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CT and MR Imaging Findings in Focal Nodular Hyperplasia of the Liver

Radiologic—Pathologic Correlation

¹ Department of Radiology, University Hospital Gent, De Pintelaan 185, B-9000 Gent, Belgium.
² Department of Pathology, University Hospital Gent, 9000 Gent, Belgium.
³ Department of Hepatology, University Hospital Gent, 9000 Gent, Belgium.
⁴ Department of Radiology, Brigham & Women's Hospital, Harvard Medical School, 75 Francis St., Boston, MA 02115.

Received October 25, 1999; accepted after revision December 7, 1999.

 
Presented at the annual meeting of the American Roentgen Ray Society, New Orleans, May 1999

Address correspondence to K. J. Mortelé

Introduction

Top Introduction General Tumor Characteristics Typical CT and MR... Atypical CT and MR... References

 
New imaging techniques, such as triple phase spiral CT and fast MR imaging, have markedly increased the detection of focal nodular hyperplasia, the second most common benign hepatic tumor. Although atypical imaging features are the exception rather than the rule, it is sometimes difficult to differentiate focal nodular hyperplasia lacking characteristic findings from other primary and secondary hepatic lesions [1]. The purpose of this essay, in which all illustrated atypical cases are pathologically proven, is to present the spectrum of common and uncommon patterns encountered in CT and MR imaging of focal nodular hyperplasia, in correlation with the pathologic features. Atypically, focal nodular hyperplasia may present as a large lesion, sometimes multiple in localization, and may show internal necrosis, hemorrhagic foci, and fatty infiltration. Other rare imaging features include nonvisualization of the central scar, nonenhancement of the central scar, and pseudocapsular enhancement on delayed imaging. Because familiarity with these varied CT and MR imaging features is essential for an accurate diagnosis, it is important for radiologists not only to be aware of these uncommon appearances of focal nodular hyperplasia but also to understand the radiologic—pathologic correlation.

General Tumor Characteristics

Top Introduction General Tumor Characteristics Typical CT and MR... Atypical CT and MR... References

 
Focal nodular hyperplasia is a rare tumor-like condition predominantly found in women during the third to fifth decade of life, although it may occur in both sexes and all age groups [1, 2]. Most commonly, it is incidentally discovered in asymptomatic patients. The cause of focal nodular hyperplasia is not well understood: congenital vascular malformation or vascular injury has been suggested as the underlying mechanism for hepatocellular hyperplasia [1]. Although the relationship between the occurrence of focal nodular hyperplasia and the use of oral contraceptives has never been proven, it is possible that endoor exogenous estrogens play a role in the growth of the lesion [1].

Generally, focal nodular hyperplasia presents as a solitary nodule smaller than 5 cm in diameter. The mass is usually lobulated and well circumscribed, although unencapsulated [1, 2]. The pathognomonic macroscopic feature is the presence of a central stellate scar with radiating fibrous septa, thereby dividing the lesion into numerous nodules of normal hepatocytes that are abnormally arranged (Fig. 1A). The central scar contains thick-walled vessels that provide excellent arterial blood supply to the lesion, and therefore, these tumors are usually homogeneous (with internal necrosis and hemorrhage being extremely rare) [1, 2]. The most characteristic microscopic features of focal nodular hyperplasia are the fibrous septae and the cellular areas of hepatocellular proliferation (Fig. 1B). The nodules seen in focal nodular hyperplasia lack normal central veins and portal tracts. The bile ductules seen in the central scar do not connect to the biliary tree. The thick-walled vessels detected in the scar often show fibromuscular hyperplasia and myxomatous changes. Inflammatory cells—both acute and chronic—may also be found [1].

View larger version (147K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1A. —Pathology of focal nodular hyperplasia in 27-year-old woman. Gross section of right lobectomy specimen shows well-circumscribed lobulated mass with central scar (arrow) and radiating septations.

