Pe d i a t r i c I m a g i n g • O r i g i n a l R e s e a r c h Cha et al. Imaging of Pediatric Focal Nodular Hyperplasia

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Pediatric Imaging Original Research

Dong Ik Cha1 So-Young Yoo Ji Hye Kim Tae Yeon Jeon Hong Eo Cha DI, Yoo SY, Kim JH, Jeon TY, Eo H

Clinical and Imaging Features of Focal Nodular Hyperplasia in Children OBJECTIVE. The purpose of this article is to review the clinical and imaging features of focal nodular hyperplasia (FNH) developed in children. MATERIALS AND METHODS. At a single institution, pediatric patients who underwent imaging studies and who had pathologically proven FNH were studied. Clinical characteristics, including presenting symptoms and signs and the presence of underlying disease, were reviewed from the medical records. Imaging features of FNHs, including the number, size, ultrasound echogenicity and vascularity, CT attenuation, MRI signal intensity and enhancement pattern, and the presence of a central scar, were evaluated. RESULTS. Twenty-five patients (11 boys and 14 girls; median age, 8.6 years) were found to have a solitary (n = 23) or multiple (n = 2) FNH lesions with a mean size of 4.9 cm (range, 1–10 cm). Multiple lesions were associated with small size of the lesions and history of malignancy treated by chemotherapy. Most patients were asymptomatic (n = 22). Biliary atresia was the most common underlying disease (n = 5). On ultrasound, FNHs most commonly appeared to be isoechoic and hypervascular. On dynamic CT and MRI, strong enhancement on the arterial phase and becoming isoattenuated or of isointense signal intensity on the portal or delayed phase was common. A central scar was usually noted in large lesions in about half the cases. CONCLUSION. Pediatric FNH is uncommon and usually is found incidentally in otherwise healthy children. However, it may occur in children who have underlying diseases, including biliary atresia. In addition, it can be encountered during surveillance of childhood cancer survivors with less common imaging features, including lack of a central scar and multiplicity.

F

Keywords: focal nodular hyperplasia, MDCT, MRI, pediatric liver, ultrasound DOI:10.2214/AJR.13.11856 Received August 30, 2013; accepted after revision October 18, 2013. 1

All authors: Department of Radiology and Center for Imaging Science, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Ilwon-Dong, Kangnam-Ku, Seoul 135-710, Korea. Address correspondence to S. Y. Yoo ([email protected]). 

AJR 2014; 202:960–965 0361–803X/14/2025–960 © American Roentgen Ray Society

960

ocal nodular hyperplasia (FNH), which is known to be the second most common benign liver tumor after hemangioma in adults, is uncommon in children, accounting for only 2% of pediatric liver tumors. The pathogenesis remains to be elucidated and has been suggested as a hyperplastic reaction to a localized vascular anomaly or acquired vascular injury [1, 2]. In adults, FNH is usually found incidentally in otherwise healthy patients with characteristic imaging features, including a central scar. In general, it is managed conservatively after a confident diagnosis [2, 3]. With the widespread use of imaging modalities such as ultrasound and CT, FNH is likely to be incidentally detected in children. In fact, over the past decade, there have been reports about the increased detection of FNH during surveillance of survivors of childhood malignancies who have undergone chemotherapy or radiotherapy [4–8].

However, because of its infrequency in childhood, FNH can be challenging to diagnose in the pediatric population. Furthermore, there are limited reports on pediatric FNH that include the imaging features [4–7]. Thus, the aim of this study is to retrospectively review the clinical and imaging features of FNH in children who are otherwise healthy or who have underlying diseases. Materials and Methods The institutional review board of Samsung Medical Center approved this study, and written informed consent was waived.

Patients and Analysis of Clinical and Imaging Data This study enrolled pediatric patients who were pathologically confirmed to have FNH and who underwent at least one imaging study, including ultrasound, CT, or MRI, in a tertiary medical center (Samsung Medical Center, Seoul, Korea).

