Large Focal Nodular Hyperplasia of the Liver: Possible to Evade Surgical Resection

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1 Osaka City Med. J. Vol. 47, , 2001 Large Focal Nodular Hyperplasia of the Liver: Possible to Evade Surgical Resection t /, r' " ~/:) SHOGO TANAKA, KAzUHIRO HIROHASHI, HIROMU TANAKA, SHOJI KOBO, TAICHI SHUTO, IKKO HIGAKI, SHIGEKAZU TAKEMURA, TAKATSUGU YAMAMOTO, YOSHIHIKO MORIMOTO, and HIROAKI KINOSHITA Department ofgastroenterological and Hepato-Biliary-Pancreatic Surgery, Osaka City University, Graduate School ofmedicine Summary Purpose Although recent advances in diagnostic imaging have allowed a number of patients with focal nodular hyperplasia (FNH) to avoid surgical treatment, the natural course of large FNH is still unknown. Case Report A 25-year-old man was admitted because of a large hepatic mass detected on routine examination in June The only laboratory abnormality was an elevated y GTP. Computed tomography, angiography, positron emission tomography using F-18 fluorodeoxyglucose (FDG - PET), and scintigraphy using technetium-99m-galactosylneoglycoalbumin(99mtc - NGA) demonstrated a spoke-wheel appearance of vessels, normal hepatocytes, and no malignancy. Histologic findings on needle biopsy were consistent with FNH. After informed consent, the patient agreed to observation. Two years after the initial diagnosis, he has no symptoms, and there are no changes in the size or character of the lesion on computed tomography. Discussion Careful observation of patients with FNH is required because its natural course is unknown and these lesions can bleed or rupture. Key Words: Focal nodular hyperplasia; Diagnostic imaging; Natural course Introduction Focal nodular hyperplasia (FNH) was first described by Edmondson!) as a benign lesion Received December 15, 2000; accepted April 10, Correspondence to: Shogo Tanaka, MD. Department of Gastroenterological and Hepato-Biliary-Pancreatic Surgery, Osaka City University, Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka, , Japan Tel ; Fax m @msic.med.osaka-cu.ac.jp

2 Tanaka et al of the liver. Patients commonly underwent hepatic resection because FNH was not easily discriminated from hepatocellular carcinoma until recent advances in diagnostic imaging. The correct therapeutic approach is controversial because the natural course of FNH is still unknown. We now report a patient with a large FNH who has been followed for 2 years after the initial diagnosis. Case Report A 25-year-old man was found to have a large hepatic mass on routine examination in June He had not had any symptoms or prior history. He did not drink alcohol and took no medications regularly. On admission, the liver edge was palpable 5 cm below the right costal margin without tenderness. There were no remarkable findings on laboratory examination except for an elevation of the serum y -glutamyl transpeptidase ( y -GTP)(248 IU/L)(normal I < 60 lull). The serum was negative for hepatitis C antibody and hepatitis B surface antigen. His serum alfa-fetoprotein, carcinoembryonic antigen, and CA19-9 concentrations were within normal limits. A contrast-enhanced computed tomography (CT) revealed a large mass, 9 cm III diameter, in the anterior segment of the liver (Fig. 1). The lesion was clearly and homogeneously enhanced, and had no central scar. Abdominal angiography showed axlelike arteries within the mass (Fig. 2). The vascular supply to the tumors appeared to arise centrally and radiate peripherally. Scintigraphy using technetium-99m-galactosylneoglycoalbumin (99mTc - NGA) and positron emission tomography (PET) using F -18 fluorodeoxyglucose (FDG) demonstrated that the mass consisted of normal hepatocytes (Fig. 3a, b). Histologic findings on the specimen obtained by an 18-gauge biopsy needle revealed normal hepatocytes, thick-walled arteries, ductal proliferation, and the absence of portal and central veins. These findings were consistent with FNH (FigA). Figure 1. Enhanced-contrast CT reveals a large lesion in the anterior segment of the liver; the lesion is clearly and homogeneously enhanced. There is no central scar

3 Natural Course oflarge FNH Figure 2. Angi()graphy from the right hepatic artery shows an anteri'br-inferior branch supplying the tumor and arising centrally and radiating peripherally in a spoke-wheel pattern. a b Figure 3. a: The tumor shows normal uptake of technetium-99mgalactosyl-neoglycoalbumin (99mTc - NGA), consistent with normal hepatocytes. b: F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) demonstrates normal uptake, similar to the surrounding liver parenchyma

4 Tanaka et al Figure 4. Histologic examination of a needle biopsy specimen of the tumor demonstrates normal hepatocytes, thick-walled arteries, ductal proliferation, and the absence of a portal and central vein. Figure 5. CT performed 2 years after the initial diagnosis revealed no changes in the size or character of the lesion. After obtaining informed consent, the patient agreed to undergo observation by CT twice a year. Two years after the initial diagnosis, he continues to have no symptoms, and there have been no changes in the size or character of the lesion on CT (Fig. 5). Discussion Edmonson!) defined focal areas which occasionally develop in a normal liver as "focal nodular hyperplasia(fnh)", and many cases have been reported. FNH may represent compensatory regeneration after localized ischemic damage of the parenchyma due to a vascular anomaly, or hepatocellular proliferation induced by vascular injury, such as thrombosis or initial hyperplasia 2 31 In 28 reported cases, the size of FNH ranged between 0.8XO.5 cm and 5.6X4.0 cm; 4 (13.3%) lesions were smaller than 1 cm; 10(33.3%) were 1.1 to 2.0 cm; 11 (36.7%) were 2.1 to

