| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Gastrointestinal Imaging |
1 From the Departments of Radiology (L.G., M.P.F., T.I., E.B.), Pathology (M.N.), and Surgery (J.M.), University of Pittsburgh Medical Center, Presbyterian Hospital, 200 Lothrop St, Room 4660 CHP MT, Pittsburgh, PA 15213; the Department of Radiology, Spedali Civili Brescia, Italy (L.G.); and the Department of Radiology, Yamanashi Medical University, Nakakoma, Japan (T.I.). Received September 15, 1999; revision requested October 14; revision received November 9; accepted November 16. Address correspondence to M.P.F. (e-mail: federlemp@radserv.arad.upmc.edu).
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
MATERIALS AND METHODS: Fifteen adult patients had more than 10 hepatic adenomas each and no history of glycogen storage disease or anabolic steroid use. Ten of them underwent bolus-enhanced dynamic computed tomography (CT) with or without magnetic resonance (MR) imaging, ultrasonography, and/or angiography.
RESULTS: Clinical abnormalities included abdominal pain in 11 (73%) and hepatomegaly in 10 (67%) patients, and abnormal liver function in 10 (91%) of 11 patients. The number of adenomas in each patient was 10–50 at imaging, but many more lesions were found in the resected specimens. Hemorrhage was commonly found within adenomas at histopathologic analysis, but only four patients had clinical and imaging evidence of substantial hemorrhage. In all patients, the adenomas increased over time, and two patients developed hepatocellular carcinoma. CT and MR features of the adenomas included evidence of hypervascularity (63%), intratumoral fat (50% of patients at CT, 80% at MR), and decreased conspicuity at portal venous and delayed-phase imaging. Fifty percent of patients had congenital or acquired hepatic vascular abnormalities.
CONCLUSION: The imaging and histopathologic features of individual adenomatous lesions are similar to those reported in young women who are taking oral contraceptives. However, the lesions in liver adenomatosis are not steroid dependent but rather multiple, progressive, and symptomatic, and they are more likely to lead to impaired liver function, hemorrhage, and perhaps malignant degeneration.
Index terms: Computed tomography (CT), phase imaging, 761.12112, 761.12114, 761.12115 • Liver neoplasms, 761.3192, 761.323 • Liver neoplasms, angiography, 761.124 • Liver neoplasms, CT, 761.12112, 761.12114, 761.12115 • Liver neoplasms, MR, 761.121411, 761.121412, 761.121414 • Liver neoplasms, US, 761.12983 • Magnetic resonance (MR), chemical shift
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
In 1985, Flejou et al (14) described, as a separate clinical entity, liver adenomatosis, which could be distinguished from isolated hepatic adenoma by the presence of multiple adenomas (arbitrarily, more than 10), lack of correlation with steroid medication, involvement in both men and women, and abnormal increases in serum alkaline phosphatase and 
-glutamyltransferase levels. The multiple adenomas arise in an otherwise normal liver and in patients without glycogen storage disease, according to common agreement (14–17).
The natural history and pathogenesis of liver adenomatosis are unclear, and only about 26 patients who have it have been reported (14–17). The risk of spontaneous hemorrhage or malignant transformation remains controversial. Very little has been reported on the current imaging characteristics of liver adenomatosis. The recommendations for surveillance and therapy have ranged from conservative monitoring or medical therapy to aggressive surgery and even orthotopic liver transplantation (3,11,14,15).
We examined 15 patients with liver adenomatosis at the University of Pittsburgh Medical Center and Spedali Civili Brescia. The purposes of our investigation were to review and compare the cases in our study with those previously reported; to correlate the clinical, histopathologic, and imaging findings; and to suggest further insights as to the pathogenesis and prognosis of and optimal therapy for this disorder.
|
MATERIALS AND METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
All 15 patients had histopathologic confirmation of at least two representative hepatic masses. Complete resection of the multiple tumors was achieved by using hepatic lobectomy in three patients and by using orthotopic liver transplantation in five. The remaining seven patients underwent laparoscopic biopsy (n = 4) or percutaneous core-needle biopsy (n = 3). The clinical and biochemical findings, including sex, age, history of other hepatic disease, steroid medication use, signs and symptoms, liver function test results, and serum 
-fetoprotein levels, were tabulated.
Ten patients underwent clinical and imaging examinations from 1991 through 1998 and had complete medical records and imaging studies available for review. Ten patients underwent CT; six, ultrasonography (US); five, magnetic resonance (MR) imaging; and three, digital subtraction angiography. Only the preoperative studies were reviewed. All patients underwent multiple CT examinations and clinical evaluations for at least 2 years.