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Imaging of Pediatric Focal Nodular Hyperplasia Electronic medical records were reviewed for the following clinical characteristics: demographic data, presenting symptoms and signs, presence of underlying disease including history of malignancy treated by chemoradiotherapy, and method of histopathologic diagnosis. For image analysis, all images were reviewed by two board-certified pediatric radiologists in consensus. The following features of the lesions were documented: number, size (defined as the maximum transverse diameter), ultrasound echogenicity and vascularity, CT attenuation, MRI signal intensity, enhancement pattern on dynamic studies, and the presence of a central scar. A central scar was considered to be present if a central stellate area, hypoattenuating on the arterial phase on CT or hyperintense on a T2-weighted image on MRI, showed delayed enhancement [9, 10]. In patients with multiple lesions, the largest one that was pathologically confirmed was considered representative. Follow-up images, if available, were also reviewed in terms of changes in size and appearance.

Image Acquisition All ultrasound examinations were performed by four pediatric radiologists (with 18, 10, 8, and 5 years of pediatric imaging experience). The equipment used included ultrasound systems from various vendors (HDI 5000, Philips Healthcare; Sequoia, Siemens Healthcare) with a 5- to 12-MHz linear-array transducer and a 2- to 6-MHz curvedarray transducer. CT was performed on MDCT scanners from various vendors (LightSpeed 16 GE Healthcare; Brillance 40, Philips Healthcare) using a low-dose technique based on the patient’s weight and with automatic exposure control. For dynam-

ic studies, the CT was obtained with a 5-mm slice thickness for a three-phase protocol including hepatic arterial, portal, and delayed phases. MRI was performed with a 3-T MRI system (Intera Achieva 3 T, Philips Healthcare) using a phased-array coil. The MRI protocol included a T1-weighted turbo field-echo in phase and opposed phase sequence, a breath-hold multishot T2-weighted sequence, and a respiratory-triggered heavily T2-weighted sequence. For dynamic imaging, arterial (20–35 seconds), portal (60 seconds), and delayed (3 minutes) phases were obtained using a T1-weighted 3D turbo-field-echo sequence (THRIVE [T1 highresolution isotropic volume examination], Philips Healthcare) after administration of non-liver-specific gadolinium chelate.

Results Clinical characteristics of patients with FNH are summarized in Table 1. There were 25 patients (11 boys and 14 girls) with ages ranging from 2 months to 18 years (median, 8.6 years). Most patients were asymp­ tomatic (n = 22). FNH was detected in these patients during investigation for the following reasons: abnormal liver function tests (n = 6), biliary atresia (n = 5), portosystemic shunt (n = 1), previous malignancy (n = 2), and workup for nonabdominal symptoms (n = 8). Abdominal symptoms, such as pain or a palpable mass, were present in three patients. Twenty-three patients (92%) had single lesions, whereas two patients with a history of malignancy had multiple lesions (Fig. 1). The mean lesion size was 4.9 cm (range, 1–10 cm). For two children, the intervals between malignancy development and FNH diagnosis were 10.9 and 12.1 years, respectively.

A

TABLE 1: Clinical Characteristics of 25 Patients With Focal Nodular Hyperplasia Characteristic

Value

Age Range

2 mo to 18 y

Median

8.6 y

Sex Male

11

Female

14

Clinical presentation Screening or surveillance History of malignancy

2

Workup for biliary atresia

5

Portosystemic shunt

1

Abdominal pain

3

Elevated liver enzyme levels

6

Other (incidentally detected)

8

Method of pathologic confirmation Ultrasound-guided biopsy

17

Hepatic resection

3

Total hepatectomya

5

Note—Except where noted otherwise, data are number of patients. aTotal hepatectomy was performed for liver transplantation in patients with biliary atresia.

The mean interval between diagnosis of biliary atresia and diagnosis of FNH was 12 months (range, 1–17 months). A total of 17 FNHs were confirmed by ultrasound-guided biopsy, and eight were con-

B

Fig. 1—18-year-old woman with history of medulloblastoma and multiple focal nodular hyperplasias (FNHs). A and B, Consecutive gadolinium-enhanced MRI scans (A obtained slightly cephalad to B) reveal multiple variably sized lesions (arrows) with strong enhancement in arterial phase. Most lesions became isointense to surrounding liver parenchyma on delayed phase (not shown). Largest lesion was found by ultrasound-guided biopsy to be FNH.

