AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Background

Focal nodular hyperplasia (FNH) is the second most common tumor of the liver, surpassed in prevalence only by hepatic hemangioma.¹ FNH is believed to occur as a result of a localized hepatocyte response to an underlying congenital arteriovenous malformation. FNH is a hyperplastic process in which all the normal constituents of the liver are present but in an abnormally organized pattern. Results of liver function tests in these patients usually are within the reference range.

While the use of contraceptive agents has not been implicated in the pathogenesis of FNH, their use is associated with an increased rate of complications in patients with FNH, and they may be a factor in the development of FNH. In symptomatic females, hemorrhagic foci or infarctions may occur within the FNH; these are aggravated by administration of contraceptive agents. The rare complication of a spontaneous rupture into the peritoneum has also been associated with contraceptive use.

In most patients, the clinical course is silent, and FNH is incidentally discovered during cross-sectional imaging, angiography, radionuclide liver scanning, or surgery. Most cases of FNH occur as a solitary lesion (80-95%), but multiple lesions may occur.² Although FNH usually has no clinical significance, recognition of the radiologic characteristics of FNH is important to avoid unnecessary surgery, biopsy, and follow-up imaging.

Malignant transformation of FNH has not been reported. FNH must be differentiated from a fibrolamellar variant of hepatocellular carcinoma, with which it shares imaging and gross features.

Pathophysiology

FNH is not a true neoplasm, but it probably represents a local hyperplastic response of hepatocytes to a congenital vascular anomaly.^{3, 2} It is a proliferation of normal, nonneoplastic hepatocytes that are abnormally arranged. Supporting this hypothesis is the fact that FNH is found in association with cavernous hemangiomas, as well as other vascular malformations of other organs and neoplasms of the brain.^{4, 5, 6} Intermediate lesions (ie, lesions with characteristics of both cavernous hemangiomas and FNH) have been reported.⁵ A rare transitional lesion that has been reported as a mixed hamartoma and found most often in infants and children has similarities to both FNH and hemangioma.^{1, 7}

It is hypothesized that a congenital vascular malformation (either an arteriovenous shunt or localized hyperperfusion) triggers focal hepatocellular hyperplasia. On pathologic examination, anomalous arterial branches, unaccompanied by portal venous branches, have been seen feeding the numerous small lobules that constitute the FNH lesion.³ As with hyperplasia and hypertrophy seen around vascular malformations in the extremities, hepatic hyperplasia is seen in the liver.

FNH is a localized, well-delineated focal lesion, not a diffuse mass, within an otherwise normal liver. It is composed of multiple, spherical aggregates of hepatocytes held together in a fibrous meshwork with a dominant scar or scars. In 80-90% of patients, the FNH lesion is solitary, and the macroscopic appearance is a highly characteristic finding. While FNH has no capsule, it tends to be a fairly well marginated, lobulated, subcapsular mass.

On naked-eye examination of a gross pathologic specimen, the lesion is often lighter than the surrounding liver tissue. In some patients, FNH blends in with normal liver tissue, so that distinguishing surrounding normal liver tissue from FNH may be difficult if a gross pathologic specimen is used. The hallmark feature of the lesion is found on a cut specimen; the lesion appears as a central stellate scar with radiating fibrous septa dividing the tumor into lobules. The central scar contains an arterial malformation with spiderlike branches supplying the component nodules. Results of microscopic examination confirm that the central stellate scar is associated with radiating fibrous septa dividing the hyperplastic nodules into smaller units.

The tumor is composed of multiple spherical aggregates of hepatocytes, which often contain increased amounts of fat (triglycerides) and glycogen. Proliferation of the biliary structures is marked, and they are surrounded by inflammatory cells, primarily at the periphery of the fibrous septa. Bile duct proliferation shows no connection to the biliary tree. Arteries in the fibrous septa have thick walls; this change is associated with intimal and medial fibromuscular hyperplasia of the larger arteries. Sinusoidal dilatation and, occasionally, hemorrhagic foci and areas of infarction are seen. Hemorrhage and infarction occurs more frequently in women using contraceptive medications. Kupffer cells are usually present in the lesion; in fact, the lesions may have a concentration of Kupffer cells higher than that of normal liver tissue.