The US studies were performed by using a model 128 XP (Acuson, Mountain View, Calif) or Sequoia (Acuson) scanner with 3.5–5.0-MHz transducers. Static gray-scale and color Doppler images were obtained.
The CT scans were obtained with a conventional transverse (9800 Advantage; GE Medical Systems, Milwaukee, Wis) or helical (CT HiSpeed Advantage; GE Medical Systems) CT scanner. The nonhelical scans (n = 2) were obtained with a monophasic injection of intravenous contrast material at 2.5 mL/sec for a total volume of 150 mL (maximum) or 2 mL/kg, with a scanning delay of 45–50 seconds. The helical CT examinations (n = 8) were performed by using a multiphasic CT protocol. All 10 patients underwent nonenhanced CT followed by contrast-enhanced CT and received either iothalarnate meglumine (Conray 60; Mallinckrodt Medical, St Louis, Mo) or ioversol (Optiray 320; Mallinckrodt Medical), which was injected intravenously at a rate of 3–5 mL/sec with a power injector (OP 100; Medrad, Pittsburgh, Pa).
The multiphasic CT protocol included the acquisition of nonenhanced, hepatic arterial phase (HAP), and portal venous phase (PVP) images in all eight patients. The HAP images were obtained after a scanning delay of 25–28 seconds, whereas the PVP images were obtained after a scanning delay of 60–70 seconds. The CT section thickness was 5–7 mm, and the table incrementation was 7.5–10.0 mm/sec, with the pitch adjusted to allow complete scanning of the liver within one breath hold. In addition, in four patients, delayed-phase liver CT images were obtained 5–10 minutes after intravenous administration of contrast material.
All of the MR examinations were obtained with a commercially available unit (1.5-T Signa Advantage; GE Medical Systems). Five patients underwent MR examinations that included the acquisition of T1-weighted spin-echo (500-600/15 [repetition time msec/echo time msec]) images and T2-weighted spin-echo or fast spin-echo (1,800-5,000/70-140) images. Chemical shift MR sequences were performed in three patients with both in-phase and opposed-phase imaging. In four patients, gadolinium-enhanced multiphasic MR images were obtained with a breath-hold fast spoiled gradient-echo sequence following rapid hand bolus administration of gadolinium-based contrast material (Magnevist; Berlex Laboratories, Wayne, NY) at a dose of 0.1 mmol/kg. Both the HAP and the PVP images were obtained with scanning delays similar to those used for the CT examinations. In two of the four patients who underwent gadolinium-enhanced multiphasic MR imaging, contrast-enhanced intermediate- and T2-weighted MR images with 0.05 mL/kg of superparamagnetic iron oxide (Endorem; Andre-Guerbet Laboratories, Aulnay-sous-Bois, France) were obtained on another day.
All of the imaging studies were reviewed retrospectively and concurrently by two experienced abdominal radiologists (L.G., T.I.) with knowledge of the diagnosis of multiple hepatic adenoma, but without knowledge of the specific number of lesions or the clinicopathologic findings in any patient. The images were interpreted by means of consensus, and no attempt was made to test for interobserver differences or accuracy because in most cases, no absolute standard was available to establish the exact number, size, and nature of the hepatic lesions.
The US tumor characteristics that were evaluated included the number, size, and echogenicity of the representative lesions relative to that of the surrounding liver. The echogenicity was classified as cystic (ie, echo free), hypoechoic, hyperechoic, or isoechoic. Bright echogenic foci with acoustic shadows were considered to be representative of calcification.
The tumor characteristics sought on CT and MR images included the number, size, and location of the lesions. A tumor capsule was judged to be present when a thin curvilinear structure surrounded all or a part of the tumor and clearly demarcated the tumor from the normal liver parenchyma. The presence and distribution of calcification were noted, along with evidence of acute hemorrhage—that is, fluid in or around the tumor that was hyperattenuating on the noncontrast CT images or hyperintense on both the T1- and T2-weighted MR images, with focal areas of low signal intensity on the T2-weighted images that suggested hemosiderin deposition. Necrosis or subacute hemorrhage was deemed to be evident when there was a fluid collection in an intermediate location between water and blood at CT. Tumor scars were defined as thin, central linear or branching hypoattenuating structures that were most evident on the HAP CT images. The presence of tumor fat (ie, lipid) was evident when the tumor components had a signal intensity that paralleled the signal intensity of known fat on the MR images, showed signal dropout on the opposed-phase chemical shift MR images, or had attenuation coefficients that were distinctly lower than those of water and/or visibly less than those of bile or urine on the nonenhanced CT images.
