the patient was a 28-year - old woman who was admitted to hospital because of a hepatic mass found incidentally on screening sonography .
she had no previous surgical and medical problems . a physical examination and the laboratory findings on admission revealed no abnormalities .
the serum alpha - fetoprotein level was 1.2 ng / ml and the carcinoembryonic antigen level was 1.3 ng / ml . test for the hepatitis - b antigen was negative and the test for hepatitis - b antibodies was positive .
ct of the abdomen showed a mass in the segment 6 measuring approximately 4.03.8-cm with a capsular retraction .
the hepatic helical ct scan during the hepatic arterial phase showed a heterogeneously enhancing mass with a lobulated margin .
the hepatic helical ct scan during the portal phase showed an isodense mass with a hypodense central scar ( fig .
these findings were compatible with the focal nodular hyperplasia except for a central scar extension to the hepatic capsule causing a retraction .
the t1-weighted axial mr image of the liver demonstrated a slightly hypointense mass demarcated by a thin hypointense rim with a central hypointense scar .
the t2-weighted axial mr image showed a slightly hyperintense mass with a hypointense central scar .
the contrast - enhanced t1-weighted axial mr image revealed a marked enhancement of the tumor with a nonenhancing central scar ( fig .
the gross specimen showed a nodular configuration with a dense fibrotic central scar . on the cut surface , a central dense fibrotic scar with radiating fibrous septa dividing the lesion into smaller nodules
the central scar extended to the surface , and the surface of the liver parenchyma adjacent to the mass was retracted .
the resected specimen showed a depressed thickened stellate scar , slightly eccentrically positioned , with tapering fibrous septa , which radiated through the mass , dividing it into multiple lobules .
focal nodular hyperplasia ( fnh ) is found predominantly in women during the third to fifth decade of life .
however , it has been reported to occur in both sexes and in all age groups .
the cause of fnh is not well understood , but a congenital vascular malformation or vascular injury has been suggested to be an underlying mechanism for the hepatocelluar hyperplasia ( 2 ) .
fnh is classically seen as a solitary , homogeneous , and slightly hypoattenuating or isoattenuating area compared to the normal liver on unenhanced ct ( 1 ) . in approximately 20% of patients , a central low - attenuating scar may be observed ( 6 ) . on enhanced ct , fnh shows an immediate and intense enhancement , with the exception of a central scar with a delayed enhancement , possibly due to abundant fibrous stroma ( 6 ) .
the atypical imaging findings of fnh include hemorrhage , necrosis , fat accumulation on an unenhanced ct , rapid contrast washout , delayed contrast accumulation , or the absence of a central scar ( 1 , 2 ) . the mr imaging of typical fnh is iso- or slightly hypointense mass with hypointense scar on the t1-weighted mr imaging and a slightly hyperintense mass with a hyperintense scar on the t2-weighted image . intensely and immediately enhancing mass with a delayed enhancing central scar is a classic finding on the gadolinum enhanced mr ( 1 , 2 ) . according to vilgrain et al ( 7 ) , when the firosis , edema , vessels , and inflammation of the central scars were carefully studied , obliterative vascular changes were observed in both hyperintense and hypointense scars on the t2-weighted images .
they reported that the distribution of fibrosis , inflammation , and vessels were not different in the hyper- and hypointense scars , but most of the hyperintense scars had predominant edema , whereas the hypointense scars showed an absence of or a lower degree of edema ( 7 ) . a similar correlation between the pathology findings and mr imaging was done to evaluate the central scars of the primary liver tumor ( 8) .
rummeny et al ( 8) described three pathologic types of the central scars : ( a ) vascular scars composed mainly of vascular channels penetrating the collagenous tissue ; ( b ) inflammatory scars with edema , necrosis , hepatocellularity and loose connective tissue ; and ( c ) collagenous scars composed predominantly of dense , sclerotic collagen .
vascular and inflammatory scars appeared hypointense relative to the liver parenchyma on the t1-weighted images , and hyperintense on the t2-weighted images , while collagenous scars were hypointense on both the t1- and t2-weighted images . in our case
, the microscopic findings showed a collagenous scar composed mainly of dense , sclerotic collagen , which explains the cause of the hypointensity on the t2-weighted image and a minimal enhancing central scar on the enhanced t1-weighted image .
the cut surface of a typical fnh revealed a central stellate scar with radiating fibrous septa dividing the lesion into smaller nodules .
the central scar contained thick - walled vessels that provided arterial blood supply to the lesion ( 2 ) .
grossly , the resected specimen showed a depressed thickened stellate scar , slightly eccentrically positioned , with tapering fibrous septa that radiated through the mass , dividing it into multiple lobules .
microscopically , numerous fibrous bands of varying thickness divided the lesion , surrounding the nodules of the hyperplastic hepatocytes and converging at the central scar .
several large blood vessels , which exhibited varying degrees of myointimal hyperplasia , mural thickening and intimal narrowing , were observed within the dense collagenous scar .
these radiating septa contained numerous thin - walled vessels , lymphocyte infiltrates and numerous proliferated bile ducts , which were closely apposed to the periseptal hepatocytes .
the hepatocytes nodules were composed of normal parenchymal elements , which were irregularly arranged with plates of one or two cells ' thickness but the normal lobular architecture was not seen .
a capsular retraction of the liver adjacent to the hepatic mass is an uncommon finding .
soyer et al . ( 3 ) reported that the prevalence of the capsular retraction adjacent to the hepatic tumor was 2% and all tumors were malignant .
seo et al ( 4 ) suggested that the prevalence was approximately 12% in malignant hepatic masses .
these findings have been observed in cases of hepatic epitheloid hemangioendothelioma ( heh ) , hepatocellular carcinoma , intrahepatic cholangiocarcinoma , and metastases from colon and breast cancers ( 3 - 5 , 10 ) .
the capsular retraction of heh was most likely due to the tumor fibrous reaction , which distorted the tumor margin and the adjacent liver capsule ( 5 ) .
the main factors causing the capsular retraction in malignant hepatic tumors are a portal venous obstruction in the hepatocelluar carcinoma , and hepatic atrophy followed by a bile duct obstruction in a cholangiocarcinoma ( 4 ) .
soyer et al . ( 3 ) reported that this finding was never associated with a benign tumor , supporting the hypothesis that a retraction of the liver capsule adjacent to a hepatic tumor is a finding specific to malignant tumors .
a capsular retraction with hemangiomas in cirrhotic livers has also been described ( 10 ) . although blachar ( 10 ) reported that the hemangioma was the only benign neoplasm associated with a capsular retraction , this study found another benign hepatic mass with a capsular retraction .
this is the first report showing a capsular retraction in focal nodular hyperplasia . in this case , the central fibrotic scar within the tumor was extended to the surface , and a retraction of the liver capsule adjacent to the tumor was made .
 focal nodular hyperplasia ( fnh ) is characterized by the presence a central scar with radiating fibrous septa . 
 our case had a capsular retraction , which was the result of an extension of the central scar to the surface . 
 in addition , a hypointense scar on the t2-weighted image and a minimal enhancing central scar on the enhanced t1-weighted image , which was due to dense , sclerotic collagenous tissue , were observed . 
 we report the first case of fnh with a capsular retraction . 
CASE REPORT
DISCUSSION