View larger version (176K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1B. —Pathology of focal nodular hyperplasia in 27-year-old woman. Photomicrograph of histopathologic specimen shows regions of nodular hepatocellular proliferation separated by radiating bands and surrounding myxomatous scar (arrows). (H and E, x80)

Typical CT and MR Findings

Top Introduction General Tumor Characteristics Typical CT and MR... Atypical CT and MR... References

 
On unenhanced CT, focal nodular hyperplasia is classically seen as a solitary, homogeneous, and slightly hypoattenuating or isoattenuating area compared with normal liver [2] (Fig. 2A). The latter may be explained by the aberrant architecture of the proliferating hepatocytes and the slightly decreased reticulum stroma. In approximately 20% of patients, a central hypoattenuating scar may be seen [3]. Related to the hypervascularity of the tumor, during the arterial phase of hepatic enhancement, focal nodular hyperplasia shows an immediate and intense enhancement (96%), with the exception of the central scar, which has delayed enhancement caused by the presence of abundant myxomatous stroma [3] (Fig. 2B). CT performed during peak portal venous enhancement shows decreased enhancement of the lesion relative to the normal enhancing hepatic parenchyma, resulting in the lesion being isoattenuating to the liver, with gradual diffusion of the contrast material into the myxomatous stroma of the central scar (Fig. 2C). Because delayed washout of contrast material from this myxomatous tissue relative to surrounding liver is also found, the central scar may appear hyperattenuating on delayed CT [1,2,3] (Fig. 2D).

View larger version (136K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2A. —Typical CT findings of focal nodular hyperplasia in 30-year-old woman. Unenhanced CT scan shows lesion in left lobe of liver (arrowheads), which is slightly hypodense to remainder of liver. Note more hypodense central scar (arrow).

View larger version (167K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2B. —Typical CT findings of focal nodular hyperplasia in 30-year-old woman. Arterial phase contrast-enhanced CT scan shows strong homogeneous enhancement of lesion, caused by arterial vascular supply. Note focal central area of low attenuation, representing central scar.

View larger version (144K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2C. —Typical CT findings of focal nodular hyperplasia in 30-year-old woman. Contrast-enhanced CT scan during the portal venous phase shows lesion being slightly hypoattenuating compared with surrounding liver because of rapid contrast material washout.

View larger version (166K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2D. —Typical CT findings of focal nodular hyperplasia in 30-year-old woman. Delayed phase contrast-enhanced CT scan shows persistent enhancement of central scar (arrowhead).

Typical MR features of focal nodular hyperplasia are iso- or hypointensity on T1-weighted images (94-100%); slight hyper- or isointensity on T2-weighted images (94-100%); homogeneity (96%); and the presence of a central scar that appears hyperintense on T2-weighted images (84%) because of its vascular channels, bile ductules, and increased edema in the myxomatous tissue [1, 4] (Figs. 3A and 3B). After administration of gadolinium chelates, the enhancement profile is identical to that seen on contrast-enhanced CT: dramatic enhancement in the arterial phase, followed by isointensity of the lesion during the portal venous phase. On delayed phase imaging, the central scar shows high signal intensity because of the accumulation of contrast material [1, 3, 4] (Figs. 3C and 3D).

View larger version (151K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 3A. —Typical MR findings of focal nodular hyperplasia in 26-year-old woman. Fat-suppressed T2-weighted turbo spin-echo MR image shows hyperintense lesion located in right lobe of liver. Hyperintense central scar is obvious (arrowhead).

View larger version (135K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 3B. —Typical MR findings of focal nodular hyperplasia in 26-year-old woman. T1-weighted fast low-angle shot (FLASH) image shows lesion slightly hypointense to surrounding parenchyma with more hypointense central scar (arrow).

View larger version (148K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 3C. —Typical MR findings of focal nodular hyperplasia in 26-year-old woman. Dynamic study with IV bolus injection of gadopentetate dimeglumine using T1-weighted FLASH MR sequence. Twenty seconds after bolus injection, lesion is hyperintense to surrounding parenchyma, and central scar remains hypointense.

View larger version (154K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 3D. —Typical MR findings of focal nodular hyperplasia in 26-year-old woman. Contrast-enhanced T1-weighted MR image, obtained 4 min after injection in C, shows that lesion remains slightly hyperintense to normal liver, but central scar is highly enhanced (arrowhead).