The attenuation and signal intensity characteristics of the tumors were judged relative to those of the surrounding liver parenchyma on the nonenhanced CT and MR images, as well as on the images obtained during all phases of contrast enhancement (ie, HAP, PVP, and delayed phase). Because many tumors were heterogeneous on the nonenhanced images because of hemorrhage, necrosis, fat, or calcification, we attempted to classify the enhancement characteristics of the remaining portions of the tumors as homogeneous or heterogeneous.
Digital subtraction angiography was performed in three patients only for the purpose of confirming the presence of vascular abnormalities, including congenital absence of the portal vein, portosystemic venous shunts, and portal venous thrombosis.
In all 15 patients, the gross and microscopic features of the resected hepatic masses or biopsy specimens, including the number and size of the lesions, evidence of hemorrhage or calcification, and unique histologic features, such as the presence and arrangement of hepatocytes, portal tracts, bile ducts, and Kupffer cells, were analyzed. The coexistence of hepatocellular carcinoma (HCC) or focal nodular hyperplasia (FNH) also was noted.
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
-glutamyltransferidase levels in 10 of the 11 patients examined. Serum -fetoprotein levels were normal in all patients at the time of diagnosis and first evaluation. All patients demonstrated an increase in the size and/or number of adenomas during the 2–12-year period of observation. The clinical and biochemical results in all 15 patients are summarized in Table 1.
|
Portal tracts and bile ducts were absent, but Kupffer cells were present in some of the nodules. The nodules were not uniform in appearance or at histologic analysis, and a minority of the nodules contained fatty components or were partially encapsulated. Coarse calcifications were noted in several nodules in one of the five patients. Many of the nodules showed evidence of subacute or chronic hemorrhage, but the bleeding did not extend beyond the tumor margins in most cases.
HCC was found in the explanted liver of one of the five patients (case 1) who underwent transplantation. The focus of HCC was present within the largest (6 x 6 cm) of the adenomas and was round, ill defined (1.7 x 1.5 cm), and distinctly different in appearance from the remainder of the adenomas. In the same liver, an intrahepatic spontaneous shunt connecting the left portal and middle hepatic veins was confirmed to be present.
Another patient (case 13) had undergone trisegmentectomy in 1981 and liver transplantation in 1982 for recurrent enlarging adenomas. In 1994, the patient was found to have HCC within the transplanted liver and died of widespread metastases.
Six patients who had a dominant mass in one lobe were treated with hepatic resection. The adenomas recurred or enlarged in all of these patients and led to liver transplantation in two of them. Another of these six patients was awaiting transplantation at the time of this study, and one died of an unrelated cause.
All four of the remaining patients underwent laparoscopic or US-guided core-needle biopsy of at least two focal masses. Attempts were made to perform biopsy on both the "representative" lesions (ie, those similar to other nodules) and the "atypical" lesions (ie, those with different imaging characteristics). The core-needle biopsy specimens were judged to be adequate for histopathologic diagnosis in all cases.
In two patients, the imaging characteristics suggested that some lesions (two lesions in one patient, solitary lesion in the other) might represent FNH because of the uniform hypervascularity and the central scar. Both the lesions that had these characteristics and on which biopsy was performed were confirmed to be FNH at histopathologic analysis; the presence of hepatocytes, Kupffer cells, primitive bile ductules, and blood vessels was noted.
The histopathologic findings in the adenomas on which biopsy was performed revealed normal hepatocytes arranged in cords of various sizes. The tumor cells were typically pale with large amounts of cytoplasmic lipid and glycogen. Large thin-walled capillaries and sinusoids were present, but distinct portal veins or bile ducts were not. Areas of hemorrhage were common.
Imaging Findings
The imaging studies from the past 9 years were available for review in 10 patients. US depicted numerous hepatic tumors in all six patients who were examined. The exact number of lesions was difficult to determine, but in general, fewer lesions were evident at US than at CT or MR imaging. The lesions were somewhat heterogeneous but predominantly hypoechoic. In three patients (cases 1, 4, and 9), several tumors demonstrated nonshadowing hyperechoic foci, which were believed to represent old hemorrhage at subsequent surgical excision. In one patient (case 3), both cystic and calcific foci were evident.