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Cha et al. firmed by surgical resection including total hepatectomy (n = 5) for liver transplantation for biliary atresia (Fig. 2). In the remaining three patients who underwent surgical resection, surgical removal was done for increase in size in one case and for difficult differentiation from other tumors such as infantile hemangioendothelioma in two cases. Imaging features of 25 FNHs are summarized in Table 2. On ultrasound (n = 24),

A

FNHs appeared to be isoechoic in 63% (15/24) of cases (Figs. 2 and 3), hyperechoic in 21% (5/24) of cases, and hypoechoic in 17% (4/24) of cases. On color Doppler studies (n = 18), 15 lesions (83%) showed hypervascularity (Fig. 3). On CT (n = 25) including 18 dynamic studies, 15 lesions showed strong and homogeneous enhancement on the arterial phase. Nine of them were isodense on the portal venous and delayed phase. Two lesions were hyperdense on the portal venous phase and became isodense on the delayed phase. Thus, 73% (11/15) of lesions showed strong enhancement on the arterial phase and became isodense on the delayed phase, 20% (3/15) showed strong enhancement on the arterial phase and became hypodense on the delayed phase, and 7% (1/15) showed high attenuation compared with the liver parenchyma, which persisted until the delayed phase. Of the remaining three lesions, one had peripheral enhancement on the arterial phase and a centripetal pattern of enhancement on the subsequent phases, one appeared isodense on the arterial phase and hypodense on the subsequent phases, and one appeared hypodense on all three phases. On CT, a central scar was seen in 52% of cases (13/25). The mean size of the nodules with a central scar was 6.3 cm (range, 3.4–10 cm), whereas that of nodules without a central scar was 3.4 cm (range, 0.6–7 cm). MRI was performed in eight patients. On T1-weighted images, 63% (5/8) of lesions showed isointense signal intensity, whereas

B

38% (3/8) showed low signal intensity. On T2weighted images, 50% (4/8) were isointense and 50% were hyperintense. On gadoliniumenhanced dynamic studies (n = 7), 86% (6/7) of the lesions enhanced on the arterial phase and became isointense on the delayed phase (Fig. 3). On MRI, a central scar was found in 71% (5/7) of lesions (Fig. 3). Four of the central scars were also visible on dynamic CT, whereas one was not visible on CT. Radiologic differential diagnoses included hepatic adenoma, hemangioma or infantile hemangioendothelioma, hepatoblastoma, and hepatocellular carcinoma. Among 17 biopsy-proven FNH lesions, follow-up images were available for 13, with a mean follow-up period of 40 months (range, 6.7–141 months). Thirty-eight percent (5/13) of them increased in size, followed by surgical resection in three. The remaining 62% (8/13) did not change in size or decreased during the follow-up. Discussion Our study showed that the common imaging features of pediatric FNH were as follows: mainly isoechoic (63%), with hypervascularity on ultrasound, and intense arterial enhancement, becoming isodense on the portal venous or the delayed phase on CT and MRI. A central scar, a well-known characteristic feature of FNH, can be absent in small lesions. We also observed that uncommon imaging features, including small size, multiplicity, and absence of a central scar, were frequent in pa-

C

Fig. 2—1-year-old girl with focal nodular hyperplasia (FNH) who had undergone Kasai operation for biliary atresia. A, On ultrasound, 2.5-cm round well-defined isoechoic mass (calipers) is seen in subcapsular area of liver. Mass showed increased vascularity on color Doppler ultrasound (not shown). B and C, On dynamic CT, mass shows strong enhancement on arterial phase (B) and becomes isodense on portal phase (not shown) and hypodense on delayed phase (C). Underlying liver shows biliary cirrhosis with multiple bile cysts in left lobe. FNH was confirmed after total hepatectomy for liver transplantation.