Atypical CT and MR Findings

Top Introduction General Tumor Characteristics Typical CT and MR... Atypical CT and MR... References

 
Atypical Presentation
Age.—Although focal nodular hyperplasia occurs in both sexes and at all ages, it is most commonly found in women (80-95%) in their third and fourth decade of life (more than 50%). In childhood (0-16 years), focal nodular hyperplasia represents only 2% of hepatic tumors (i.e., approximately 0.02% of all pediatric tumors) [5] (Fig. 4A,4B).

View larger version (142K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 4A. —Focal nodular hyperplasia in 4-year-old girl. Gadolinium-enhanced T1-weighted fast low-angle shot MR images show 3-cm lesion in caudate lobe of liver. On arterial phase image, lesion is markedly enhanced compared with liver, with exception of central scar.

View larger version (148K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 4B. —Focal nodular hyperplasia in 4-year-old girl. Gadolinium-enhanced T1-weighted fast low-angle shot MR images show 3-cm lesion in caudate lobe of liver. On delayed phase image, mass shows isointense appearance compared with normal liver with delayed enhancement of central scar (arrow).

Tumor volume.—Because the growth of focal nodular hyperplasia is exactly proportional to the inherent vascular supply of the tumor, it is mostly limited to smaller than 5 cm in diameter [1]. In a large study by Ishak and Rabin [6], of the 130 patients with focal nodular hyperplasia, 110 (85%) had a single nodule less than 5 cm in diameter, 16 (12%) had a focal nodular hyperplasia between 5 and 10 cm, and only four (3%) had a lesion larger than 10 cm. Unlike the "classic" asymptomatic small lesions, larger tumors may cause symptoms, such as abdominal pain or awareness of the presence of an abdominal mass. The pain is usually caused by the expansion of the Glisson's capsule or focal mass effect on surrounding organs or vascular structures (Figs. 5 and 6A,6B).

View larger version (158K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 5. —Large focal nodular hyperplasia in 42-year-old woman. Delayed phase contrast-enhanced CT scan shows large well-circumscribed nearly isodense mass in medial segment of left lobe of liver (black arrows). Left portal vein and hepatic artery (arrowhead) are adjacent to and displaced by the lesion. Additionally, bile ducts of segments II and VII of liver are slightly dilated (white arrows).

View larger version (154K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 6A. —Large focal nodular hyperplasia in 37-year-old woman. T1-weighted fast low-angle shot MR image shows large (11 cm) and slightly hypointense lesion in caudate lobe of liver. Note its mass effect on left portal vein (arrowhead), inferior caval vein, and hepatic veins (black arrow), with presence of intrahepatic venous collateral (white arrows), caused by limited normal venous outflow.

View larger version (157K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 6B. —Large focal nodular hyperplasia in 37-year-old woman. Gadopentetate dimeglumine—enhanced T1-weighted MR image during portal venous phase shows isointensity of lesion to normal liver, enhancement of central scar (arrowhead), and extreme stretching of middle hepatic vein around lesion (arrows).

Multiplicity of lesions.—Most focal nodular hyperplasia occurs as solitary lesions. In a study by Vilgrain et al. [4], of 37 patients with pathologically proven focal nodular hyperplasia, only eight patients (22%) had multiple lesions. Two lesions were present in each of six patients, three in one patient, and four in another patient [4] (Figs. 7 and 8).

View larger version (146K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 7. —Multiple focal nodular hyperplasias in 28-year-old woman. Contrast-enhanced CT scan during arterial phase shows multiple hypervascular lesions disseminated throughout liver.

View larger version (128K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 8. —Multiple focal nodular hyperplasias in 49-year-old woman. Portal venous phase gadolinium-enhanced T1-weighted MR image shows three lesions (arrows) in plane of image. Presence of enhancing central scar in smallest lesion (arrowhead) made these lesions consistent with focal nodular hyperplasia. Finding was confirmed at biopsy.

Atypical Density and Signal Intensity Characteristics
Lesion heterogeneity.—Because the growth of focal nodular hyperplasia remains proportional to the blood supply of the lesion rather than exceeding it, hemorrhage and necrosis are unusual findings in focal nodular hyperplasia [1]. Infarction (ischemic necrosis) of focal nodular hyperplasia occurs even more rarely than hemorrhage and has been reported previously as a focal finding in three women, each with a history of oral contraceptive use [7]. Estrogens may have an effect on the vascular changes seen in focal nodular hyperplasia (Fig. 9A,9B).