The detailed CT findings in 10 patients with adenomatosis are summarized in Table 2. The estimated number of discrete tumors was 10–20 in two patients, 21–40 in five, 41–50 in one, and more than 50 lesions in two. There was no right or left lobe predominance, and multiple hepatic segments were involved in all cases. The largest diameter of the tumors ranged from 0.5 to 15.0 cm. Subcapsular tumors distorted the liver contour in six patients. The surface and borders of most adenomas were smooth and well defined. Calcifications were evident in two patients (Fig 1), and five patients had multiple adenomas with fat content (Fig 2). Three patients had at least partial encapsulation of some of the larger adenomas. In two patients, cystic and hemorrhagic areas were identified within some adenomas, and one of these patients had a subcapsular hematoma as well (Fig 3). The single case of malignant degeneration of an adenoma to HCC with CT data available for review was not recognized prospectively or retrospectively.
|
|
|
|
|
|
|
|
Five patients had congenital or acquired abnormalities of the major hepatic veins that were recognized at CT and MR imaging. Two patients appeared to have congenital absence of the portal vein (Fig 4), and one had portal venous thrombosis with cavernous transformation (Fig 1). Two patients had intrahepatic portosystemic shunts (Fig 5). Three patients underwent catheter angiography, which confirmed the vascular abnormalities that were depicted at CT.
|
|
|
|
|
On the T1-weighted images, several tumors in three patients showed heterogeneous hyperintensity, which seemed to correlate with the intratumoral fat demonstrated at CT in two patients or at histopathologic analysis in one patient (Fig 2). In the remaining two patients, most of the tumors were nearly isointense to the liver parenchyma on T1-weighted images. On T2-weighted images, most of the adenomas were heterogeneously moderately hyperintense in three patients or homogeneously nearly isointense in two patients. The images obtained in the three patients in whom opposed-phase chemical shift imaging was performed all showed lesions with signal dropout, which indicated lipid content.
On the multiphasic, gadolinium-enhanced MR imaging studies, which were performed in four patients, most of the adenomas were predominantly hyperintense on the HAP and early PVP images and became progressively more isointense on the later PVP or delayed-phase images. The lesions also appeared to be more homogeneously enhanced on the PVP and delayed-phase images.
Two patients underwent MR imaging that was repeated after the intravenous administration of ferumoxide particles. The adenomas showed variable uptake of the contrast material, and lesion conspicuity decreased at intermediate-weighted and T2-weighted imaging in both cases.
MR imaging demonstrated the same hepatic vascular anomalies as did CT in the three patients who underwent both imaging examinations—namely, left portohepatic shunt (Fig 5), congenital absence, and acquired thrombosis of the portal vein.
Angiography performed in three patients helped to confirm one case each of portal venous thrombosis, congenital absence of the portal vein (Fig 4), and portosytemic venous shunt (Fig 5).
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Most steroid-induced or steroid-augmented adenomas are solitary, or, at most, two or three of these lesions manifest in a patient and typically regress with cessation of exogenous steroid use (1–13). Most are asymptomatic, unless there is a hemorrhage, which occurs in a minority of patients. The exact frequency of hemorrhage is uncertain, because symptomatic patients are more likely to seek medical attention. Malignant degeneration to HCC has been reported rarely in adenomas related to exogenous steroid use or glycogen storage disease. Liver function tests are almost invariably normal (1–13).
Liver adenomatosis, on the other hand, affects both men and women. Although other investigators (14–17) have cited no sex-based predominance, only one of the 15 patients in our study was male. The reason for this discrepancy is not apparent, although to our knowledge, our study was the largest series of cases reported by a single group of investigators. The tumors in patients with liver adenomatosis do not appear to be steroid dependent, and they do not regress with steroid withdrawal or blockage (eg, with tamoxifen or oophorectomy) (15). Liver function abnormalities, particularly those related to serum alkaline phosphatase and -glutamyltransferidase levels, are almost always present because of the tremendous number of space-occupying tumors. Malignant degeneration to HCC with liver adenomatosis, which we encountered in two patients, has been reported by several investigators (3,15). Hemorrhage is common in liver adenomatosis, particularly with large and subcapsular adenomas. Hemorrhage occurred in more than 60% of the patients in the Mayo Clinic experience with eight patients who had liver adenomatosis (15).
The conditions that may predispose patients to liver adenomatosis are poorly understood. One of the most intriguing speculations has to do with congenital or acquired abnormalities of the hepatic vasculature. Other investigators (9,18–24) have noted that both FNH and hepatic adenomas occur more often in patients who have coexistent vascular tumors, portal venous absence or occlusion, or portohepatic venous shunts. Five of the patients in our study had these vascular abnormalities, and two had coexistent FNH that was biopsy proved. We speculate that a focal disturbance of the hepatic blood supply somehow facilitates the hyperplastic development of these two similar benign lesions. Moreover, the histologic features of liver adenomas, with a proliferation of hepatocytes and sinusoids and weak connective tissue support, predisposes them to hemorrhage, particularly because these lesions are perfused almost exclusively by high-pressure arterial flow.
