; however, some HAs and some well-differentiated HCCs show some signal intensity loss, which may be explained by the presence of some Kupffer cells in the lesions.
Mangafodipir trisodium (formerly termed Mn-DPDP) is a hepatobiliary MRI contrast agent. It is taken up by hepatocytes and excreted into bile. Because HA, FNH, and HCC all contain hepatocytes, they may demonstrate enhancement with this agent. Metastases and hemangiomas do not contain hepatocytes and do not enhance; therefore, this agent can help differentiate HA, which enhances, from metastases, which do not enhance.

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans. As of late December 2006, the FDA had received reports of 90 such cases. Worldwide, over 200 cases have been reported, according to the FDA. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.

Degree of Confidence: Generally, on routine MRI of the liver using T1-weighted, T2-weighted, chemical-shift, and dynamic gadolinium-enhanced imaging, certain hepatic masses can be diagnosed with confidence while others cannot.

If a hepatic mass contains a low signal central scar on T1-weighted images that enhances after gadolinium administration, the diagnosis of FNH is fairly certain.

However, overlap exists in the imaging and enhancement characteristics of HAs, HCC, and hypervascular metastases such as melanoma. Clinical correlation in such cases is most helpful. A history of cirrhosis and high AFP levels favor HCC. A history of melanoma or other primary tumors favors metastases. In otherwise healthy young women using oral contraceptives, HA is favored. Patients with glycogen storage disease, hemochromatosis, acromegaly, or males on anabolic steroids also are more prone to developing HAs.

False Positives/Negatives: Although most HAs are hyperintense to normal liver on T1-weighted images, this is not a specific finding. Other hepatic masses, such as HCC, melanoma metastases, and protein material in hepatic abscess cavities, can be hyperintense on T1-weighted images as well.

ULTRASOUND Section 7 of 12

Author Information Introduction Differentials Radiograph CT Scan MRI Ultrasound Nuclear Medicine Angiography Intervention Pictures Bibliography

Findings: On ultrasound, HAs demonstrate variable echogenicity. They may be hypoechoic, isoechoic, or hyperechoic to liver parenchyma. Usually, differentiating HAs from other liver lesions such as FNH or HCC is not possible based on either gray scale or Doppler characteristics. Cherqui et al described increased intralesional venous structures with a paucity of intra-arterial structures in HAs; however, Rumack et al failed to replicate this finding and it is not a reliable differentiating feature. The primary role of ultrasound is to screen patients with hepatic masses that are discovered incidentally or who have a clinical history of abnormal liver function test results. Further imaging then is indicated using MRI, CT, and/or nuclear medicine.

NUCLEAR MEDICINE Section 8 of 12

Author Information Introduction Differentials Radiograph CT Scan MRI Ultrasound Nuclear Medicine Angiography Intervention Pictures Bibliography

Findings: A combination of radiotracers may help make the diagnosis of HAs in equivocal cases.

On gallium-67 (Ga-67) scans, HAs demonstrate decreased uptake compared to healthy liver tissue, which can be explained by the benign nature of the cells. In contrast, HCC often demonstrates equivocal or greater Ga-67 uptake than liver, with studies reporting that 90-95% of HCCs demonstrate uptake or equivocal uptake of Ga-67.
Since HAs usually have few or absent Kupffer cells, they show focal defects on sulfur-colloid liver-spleen scans. However, an occasional HA contains enough Kupffer cells to demonstrate normal uptake of sulfur colloid. HCCs almost always appear as defects on sulfur-colloid scintigraphy because they lack Kupffer cells. FNH contains Kupffer cells and usually demonstrates uptake of sulfur colloid. In summary, sulfur-colloid uptake strongly favors a diagnosis of FNH. Lack of sulfur-colloid uptake is not specific and can be attributed to many other hepatic lesions, including HCC, HAs, and metastases.
Using hepatobiliary agents, HAs usually demonstrate early uptake with subsequent retention of the radiotracer because HAs do not contain bile ducts, thus, the radiotracer is not excreted by the lesion, which remains hot on delayed images. This is in contrast to HCC, which shows focal defects on early scans. Avid uptake becomes detectable only after 2-5 hours.
Recently, positron emission tomography (PET) using fluorine-18-fluorodeoxyglucose (¹⁸FDG), has been shown to be useful in evaluating many tumors. Malignant tumors usually show uptake of ¹⁸FDG, while benign tumors do not. Occasionally, benign lesions such as sarcoids, inflammatory processes, and abscesses can show uptake. A case has been reported of ¹⁸FDG uptake in an HA.
When HA is indistinguishable from HCC and FNH radiologically, a combination of radionuclide imaging including sulfur-colloid, Ga-67, and technetium Tc-99m pyridoxyl-5-methyltryptophan (PMT) uptake may help establish the correct diagnosis. Most HAs demonstrate decreased gallium uptake, decreased sulfur-colloid uptake, and early and retained uptake of hepatobiliary agents.