In a study correlating MRI results with pathologic findings, a central scar was seen in 30 of 38 lesions. In a large series of 130 patients with FNH, 84% had a single nodule smaller than 5 cm in diameter, 13% had FNH with a 5- to 10-cm nodule, and only 3% of patients had a lesion greater than 10 cm in diameter. Calcification is rare in patients with FNH, but it has been described.

Frequency

United States

FNH is the second most common benign hepatic tumor (after hemangioma), constituting about 8% of primary hepatic tumors in an autopsy series (Craig JR, Peters RL, Edmondson HA).¹

Mortality/Morbidity

• Mortality and morbidity are related to hepatic surgery; surgery is occasionally performed in patients who are symptomatic or in patients in whom imaging findings are equivocal.
• The natural morbidity resulting from the lesions is low, and no deaths due to FNH have been reported, at least to our knowledge.

Sex

FNH is found most commonly in women (80-95% of cases) in their third and fourth decades of life.^{7, 8, 9, 10, 11, 12, 13, 14}

Age

FNH is found most commonly in the third and fourth decades of life.^{7, 8, 9, 10, 11, 12, 13, 14} However, cases can be seen in childhood or late adulthood.

Clinical Details

In 50-80% of cases, FNH is detected as an incidental finding at autopsy, by laparotomy, or during radiologic investigation.^{7, 8, 12} The most common mode of discovery of  FNH is usually as an incidental finding during ultrasonography (US) or computed tomography (CT). Symptomatic patients most often complain of an abdominal mass (10-15% of all patients) or abdominal pain.^{7, 8, 12}  The pain is usually caused by larger lesions, which stretch the liver capsule or have a mass effect on adjacent organs. Results of liver function tests are usually normal.

Patients using oral contraceptives are more likely to present with symptoms, because contraceptive use is often linked to tumor hemorrhage or infarction. The relationship between FNH and the use of oral contraceptives, however, is often misunderstood, in that FNH itself is not caused or even associated with the use of oral contraceptives.^{12, 15, 16} We believe that this misconception most likely arose because hepatocellular adenoma, a neoplasm that has been definitively related to the use of oral contraceptives, was mistakenly included in early series of FNH. On the other hand, however, oral contraceptives may promote the growth of FNH.^{1, 15}

Classification
Currently, FNH is subdivided into 2 types: classic (80%) and nonclassic (20%).¹⁷  Nonclassic FNH is further divided into 3 subtypes: telangiectatic FNH, FNH with cytologic atypia, and mixed hyperplastic and adenomatous FNH.  Classic FNH contains all of the 3 characteristics: abnormal nodular architecture, malformed vessels, and cholangiolar proliferation. Nonclassic FNH contains 2 of the 3 components but always includes bile duct proliferation.¹⁷

Because telangiectatic FNH shares several morphologic patterns with hepatocellular adenomas, Paradis et al conducted a study in which they attempted to reclassify telangiectatic FNH by molecular analysis.¹⁸ Their results showed that telangiectatic FNH has a molecular pattern closer to that of hepatocellular adenomas than to FNH and suggest that telangiectatic FNH instead be referred to as "telangiectatic hepatocellular adenomas."

Preferred Examination

FNH is increasingly being recognized as an incidental finding because of the widespread use of diagnostic imaging for unrelated conditions. For imaging of the right upper quadrant, US is more widely used than other modalities, and usually, US findings raise the possibility of FNH. US, particularly when combined with duplex Doppler US, may be the only type of imaging required. However, further confirmation may be required, particularly in patients in whom cancer is suspected at other sites. In this context, CT, MRI, angiography, and radionuclide imaging may be used to increase diagnostic confidence.