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4y

7.0

1.0

4.0

2y

18 y

5.6

Male

Female 7 mo 3.0

2.8

Male

Male

Female 4 y

Male

Male

Male

Female 16 y

13

14

15

16

17

18

19

20

2.7

Male

Female 15 y

Female 1 y

23

24

25

2.3

7.0

4.7

9.7

4.6

10

8.3

Positive

Positive

Positive

Negative

Positive

Negative

Positive

NA

NA

Positive

Negative

Negative

NA

Positive

NA

Positive Positive

Isoechoic

Isoechoic Positive

Positive

Hyperechoic Positive

Isoechoic

Isoechoic

Hyperechoic Positive

Isoechoic

Hypoechoic

Isoechoic

Hypoechoic

Isoechoic

Isoechoic

Hyperechoic Positive

NA

Hyperechoic Negative

Hyperechoic Positive

Isoechoic

Isoechoic

Isoechoic

Isoechoic

Isoechoic

Hypoechoic

Isoechoic

Isoechoic

Hypoechoic Isointense

Isointense

Hypointense

Isointense

Hypointense

Isointense

Isointense

Hypointense

Isointense

Isointense

Hypointense Hypointense

Isointense

Isointense

Hypointense Hypointense

Hyperintense

Hyperintense Isointense

Delayed Phase

Hyperintense

Hyperintense

Hyperintense

Hyperintense

Hyperintense

Hyperintense

Hyperintense

Hyperintense

Hyperintense

Hyperintense

Hypointense

Hyperintense

Isointense Isointense

Hyperintense

Isointense

Isointense

Isointense

Isointense

Isointense

Isoinstense

Isointense

Isointense

Isointense

Hyperintense Isointense

Hyperintense Hyperintense

Hyperintense

Isointense

Hypointense Hypointense

Isointense

MRI

No

No

Yes

Yes

No

Yes

No

No

Yes

No

Yes

No

Yes

Yes

No

No

Yes

Yes

Yes

Yes

Yes

No

Yes

Isointense

Hyperintense

Isointense Isointense

Hyperintense Isointense

Hyperintense Isointense

Hyperintense Isointense

Isointense

Isointense

Isointense

Hyperintense Hyperintense Isointense

Yes

Yes

No

Yes

Isointense

Isointense

Isointense

Hyperintense Isointense

Hyperitense Hyperintense Isointense

Isointense

Isointense

Yes

Yes

Hypoitense Hyperitense Hyperintensea Hyperintensea Hyperintensea No

Isointense

Isointense

Hypointense Hyperintense

Isointense

Hypointense

Central Central Scar Scar Present T1-Weighted T2-Weighted Arterial Phase Portal Phase Delayed Phase Present

Hyperintensea Hyperintensea Hyperintensea No

Hyperintense

Hyperintense

Hyperintense

Isointense

Hyperintense

Hyperintense

Hyperintense

Hyperintense

Note—NA = not applicable. aCentripetal pattern of enhancement was seen on both liver CT and liver MRI.

0.6

3.4

3 mo 5.2

Female 12 y

Female 1 y

21

22

16 y

16 y

14 y

13 y

17 y

2 mo 4.0

5.5

12

1y

Male

Female 3 y

6.7

7.0

7.0

3.7

2.7

10

Female 8 y

Female 16 y

Male

Male

Female 1 y

Female 6 mo 4.0

Male

Female 12 y

Female 18 y

Sex

CT

Mass Size Age (cm) Echogenicity Hypervascularity Arterial Phase Portal Phase

11

9

8

7

6

5

4

3

2

1

Patient No.

Ultrasound

TABLE 2: Imaging Features of Focal Nodular Hyperplasia in 25 Patients

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Biliary atresia

NA

NA

Biliary atresia

NA

NA

NA

NA

NA

NA

NA

Biliary atresia

NA

Portosystemic shunt

NA

Biliary atresia

NA

NA

NA

NA

Biliary atresia

NA

NA

Neuroblastoma

Medulloblastoma

Underlying Condition

Imaging of Pediatric Focal Nodular Hyperplasia

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Cha et al. Fig. 3—13-year-old boy with focal nodular hyperplasia who presented with elevated liver enzyme levels. A, Ultrasound shows 10-cm isoechoic mass (calipers). B, Hypervascularity is seen on color Doppler study. C, On T2-weighted MRI, mass (arrow) appears to have isointense to slightly hyperintense signal intensity. D, On dynamic arterial phase study, mass (arrow) shows strong enhancement. E, On delayed phase, mass becomes isointense. Note central scar (arrowhead), which shows delayed enhancement.