Degree of Confidence: Most HAs demonstrate decreased gallium uptake, decreased colloid uptake, early and retained uptake of hepatobiliary agents, and no uptake on PET scanning; therefore, HA often can be diagnosed confidently using nuclear medicine studies.

False Positives/Negatives: Cases have been reported of hot HAs on PET ¹⁸FDG scans. In addition, reports exist of HAs with enough Kupffer cells to demonstrate uptake on sulfur colloid scans.

ANGIOGRAPHY Section 9 of 12

Author Information Introduction Differentials Radiograph CT Scan MRI Ultrasound Nuclear Medicine Angiography Intervention Pictures Bibliography

Findings: In the diagnostic workup of HAs, angiography does not have a significant role. Angiography can be helpful for technical reasons when considering resection. On angiography, HAs typically appear as hypervascular masses with the vascular supply arising peripherally. However, HAs may be hypovascular (as many as 50%) or have areas of hypovascularity within the mass corresponding to hemorrhage and necrosis.

In contrast, FNH typically is hypervascular with dense capillary blushing. In large lesions, a dilated branch of the hepatic artery can enter the center of the mass then divide into small branches that radiate similar to the spokes on a wheel (spoke-wheel appearance). If the spokelike appearance is noted, FNH is the likely diagnosis. HCC demonstrates hypervascularity, irregular tumor vessels, and arteriovenous shunting. In patients with HCC, tumor thrombus in the portal or hepatic veins also may be seen. Most liver metastases are hypervascular with a capillary stain.

Degree of Confidence: Currently, angiography usually is not performed for the detection and differentiation of hepatic masses. Angiography can be performed preoperatively to better define the vascular anatomy prior to resection, although the information can be obtained noninvasively using CT or MR angiography.

INTERVENTION Section 10 of 12

Author Information Introduction Differentials Radiograph CT Scan MRI Ultrasound Nuclear Medicine Angiography Intervention Pictures Bibliography

Intervention: As a result of the risk of intraperitoneal hemorrhage and the rare occurrence of malignant transformation to HCC, surgical resection has been advocated in most patients with presumed HA. The risk of significant bleeding from the tumor is as high as 30%. Unfortunately, the exact risk of malignant transformation is unknown. Other physicians have advocated surgical resection only when tumors are larger than 5 cm or when AFP levels are elevated, since these two findings are associated with higher risk of malignancy.

The value of percutaneous fine needle biopsy for the diagnosis of HA is controversial for two reasons. First, histologic studies may lead to misdiagnosis when differentiating HA from FNH. In addition, a considerable risk of hemorrhage exists when biopsy is performed on these hypervascular tumors. HA lesions may diminish after oral contraceptives are discontinued; however, discontinuing oral contraceptives does not lower the risk of malignant transformation.

When a definitive diagnosis of FNH can be made using imaging studies, surgery can be avoided and lesions can be observed safely using radiologic studies. However, if HA or HCC remains in the differential diagnosis, surgery usually is indicated.