Limitations of Techniques

The diagnosis of FNH is based on the demonstration of a central scar; however, a typical central scar is not demonstrated in every patient. A scar may not be visible in as many as 20% of patients. Moreover, a central scar may be found in some patients with fibrolamellar hepatocellular carcinoma, hepatic adenoma, or intrahepatic cholangiocarcinoma. This limitation applies to all cross-sectional imaging techniques, including US, CT, and MRI.

The detection of lesions by using radionuclide scans with technetium-99m sulfur colloid depends on the concentration of Kupffer cells in the FNH. If the concentration of Kupffer cells is low, FNH may be demonstrated as a photon-deficient mass indistinguishable from other liver mass lesions. The characteristic spokelike appearance on angiograms is demonstrated in only 33% patients; moreover, FNH may be avascular in 10% of patients.

Diagnosis of FNH is achieved by using several complementary imaging techniques. Thus, in patients in whom the diagnosis is not clearly determined with imaging findings, open biopsy or surgical resection may be needed because needle-biopsy findings can substantially overlap with those of a well-differentiated hepatocellular carcinoma.

DIFFERENTIALS

Section 3 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Other Problems to Be Considered

Well-differentiated hepatocellular carcinoma
Giant cavernous hemangioma
Hypervascular liver metastases
Intrahepatic cholangiocarcinoma

RADIOGRAPH

Section 4 of 12  

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• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Plain radiographs have little to offer in the diagnosis of FNH. Radiographs may demonstrate other causes of abdominal pain in symptomatic patients, including gallstones, nonspecific hepatomegaly, and other soft-tissue masses. The presence of calcification in a liver lesion suggests a diagnosis other than FNH because only 1% of patients with FNH have calcification.¹⁹

Degree of Confidence

Plain radiography has low specificity and sensitivity in the diagnosis of FNH.

CT SCAN

Section 5 of 12  

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• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

On nonenhanced CT scans, FNH may appear as an isoattenuating or slightly hypoattenuating mass. Nonenhanced images are important because FNH may be missed without a precontrast study.

For the optimal evaluation of FNH, a helical CT scan with a 4-phase study should be performed. This evaluation should include nonenhanced and hepatic arterial, portal venous, and delayed–phase examinations.

After the administration of contrast material, the lesion becomes hyperattenuating relative to the surrounding liver in the arterial phase; this occurs approximately 20-30 seconds after the bolus of contrast agent is administered. In the portal venous phase, 70-90 seconds after the bolus injection, FNH is less conspicuous and becomes isoattenuating to the rest of the liver. During the delayed phase, approximately 5-10 minutes after the bolus injection, FNH is isoattenuating with normal liver.

In 15-33% of patients, conventional CT scans show the hypoattenuating stellate central scar with a central core and radiating fibrous septa. The central scar may become hyperattenuating on delayed images because of delayed contrast washout from the scar; however, the central scar does not go through a hypoattenuating phase on helical CT scans. The scar is demonstrated as a hyperattenuating region in the portal venous phase. The central artery traversing the central scar may show early enhancement in the arterial phase.

Attal et al described US, CT and MR features of telangiectatic FNH and correlated their findings with histopathologic findings in 13 cases.²⁰  The study showed that there are a number of differences between telangiectatic FNH lesions and typical FNH lesions: atypical FNH features that are often observed in telangiectatic FNH include the lack of a central scar, lesion heterogeneity, hyperintensity on T1-weighted MRI, strong hyperintensity on T2-weighted MRI, and persistent contrast enhancement on delayed contrast-enhanced CT or T1-weighted MRI.²⁰

Degree of Confidence

When characteristic features are seen in the appropriate clinical setting, a fairly confident diagnosis can be made. Unfortunately, CT features of other benign and malignant lesions can mimic those of FNH.