A

B

C

D

E

tients with underlying diseases including biliary atresia and previous malignancy. It is notable that, in our study, four children were younger than 1 year, and two of those four children had underlying abnormalities, including portosystemic shunt and biliary atresia, respectively. The youngest patient was 2 months old and had a portosystemic shunt. In the literature, the occurrence of FNH in the liver of infants is very rarely reported, and the youngest patient we found in the literature was a 43-day-old infant with isolated hemihyperplasia [11–13]. Our study is in line with a previous report by Towbin et al. [4], who found that characteristics of FNH depended on the presence or absence of a history of malignancy. Patients with a history of malignancy had multiple lesions, smaller lesions, and a much lower frequency of a central scar. On the other hand, patients without a history of malignancy usually had a single lesion with a larger size and were more likely to have a central scar. Although there were only two cases with a history of malignancy in this study, both cases presented with multiple lesions, whereas all patients without a history of malignancy had a single lesion. The mean size of lesions was smaller in patients with a history of malignancy (2.5 cm; range, 1–4 cm) than in otherwise healthy children (5.6 cm; range, 2.7–10 cm). Although this study included only a few patients with a history of malignancy, we found

more FNH lesions that were diagnosed noninvasively by imaging follow-up in the longterm survivors of childhood cancers. According to previous reports, it seems that acquired vascular injury by chemotherapy with or without radiotherapy followed by subsequent localized circulatory disturbances, such as thrombosis, high sinusoidal pressure, or increased flow, leads to the development of FNH in those populations long after completion of anticancer therapy [5–7, 14–16]. The discovery of a hepatic nodule in these patients often raises concerns about malignancy. Furthermore, the exact histologic diagnosis of a small hepatic nodule by an invasive procedure can be challenging in children. On the basis of our experience and previous reports, it appears that, in general, FNH can be distinguished from metastases by its imaging appearance because FNH lesions are hyperdense, whereas metastatic lesions are hypodense in the arterial or early portal venous phase after IV administration of contrast material [17]. Although these results may be limited for children with a history of hypervascular malignancy, such as neuroendocrine carcinoma, a hypervascular malignancy is very rare in childhood, and appropriate knowledge of a patient’s history may aid in differentiating FNH from metastases. Similar to the two cases in this study, FNHs developing in childhood cancer survivors are reported to have a tendency to be multiple and small and lacking a central scar [4, 6, 8, 18].

FNH in adults is often diagnosed with imaging modalities because of its characteristic imaging features. It is usually a single mass less than 5 cm in diameter with a central scar. On CT, it is either hypo- or isodense compared with the surrounding liver parenchyma. On the arterial phase, it usually shows homogeneously intense enhancement except for the central scar. On the portal venous or delayed phase, the mass becomes isodense to the surrounding liver. The central scar, which is found in approximately 20% of lesions on CT, may enhance [9, 14]. On MRI, it is usually hypo- or isointense to the surrounding liver on T1-weighted images and isointense to slightly hyperintense on T2-weighted images. It has homogeneously intense enhancement on the arterial phase and becomes isointense to the surrounding liver on the portal venous phase. The central scar, which is present in approximately 85% of cases on MRI, is hyperintense compared with the mass and may enhance in the later phases of imaging [9, 14]. Our study also shows that most FNHs in children are similar to FNHs in adults with regard to imaging features. Biliary atresia with biliary cirrhosis was the most common underlying disorder in this study, accounting for 20% (5/25) of cases. Although, by definition, FNH develops in an otherwise histologically normal or nearly normal liver [16], several studies have reported FNHlike nodules that are radiologically, macroscopically, microscopically, and immunohisto-