View larger version (165K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 9A. —Internal necrosis and hemorrhage in focal nodular hyperplasia in 52-year-old woman who presented with persistent abdominal pain. Arterial phase gadolinium-enhanced T1-weighted fast low-angle shot MR image shows inhomogeneous enhancement of mass with areas of necrosis present (black arrow). Note second smaller lesion (arrowhead) in right liver lobe with central scar (white arrow).

View larger version (156K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 9B. —Internal necrosis and hemorrhage in focal nodular hyperplasia in 52-year-old woman who presented with persistent abdominal pain. Photomicrograph of histopathologic specimen of lesion shows cellular arrangement consistent with focal nodular enhancement and area of hemorrhagic necrosis (arrows) in lesion. (H and E, x40)

Fat accumulation.—Fatty infiltration of focal nodular hyperplasia is rare and only sporadically mentioned in literature [8]. In previous reports describing the presence of fat in focal nodular hyperplasia, fatty infiltration of the lesion was thought to be a result of the extension of the patient's underlying disease, which was hepatic steatosis (Fig. 10A,10B). Hypothetically, intralesional steatosis in focal nodular hyperplasia can be expected in several types of hepatic injury associated with steatosis, such as alcoholic toxicity, obesity, diabetes, malnutrition, and protein malabsorption. Fatty infiltration of focal nodular hyperplasia without coexistence of diffuse steatosis has been mentioned only twice in the literature with no explicit underlying cause detected [8].

View larger version (148K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 10A. —Fatty infiltration in focal nodular hyperplasia in 47-year-old woman. Unenhanced axial CT scan shows total fatty replacement of liver and well-delineated, inhomogeneous, and hypodense mass (arrows) in right liver lobe.

View larger version (145K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 10B. —Fatty infiltration in focal nodular hyperplasia in 47-year-old woman. Photomicrograph of histopathologic specimen shows central stellate scar (large arrow) with ductular proliferation surrounded by normal and steatotic (small arrows) hepatic parenchyma. (H and E, x40)

Nonvisualization of the central scar.—In some cases, the scar may be extremely small or even undetectable on CT (16-40%) and on MR imaging (22%) [1,2,3,4]. In such cases, the lesion is usually difficult to visualize, except for a bulge or deformity of the liver contour or displacement of adjacent hepatic vessels (Figs. 11 and 12).

View larger version (167K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 11. —Nonvisualization of central scar in focal nodular hyperplasia of 53-year-old woman. Arterial phase contrast-enhanced CT scan shows small hypervascular lesion in right lobe of liver (arrow). No central scar is visible.

View larger version (171K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 12. —Nonvisualization of central scar in focal nodular hyperplasia in 45-year-old man. T2-weighted half-Fourier acquisition single-shot turbo spin-echo MR image shows small isointense mass in right lobe of liver (arrows). No scar is present.

Atypical Enhancement Characteristics
Pseudocapsular enhancement.—Though rare, focal nodular hyperplasia can be surrounded by a pseudocapsule [9]. Whenever the capsule is present in such cases, it implies that the underlying lesion is growing slowly, allowing a passive thickening of the surrounding liver stroma; the capsule tissue in such cases is fibrous, thick, and hyaline [4] (Figs. 13A and 13B). In some cases, however, a pseudocapsule can be mimicked because of eccentric compression of the lesion on normal surrounding vascular structures or hypertrophied feeding vessels (Fig. 13C).

View larger version (161K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 13A. —Pseudocapsular enhancement of focal nodular hyperplasia. Delayed phase gadolinium-enhanced T1-weighted fast low-angle shot MR image of 34-year-old woman shows isointense lesion in lateral segment of left liver lobe with marked enhancement of central scar and pseudocapsule (arrows).

View larger version (144K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 13B. —Pseudocapsular enhancement of focal nodular hyperplasia. Low-power photomicrograph of histopathologic specimen of pseudocapsule in same patient as A shows prevalent stromal component (arrow) between lesion and normal parenchyma. (reticulum stroma stain)

View larger version (150K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 13C. —Pseudocapsular enhancement of focal nodular hyperplasia. Delayed phase gadolinium-enhanced T1-weighted fast low-angle shot MR image in 26-year-old woman shows peripheral enhancement (arrows) of lesion located in right lobe of liver.