Because of the nature and pathogenesis of FNH, it is difficult to obtain an accurate diagnosis of FNH on the basis of the clinical presentation and radiographic studies. Shen et al explored the diagnosis and treatment of FNH by studying 86 patients with a diagnosis of FNH that was confirmed pathologically between 1999 and 2006.²¹ In 80 of the patients, there was a solitary focus; and in 6 patients, there were multiple foci. In 69 patients, the diameter of the tumor was less than 5 cm; in 15 patients, the tumor diameter was 5-10 cm; and in 2 patients, the diameter of the tumor was greater than 10 cm. ²¹ 

Overall, a correct preoperative diagnosis was made in 59.3% of patients (51/86). Doppler color flow imaging provided a correct preoperative diagnosis in 32.9%, CT in 60.3%, and MRI in 77.4%. All of the patients underwent tumor resection, and all displayed good curative results.²¹ 

The investigators concluded that CT and MRI are both important methods for diagnosing FNH but that it is difficult to make a definitive preoperative diagnosis for partial classic and for all nonclassic cases of FNH. As a result of their findings, Shen et al suggested that patients undergo tumor resection if they have clinical symptoms or have an indefinite diagnosis.²¹

False Positives/Negatives

Although triple-phase CT scanning accurately characterizes most FNH lesions, CT findings are not as definitive in some patients with FNH. Rarely, a false-positive diagnosis of FNH may occur with fibrolamellar hepatocellular carcinoma as well as other well-differentiated variants of hepatocellular carcinoma.

MRI

Section 6 of 12  

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• Introduction
• Differentials
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• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
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• Intervention
• Multimedia
• References

Findings

FNH usually displays a homogeneous signal intensity on MRIs.

In 94-100% of FNH patients,the FNH lesion is isointense to hypointense on T1-weighted images; in 6%, the signal intensity on T1-weighted images may be hyperintense; and on T2-weighted images, the lesion is slightly hyperintense to isointense in 94-100% of patients.

The central scar of FNH is hypointense on T1-weighted images, but on T2-weighted images, the central scar shows a variable signal-intensity pattern. On T2-weighted images, the scar appears hyperintense in 75% of patients and hypointense in 25% of patients.¹⁹

After the administration of a gadolinium-based contrast agent, the enhancement pattern parallels that of contrast-enhanced CT. Dense enhancement is seen in the arterial phase, and the lesion becomes isointense during the portal venous phase and isointense on delayed images. Late and prolonged enhancement of the central stellate scar occasionally occurs.

MRI findings are not pathognomonic for FNH, but the use of MRI reticuloendothelial agents, such as superparamagnetic iron oxide (SPIO) and ultrasmall superparamagnetic iron oxide (USPIO), increase the specificity. On SPIO-enhanced T2-weighted images, FNH shows decreased signal intensity because of iron uptake by Kupffer cells. This finding is not specific to FNH, because hepatocellular adenoma and hepatocellular carcinoma also may contain Kupffer cells.

Attal et al described the features of US, CT, and MRI regarding telangiectatic FNH, and they compared the findings with histopathologic findings in 13 cases of FNH.  The results of the study showed that telangiectatic FNH differs from typical FNH on images: the atypical features that were often observed with telangiectatic FNH were the lack of a central scar, heterogeneous lesions, hyperintensity on T1-weighted MRI, strong hyperintensity on T2-weighted MRI, and persistent contrast enhancement on delayed contrast-enhanced CT or T1-weighted MRI.²⁰

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

The MRI findings in patients who have FNH are not pathognomonic for the disease. However, the use of MRI reticuloendothelial agents, such as USPIO and SPIO, can increase MRI's specificity. In the diagnosis of FNH, MRI has a sensitivity of 70% and a specificity of 98%.¹⁹
.

False Positives/Negatives

A false-positive diagnosis of FNH may occur with fibrolamellar hepatocellular carcinoma and other well-differentiated forms of hepatocellular carcinoma. On SPIO-enhanced T2-weighted images, hepatocellular adenoma and hepatocellular carcinoma can also show decreased signal intensity, because Kupffer cells may be present.

ULTRASOUND

Section 7 of 12  

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• Ultrasound
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• Multimedia
• References

Findings

The US findings of FNH are variable. The lesion may appear as a homogeneous mass that is isoechoic, hypoechoic, or hyperechoic. FNH has a mass effect that may displace intrahepatic blood vessels. Only 18% of patients have a central scar.