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Imaging of Pediatric Focal Nodular Hyperplasia chemically identical to FNH in a cirrhotic liver [17–20]. Because an arterial enhancing nodule in a cirrhotic liver can simulate hepatocellular carcinoma, knowing the imaging features of these FNH-like nodules in patients with biliary cirrhosis due to biliary atresia is important to avoid unnecessary invasive procedures. As our study shows, FNH that develops in the liver of biliary atresia preferentially has a peripheral subcapsular location. In previous reports about FNH in patients with portal vein obstruction, it has been suggested that increased arterial blood flow with impaired portal supply to the liver is likely to cause the development of FNH, especially in the peripheral areas where the portal supply may decrease further compared with the central area [19, 20]. Furthermore, previous studies showed that hepatic subcapsular flow increases in biliary atresia [21, 22]. Although, in our study, the patients with biliary atresia did not show portal vein obstruction, the portal vein was relatively decreased in diameter and there was also enlargement of the hepatic artery in all of them (n = 5). Therefore, we speculate that the preferential location of FNH observed in patients with biliary atresia may be related to the decreased portal flow, increased arterial supply, or both. In our study, follow-up imaging found that FNH increased in size in about 40% of cases over a mean period of 40 months, a higher frequency than in the previous studies. Although studies about the natural course of FNH are very limited and there have been conflicting results, some researchers have shown that FNH can grow in a minority in the adult studies [23– 25]. FNH is assumed to grow in the early stages of development until it reaches its maximum size. Therefore, in children, especially when FNH is found to be small, there may be a higher chance of observing a growing FNH. There are several limitations to our study. First, because of the retrospective nature of this study, the imaging investigations were not uniform. Second, although this is one of the largest studies that included pathologically proven FNH in children, the sample size is still small. Third, because the diagnosis of FNH can sometimes be made by characteristic imaging features without a biopsy, selection bias is implied in this study, which enrolled only pathologically confirmed cases. Therefore, we might have excluded typical FNH cases diagnosed in a noninvasive way. Regarding hepatobiliaryspecific MRI, which is highly useful in diagnosing FNH, its use in children has not been

established yet [26], and, currently, we do not use a he­pa­to­biliary-specific contrast agent for pediatric cases in our institution. In conclusion, although it is uncommon, FNH should be considered as one of the differential diagnoses of a pediatric liver mass, which is increasingly being encountered in imaging not only in healthy children but also in childhood cancer survivors during their surveillance and in patients with underlying diseases, such as biliary atresia. Knowledge of the imaging and clinical features will be crucial in making a confident diagnosis of FNH in children. References 1. Wanless IR, Mawdsley C, Adams R. On the pathogenesis of focal nodular hyperplasia of the liver. Hepatology 1985; 5:1194–1200 2. 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 3. Belghiti J, Pateron D, Panis Y, et al. Resection of presumed benign liver tumours. Br J Surg 1993; 80:380–383 4. Towbin AJ, Luo GG, Yin H, Mo JQ. Focal nodular hyperplasia in children, adolescents, and young adults. Pediatr Radiol 2011; 41:341–349 5. Bouyn CI, Leclere J, Raimondo G, et al. Hepatic focal nodular hyperplasia in children previously treated for a solid tumor: incidence, risk factors, and outcome. Cancer 2003; 97:3107–3113 6. Joyner BL Jr, Levin TL, Goyal RK, Newman B. Focal nodular hyperplasia of the liver: a sequela of tumor therapy. Pediatr Radiol 2005; 35:1234–1239 7. Marabelle A, Campagne D, Dechelotte P, Chipponi J, Demeocq F, Kanold J. Focal nodular hyperplasia of the liver in patients previously treated for pediatric neoplastic diseases. J Pediatr Hematol Oncol 2008; 30:546–549 8. Anderson L, Gregg D, Margolis D, Casper J, Talano J. Focal nodular hyperplasia in pediatric allogeneic hematopoietic cell transplant: case series. Bone Marrow Transplant 2010; 45:1357–1359 9. Hussain SM, Terkivatan T, Zondervan PE, et al. Focal nodular hyperplasia: findings at state-of-the-art MR imaging, US, CT, and pathologic analysis. RadioGraphics 2004; 24:3–17; discussion, 18–19 10. Brancatelli G, Federle MP, Grazioli L, Blachar A, Peterson MS, Thaete L. Focal nodular hyperplasia: CT findings with emphasis on multiphasic helical CT in 78 patients. Radiology 2001; 219:61–68 11. Demir HA, Varan A, Akcoren Z, Haliloglu M, Buyukpamukcu M. Focal nodular hyperplasia of the liver and elevated alpha fetoprotein level in an infant with isolated hemihyperplasia. J Pediatr Hematol Oncol 2008; 30:775–777