Nonenhancement of the central scar.—In unusual cases, the central scar can appear hypodense on contrast-enhanced CT and hypointense on T1-weighted MR images after administration of IV contrast material, mimicking the collagenous scar seen in hepatic adenoma, fibrolamellar carcinoma, hepatocellular carcinoma, or intrahepatic cholangiocarcinoma [9]. This scar hypodensity and hypointensity after administration of contrast material has been attributed to obliterative vascular hyperplasia of the central arteries (Figs. 14A,14B and 15A,15B). This vascular hyperplasia is also thought to be the underlying mechanism to explain scar hypointensity on T2-weighted images, another atypical feature of focal nodular hyperplasia [1].

View larger version (168K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 14A. —Nonenhancement of central scar in 48-year-old woman. Contrast-enhanced CT scan shows 8-cm lesion in segment IV of left lobe of liver. Centrally, 4-cm hypodense scar is shown. Nonenhancement of scar is seen either on arterial (A) or delayed (B) phase CT scans.

View larger version (159K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 14B. —Nonenhancement of central scar in 48-year-old woman. Contrast-enhanced CT scan shows 8-cm lesion in segment IV of left lobe of liver. Centrally, 4-cm hypodense scar is shown. Nonenhancement of scar is seen either on arterial (A) or delayed (B) phase CT scans.

View larger version (162K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 15A. —Nonenhancement of central scar in 53-year-old man. T2-weighted half-Fourier acquisition single-shot turbo spin-echo MR image reveals small mass in lateral segment of left lobe. Compared with normal liver, lesion is slightly hyperintense. Central scar (arrow) shows typical hyperintensity pattern.

View larger version (146K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 15B. —Nonenhancement of central scar in 53-year-old man. After administration of gadopentetate dimeglumine, delayed phase (24 min) T1-weighted MR image shows gradual but incomplete enhancement of central scar (arrow).

Conclusion

During the past few years, technical advances in CT and MR imaging have led to a marked increase in detection and characterization of focal nodular hyperplasia. Fortunately, focal nodular hyperplasia usually presents with classic imaging features, helping to narrow the differential diagnosis and negating the need for biopsy or further studies. Infrequently, however, focal nodular hyperplasia may show an unusual imaging appearance. These "atypical" CT and MR imaging features, which do not exclude the diagnosis of focal nodular hyperplasia (as shown in this essay), are important for the radiologist to understand and recognize.

References

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1. Mathieu D, Vilgrain V, Mahfouz AE, Anglade MC, Vullierme MP, Denys A. Benign liver tumors. Magn Reson Imaging Clin N Am 1997:5:255 -288[Medline]
2. Shirkhoda A, Farah MC, Bernacki E, Madrazo B, Roberts J. Hepatic focal nodular hyperplasia: CT and sonographic spectrum. Abdom Imaging 1994;19:34 -38[Medline]
3. Shamsi K, De Schepper A, Degryse H, Deckers F. Focal nodular hyperplasia of the liver: radiologic findings. Abdom Imaging 1993;18:32 -38[Medline]
4. Vilgrain V, Flejou JF, Arrive L, et al. Focal nodular hyperplasia of the liver: MR imaging and pathologic correlation in 37 patients. Radiology 1992;184:699 -703[Abstract/Free Full Text]
5. Reymond D, Plaschkes J, Luthy AR, Leibundgut K, Hirt A, Wagner HP. Focal nodular hyperplasia of the liver in children: review of follow-up and outcome. J Pediatr Surg 1995;30:1590 -1593[Medline]
6. Ishak KG, Rabin L. Benign tumors of the liver. Med Clin North Am 1975;59:995 -1013[Medline]
7. Brunt EM, Flye MW. Infarction in focal nodular hyperplasia of the liver: a case report. Am J Clin Pathol 1991;95:503 -506[Medline]
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9. Choi CS, Freeny PC. Triphasic helical CT of hepatic focal nodular hyperplasia: incidence of atypical findings. AJR 1998;170:391 -395[Abstract/Free Full Text]

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