Doppler sonograms demonstrate an enlarged afferent blood vessel with central arterial hypervascularity and centrifugal filling to the periphery in a spokelike manner. Large draining veins may be seen at the periphery of the mass. High-velocity Doppler signals with arterial pulsatility may be recorded from arteriovenous shunts. Echo-enhanced Doppler US has a high sensitivity for detection of the feeding artery and for depiction of the radial vascular architecture in FNH, especially for lesions that are located in the liver's left lobe. Power Doppler US has increased sensitivity for FNH and may help distinguish it from hepatocellular carcinoma.

The use of dynamic contrast-enhanced US is increasingly being used to diagnose FNH. Ungermann et al used dynamic contrast-enhanced US to study the presence of a spoke-wheel pattern and the typical symptoms of FNH, in relation to lesion size, in 28 patients.²² According to the investigators, contrast-enhanced US can be the final diagnostic method for lesions that are larger than 3 cm and have a typical spoke-wheel structure on contrast-enhanced US. They concluded, however, that if the spoke-wheel pattern is not present and if there is no central scar, the diagnosis of FNH cannot be made specifically by contrast enhanced US alone.²²

In a study of 13 cases of FNH, Attal et al described US, CT, and MR features of telangiectatic FNH and correlated the findings with histopathologic finding.  They found that telangiectatic FNH differed from typical FNH. The atypical FNH findings that were often observed with telangiectatic FNH were the lack of a central scar, heterogeneous lesion formation, hyperintensity on T1-weighted MRI, strong hyperintensity on T2-weighted MRI, and contrast enhancement on delayed contrast-enhanced CT or T1-weighted MRI.²⁰

Degree of Confidence

The FNH lesion may be difficult to detect, because it is often hypoechoic to normal liver tissue. US specificity is low, but the specificity can be increased with Doppler US and echo enhancement. As is the case with other cross-sectional imaging, however, a specific diagnosis is sometimes not possible because the FNH lesion is similar to lesions of other benign and malignant diseases.

False Positives/Negatives

The lesion may be missed entirely if the signal is isoechoic. US findings of FNH overlap with those of hepatic adenomas and hepatocellular carcinomas, although the use of Doppler US, particularly power Doppler and echo-enhanced Doppler US, improves the sensitivity and specificity.

NUCLEAR MEDICINE

Section 8 of 12  

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• Intervention
• Multimedia
• References

Findings

The best imaging modalities for characterizing FNH are those modalities that can delineate the lesion's central scar or can show Kupffer cell activity. The best modalities for identifying the central scar are CT and MRI, and Kupffer cell activity is best demonstrated by radionuclide scans. In the future, however, MRI superparamagnetic contrast agents may challenge radionuclide scanning.

Detection of Kupffer cells in FNH has historically been achieved using technetium-99m (^99mTc) sulfur colloid scanning. In 60-70% of FNH patients, these scans show normal or increased uptake of ^99mTc sulfur colloid. In 30-40% of patients, Kupffer cells are not sufficiently concentrated in the FNH lesion; the lesion may even be photon deficient.¹⁹ The uptake of ^99mTc–hepatoiminodiacetic acid (HIDA) may be normal to increased in 40-70% of patients, but the lesion may be photon deficient in as many as 60% of patients. With ^99mTc-tagged RBCs, uptake is increased during the early phase, followed by decreased uptake.¹⁹

Degree of Confidence

^99mTc sulfur colloid uptake in patients with FNH depends on the concentration of Kupffer cells in the FNH lesion. Unfortunately, other hepatocellular neoplasms, such as a hepatocellular adenoma and hepatocellular carcinoma, can also have Kupffer cells and demonstrate ^99mTc sulfur colloid uptake.

False Positives/Negatives

Hepatic adenoma, hemangioma, hepatoblastoma, liver herniation, and hepatocellular carcinoma can give rise to similar appearances on ^99mTc sulfur colloid scans.

ANGIOGRAPHY

Section 9 of 12  

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• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Angiographic findings demonstrate a discretely marginated mass. When the mass is small, the arteries supplying the mass break up into small branches, which appear to permeate the FNH and form a reticular pattern. These branches are not dilated, but the overall impression is that of increased vascularity. Vascularity may be decreased within the central stellate scar.