5 Natural Course oflarge FNH 3.0 em; 3 (10.0%) were 3.1 to 5.0 em, and 2 were larger than 5.1 em"). Lesions may be as large as 24 cm 5 ). In our case, a central scar,, 6) was not detected, but the spoke-wheel appearance on angiogram 2,6), the presence of normal hepatocytes by PET 7 ) (in this exam, focal FDG accumulation is regarded as a sign of malignancy), and 99mTc-NGAB), (in this test, the accumulation of 99mTc - NGA is related to the functional activity and to the number of the functional hepatocytes), were all compatible with FNH. Histologically normal liver cells, without a portal triad and central vein 9 )but with thick-walled arteries B ), were noted. Although some authors have reported patients with FNH who have had rupture or massive intraabdominal hemorrhage 9 ' 15 ), most patients with FNH have no symptoms, and malignant degeneration of FNH has not been reported. Leconte, et al. 16 ) also indicated the variety of natural course of FNH; they reported 18 FNHs followed for at least 6 months with no treatment, in which the volume was stable in 6 cases, decreased in 10 cases, and increased in 2 cases. Some patients with a small FNH were successfully treated with percutaneous ethanol injection therapy17j; however, vascular intervention (embolization or ligation of the hepatic artery) is not often effective 1B,19). In our patient, although surgical resection was not contraindicated, observation was chosen after adequate informed consent was obtained. Mter 2 years of observation, no changes have been noted in the lesion, although continued observation is still required because of the unknown natural course and the possibility ofbleeding or rupture. References 1. Edmondson H A: Tumors of the liver and intahepatic bile ducts. In Atlas of Tumor Pathology, fasc. 25, sect. 7, Edmondson HA, Armed Forces Institute of Pathology, Washington DC , (1958) 2. Whelen J J, Baugh J H, Chandor S: Focal nodular hyperplasia of the liver. Ann Surg 177: (1973) 3. Wanless I R, Mawdsley C, Adams R: On the pathogenesis of focal nodular hyperplasia of the liver. Hepatology 5: (1985) 4. Kojiro M, Okumura S, Nakashima 0: Clinicopathologic characteristics of focal nodular hyperplasia(fnh) of the liver. J Hep Bil Pancr Surg 3: (1996) 5. Gold J H, Guzman I J, Rosai J: Bengin tumors of the tumor: Pathological examination of 45 cases. Am J Clin Pathol 70: 6-17 (1978) 6. Rogers J V, Mack L A, Freeny PC, Johnson M L, Sones P J: Hepatic focal nodular hyperplasia; angiography, CT, sonography, and scintigraphy. Am J Roentgenol 70: 6-17 (1981) 7. Bares R, Klever P, Hauptmann S, Hellwig D, Fass J, Cremerius U, Schumpelick V, Mittermayer C, Bull U: F-18 fluorodeoxyglucose PET in vivo evaluation of pancreatic glucose metabolism for detection of pancreatic cancer. Radiology 192: (1994) 8. Kurtaran A, Muller C, Novacek G, Kaserer K, Mentes M, Raderer M, Pidlich J, Eibenberger K, Angelberger P, Virgolini I: Distinction between hepatic focal nodular hyperplasia and malignant liver lesions using technetium- 99m-galactosyl-neoglycoalbumin. J Nuc Med 38: (1997) 9. Catalano P W, Early M E, Topolosky H W, Martin E W Jr, Carey L C: Focal nodular hyperplasia of the liver; Report of six patients. Cancer 39: (1977) 10. Becker Y T, Raiford D S, Webb L, Wright J K, Chapman W C, Pinson C W: Rupture and hemorrhage of hepatic focal nodular hyperplasia. The Am Surg 61: (1995) 11. Stauffer J Q, Lapinski M W, Honold D J, Myers J K: Focal nodular hyperplasia of the liver and intrahepatic hemorrhage in young women on oral contraceptives. Ann Intern Med 83: (1975)

6 Tanaka et al 12. Nime F, Pickren J W, Vana J, Aronoff B L, Baker H W, Murphy G P: The histology of liver tumors in oral contraceptive users observed during a national survey by the American College of Surgeons Commission on Cancer. Cancer 44: (1979) 13. Ishak K G, Rabin L: Benign tumors of the liver. Med Clin N Amer 59: 6-17 (1975) 14. Green M T Jr, Brown J R: Avulsion of pedunculated focal nodular hyperplasia: an unusual football injury. J La State Med Soc 124: (1973) 15. Barrows G H, Christopherson W M: Human liver tumors in relation to steroidal usage. Environ Health Perspect 50: (1983) 16. Leconte I, Van Beers B E, Lacrosse M, Sempoux: C, Jamart J, Materne R, Baudrez V, Horsmans Y: Focal nodular hyperplasia: natural course observed with CT and MRI. J Comput Assist Tomogr 24: (2000) 17. Soucy P, Rasuli P, Chou S, Carpenter B: Definitive treatment of focal nodular hyperplasia of the liver by ethanol embolization. J Pediatr Surg 24: (1989) 18. Pain J A, Gimson A E, Williams R, Howard E R: Focal nodular hyperplasia of the liver; Results of treatment and options in management. Gut 32: (1991) 19. Reymond D, Plaschkes J, Ridolfi L A, Leibundgut K, Hirt A, Wagner H P: Focal nodular hyperplasia of the liver in children: Review of follow-up and outcome. J Pediatric Surg 30: (1995)