PICTURES Section 11 of 12

Author Information Introduction Differentials Radiograph CT Scan MRI Ultrasound Nuclear Medicine Angiography Intervention Pictures Bibliography

Arrive L, Flejou JF, Vilgrain V, et al: Hepatic adenoma: MR findings in 51 pathologically proved lesions. Radiology 1994 Nov; 193(2): 507-12 [Medline].
Ault GT, Wren SM, Ralls PW, et al: Selective management of hepatic adenomas. Am Surg 1996 Oct; 62(10): 825-9[Medline].
Casillas VJ, Amendola MA, Gascue A, et al: Imaging of nontraumatic hemorrhagic hepatic lesions. Radiographics 2000 Mar-Apr; 20(2): 367-78[Medline].
Cherqui D, Rahmouni A, Charlotte F, et al: Management of focal nodular hyperplasia and hepatocellular adenoma in young women: a series of 41 patients with clinical, radiological, and pathological correlations. Hepatology 1995 Dec; 22(6): 1674-81[Medline].
Davis LP, McCarroll K: Correlative imaging of the liver and hepatobiliary system. Semin Nucl Med 1994 Jul; 24(3): 208-18[Medline].
deMenis E, Tramontin P, Conte N: Successful resection of multifocal hepatic adenoma in pregnancy. South Medical Journal 1997; 22(8): 357-361.
Dunphy T: Magnetic resonance imaging of focal liver lesions. Appl Radiol 2001; 30(suppl): 69-70.
Gyorffy EJ, Bredfeldt JE, Black WC: Transformation of hepatic cell adenoma to hepatocellular carcinoma due to oral contraceptive use. Ann Intern Med 1989 Mar 15; 110(6): 489-90[Medline].
Herman P, Pugliese V, Machado MA, et al: Hepatic adenoma and focal nodular hyperplasia: differential diagnosis and treatment. World J Surg 2000 Mar; 24(3): 372-6[Medline].
Hill MA, Albert T, Zieske A, Levine EA: Successful resection of multifocal hepatic adenoma during pregnancy. South Med J 1997 Mar; 90(3): 357-61[Medline].
Ichikawa T, Federle MP, Grazioli L, Nalesnik M: Hepatocellular adenoma: multiphasic CT and histopathologic findings in 25 patients. Radiology 2000 Mar; 214(3): 861-8[Medline].
Kume N, Suga K, Nishigauchi K, et al: Characterization of hepatic adenoma with atypical appearance on CT and MRI by radionuclide imaging. Clin Nucl Med 1997 Dec; 22(12): 825-31[Medline].
Paley MR, Mergo PJ, Torres GM, Ros PR: Characterization of focal hepatic lesions with ferumoxides-enhanced T2- weighted MR imaging. AJR Am J Roentgenol 2000 Jul; 175(1): 159-63[Medline].
Patel PM, Alibazoglu H, Ali A, et al: 'False-positive' uptake of FDG in a hepatic adenoma. Clin Nucl Med 1997 Jul; 22(7): 490-1[Medline].
Paulson EK, McClellan JS, Washington K, et al: Hepatic adenoma: MR characteristics and correlation with pathologic findings. AJR Am J Roentgenol 1994 Jul; 163(1): 113-6[Medline].
Rooks JB, Ory HW, Ishak KG, et al: Epidemiology of hepatocellular adenoma. The role of oral contraceptive use. JAMA 1979 Aug 17; 242(7): 644-8[Medline].
Rumack CM, Wilson SR, Charboneau JW: Diagnostic Ultrasound. Vol 1. 2nd ed. Mosby-Year Book; 1998: 129-30.
Weimann A, Ringe B, Klempnauer J, et al: Benign liver tumors: differential diagnosis and indications for surgery. World J Surg 1997 Nov-Dec; 21(9): 983-90; discussion 990-1[Medline].
Welch TJ, Sheedy PF 2nd, Johnson CM, et al: Focal nodular hyperplasia and hepatic adenoma: comparison of angiography, CT, US, and scintigraphy. Radiology 1985 Sep; 156(3): 593-5[Medline].
Wojtowycz M: Handbook of Interventional Radiology and Angiography. 2nd ed. Mosby-Year Book; 1995: 77-83.

Hepatic Adenoma excerpt