In the parenchymal phase, a fine, homogeneous granularity is demonstrated, with an occasional lucent ring around the mass.

In large tumors, the dilated main feeding artery perforates the center of the tumor. Peripheral arteries arise from the central artery, arranged in a spoke-wheel pattern.

Degree of Confidence

Although the typical angiographic findings are present in only 33% of patients, the diagnosis of FNH may still be suggested.¹⁹. FNH may instead appear similar to an adenoma.

False Positives/Negatives

Only 33% of patients have the characteristic findings of FNH; therefore, lesions may be missed, or an incorrect diagnosis, such as a hepatocellular adenoma, may be derived in up to 67% of patients.¹⁹

INTERVENTION

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• Intervention
• Multimedia
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Surgery is occasionally performed in patients who are symptomatic or in patients in whom imaging findings are equivocal.

MULTIMEDIA

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• Multimedia
• References

Media file 1:  Dynamic MRIs in a 36-year-old woman referred for a gallbladder sonography, during which the patient was found to have a vague ill-defined hypoechoic mass in the right lobe of the liver (not shown). (Top left) Gadolinium-enhanced T1-weighted MRI demonstrates an ill-defined low-signal-intensity mass. (Top right) The mass enhances intensely in the arterial phase after the administration of contrast medium. (Bottom left) Minor enhancement persists in the portal venous phase. (Bottom right) The lesion becomes isointense relative to the liver on delayed images.
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Media type:  MRI

Media file 2:  Longitudinal sonogram through the liver and gallbladder in a 38-year-old woman referred for a gallbladder scanning. Image shows an ill-defined hyperechoic mass in the right lobe of the liver.
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Media type:  Image

Media file 3:  Longitudinal sonogram (more medial section than in Image 2) in a 38-year-old woman referred for a gallbladder scanning. Sonogram shows mass effect from the tumor, as demonstrated by the arching of the portal vein anteriorly.
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Media type:  Image

Media file 4:  Enhanced axial CT scan through the liver in the arterial phase in a 38-year-old woman referred for gallbladder scanning (same patient as in Images 2-3). The mass demonstrates intense enhancement.
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Media type:  CT

Media file 5:  Delayed portal venous phase enhanced axial CT scan in a 38-year-old woman referred for gallbladder scan (same patient as in Images 2-4). Image shows stretching of the portal vein and the right hepatic vein around the mass (M).
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Media type:  CT

Media file 6:  Technetium-99m sulfur colloid scans in a 38-year-old woman referred for gallbladder scan (same patient as in Images 2-5). Images show complete filling of the mass depicted on sonograms and CT scans.
	View Full Size Image
Media type:  Image

REFERENCES

Section 12 of 12

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• Introduction
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• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

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2. Wanless IR, Albrecht S, Bilbao J, Frei JV, Heathcote EJ, Roberts EA. Multiple focal nodular hyperplasia of the liver associated with vascular malformations of various organs and neoplasia of the brain: a new syndrome. Mod Pathol. Sep 1989;2(5):456-62. [Medline].
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12. Knowles DM 2nd, Casarella WJ, Johnson PM, Wolff M. The clinical, radiologic, and pathologic characterization of benign hepatic neoplasms. Alleged association with oral contraceptives. Medicine (Baltimore). May 1978;57(3):223-37. [Medline].
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16. Kerlin P, Davis GL, McGill DB, Weiland LH, Adson MA, Sheedy PF 2nd. Hepatic adenoma and focal nodular hyperplasia: clinical, pathologic, and radiologic features. Gastroenterology. May 1983;84(5 Pt 1):994-1002. [Medline].
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18. Paradis V, Benzekri A, Dargère D, Bièche I, Laurendeau I, Vilgrain V. Telangiectatic focal nodular hyperplasia: a variant of hepatocellular adenoma. Gastroenterology. May 2004;126(5):1323-9. [Medline].
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Article Last Updated: May 23, 2007