12. Mindikoglu AL, Regev A, Levi JU, Casillas J, Schiff ER. Focal nodular hyperplasia in identical twins. Am J Gastroenterol 2005; 100:1616–1619 13. Bordeianou L, Ryan DP, Goldstein AM. Focal nodular hyperplasia in a child with Beckwith-Wiedemann syndrome. Pediatr Surg Int 2005; 21:742–744 14. Kumagai H, Masuda T, Oikawa H, Endo K, Endo M, Takano T. Focal nodular hyperplasia of the liver: direct evidence of circulatory disturbances. J Gastroenterol Hepatol 2000; 15:1344–1347 15. Wanless IR, Lentz JS. Fatty liver hepatitis (steatohepatitis) and obesity: an autopsy study with analysis of risk factors. Hepatology 1990; 12:1106–1110 16. Castellino S, Muir A, Shah A, et al. Hepato-biliary late effects in survivors of childhood and adolescent cancer: a report from the Children’s Oncology Group. Pediatr Blood Cancer 2010; 54:663–669 17. Smith EA, Salisbury S, Martin R, Towbin AJ. Incidence and etiology of new liver lesions in pediatric patients previously treated for malignancy. AJR 2012; 199:186–191 18. Gobbi D, Dall’Igna P, Messina C, Cesca E, Cecchetto G. Focal nodular hyperplasia in pediatric patients with and without oncologic history. Pediatr Blood Cancer 2010; 55:1420–1422 19. Bureau C, Peron JM, Sirach E, Selves J, Otal P, Vinel JP. Liver nodules resembling focal nodular hyperplasia after portal vein thrombosis. J Hepatol 2004; 41:499–500 20. Marin D, Galluzzo A, Plessier A, Brancatelli G, Valla D, Vilgrain V. Focal nodular hyperplasia-like lesions in patients with cavernous transformation of the portal vein: prevalence, MR findings and natural history. Eur Radiol 2011; 21:2074–2082 21. El-Guindi MA, Sira MM, Konsowa HA, El-Abd OL, Salem TA. Value of hepatic subcapsular flow by color Doppler ultrasonography in the diagnosis of biliary atresia. J Gastroenterol Hepatol 2013; 28:867–872 22. Lee MS, Kim MJ, Lee MJ, et al. Biliary atresia: color Doppler US findings in neonates and infants. Radiology 2009; 252:282–289 23. Kuo YH, Wang JH, Lu SN, et al. Natural course of hepatic focal nodular hyperplasia: a long-term follow-up study with sonography. J Clin Ultrasound 2009; 37:132–137 24. Leconte I, Van Beers BE, Lacrosse M, et al. Focal nodular hyperplasia: natural course observed with CT and MRI. J Comput Assist Tomogr 2000; 24:61–66 25. Halankar JA, Kim TK, Jang HJ, Khalili K, Masoom HA. Understanding the natural history of focal nodular hyperplasia in the liver with MRI. Indian J Radiol Imaging 2012; 22:116–120 26. Tamrazi A, Vasanawala SS. Functional hepatobiliary MR imaging in children. Pediatr Radiol 2011; 41:1250–1258

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Clinical and imaging features of focal nodular hyperplasia in children.

The purpose of this article is to review the clinical and imaging features of focal nodular hyperplasia (FNH) developed in children...
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