Even with the additional data gleaned from our cases, the nature and prognosis of and optimal therapy for liver adenomatosis remain uncertain. It may seem arbitrary and illogical to consider liver adenomatosis as a completely separate entity from the more common solitary or sporadic adenomas. We and others have encountered multiple "typical" adenomas, such as those that occur in young women who are taking oral contraceptives, and have seen as many as 10 adenomas each in patients with glycogen storage disease or anabolic steroid use (4–13). According to the definition of Flejou et al (14), which is accepted by other investigators, these cases do not warrant classification as liver adenomatosis.
Nevertheless, we agree that patients with multiple adenomas seem likely to develop additional adenomas that often result in hepatomegaly and abdominal pain, adversely affect liver function, are likely to hemorrhage, and may undergo malignant transformation. In the relatively few patients with liver adenomatosis in whom autopsy or liver transplantation has been performed, many more adenomatous lesions were found at gross examination of the liver than were identified at imaging studies, including CT (14,15).
In our series, two of 15 patients with liver adenomatosis developed HCC within an adenoma. One patient (case 1) had an elevating -fetoprotein level that was discovered during clinical surveillance and HCC within a large adenoma at liver transplantation that was not detected at preoperative CT. The other patient (case 13) developed HCC 12 years after undergoing liver transplantation for multiple benign adenomas. We agree with other investigators (3,15) that patients with liver adenomatosis are at increased risk for development of HCC and should be closely monitored with CT or MR imaging and serum -fetoprotein or other tumor marker examinations.
Most adenomas in liver adenomatosis do not seem to be responsive to estrogen stimulation. Ribeiro et al (15) performed an examination of eight patients with liver adenomatosis, including analysis of tumors for estrogen receptors, and concluded that attempts to eliminate endogenous estrogens (by using oophorectomy or tamoxifen therapy) usually were not warranted, whereas removal of exogenous steroids seemed to be prudent.
Because of the chance of malignant degeneration and hemorrhage, resection of adenomas, or at least of the largest and most "vulnerable" lesions (eg, subcapsular, exophytic, and hemorrhagic lesions), seems to be warranted in many cases, even if some smaller adenomas must remain in place (10,14,15). Ribeiro et al (15) reported decreased abdominal pain and longer hemorrhage-free intervals in patients who underwent partial or complete surgical resection of adenomas in liver adenomatosis. Orthotopic liver transplantation may be reserved for patients who have progressive signs or symptoms after partial resection, or in whom HCC is suspected.
The multiple adenomas in liver adenomatosis may have a variety of appearances, but the CT and MR characteristics of individual lesions are similar to those reported for sporadic or solitary adenomas (7,9). Fewer than half of all patients with adenomas and less than 10% of adenomas have a fat (ie, lipid) component identified at CT, whereas MR images depict fat in 35%–77% of adenomas (7). Obvious hemorrhage is not commonly identified in individual adenomas at CT, but it is commonly recognized at MR imaging and even more commonly at histopathologic analysis. Calcification is rare (prevalence <5%) and seems to occur in areas of prior hemorrhage.
Adenomas consist almost entirely of uniform hepatocytes, with the exception of areas of focal fat, hemorrhage, or calcification; however, the hepatocytes may contain large amounts of lipid and glycogen. Therefore, it is not surprising that many adenomas are not evident on CT scans, particularly those obtained during slow infusion of contrast material or during the portal venous, equilibrium, or delayed phases of enhancement. Even in our cases of bolus contrast-enhanced CT, three patients had adenomas that were almost entirely isoattenuating on PVP images.
In our experience, the HAP of enhancement, occurring about 20–30 seconds after rapid bolus administration of contrast material, is the most useful for both CT and MR detection of adenomas. Most hepatic adenomas are uniformly or heterogeneously hyperattenuating on HAP images. However, noncontrast CT images are valuable, particularly for the identification of focal fat and hemorrhage, and PVP images are essential for further characterization and recognition of vascular abnormalities, which are an important clue for the diagnosis of liver adenomatosis. We did not find US to offer useful additional information for the identification or characterization of lesions.
Because adenomas may have a variable appearance and patients with sporadic adenomas or adenomatosis may have coexistent HCC and/or FNH, achieving a confident diagnosis of each lesion in each patient can be challenging. We failed to diagnose either case of HCC within an adenoma, whereas we accurately identified the FNH in two patients owing to the presence of uniformly hypervascular, nonencapsulated lesions with a central scar.
The CT and MR imaging characteristics that we have described seem to correlate well with the findings in the available gross pathologic specimens. Intra- and extracellular fat and hemorrhage were often evident at imaging and were even more prevalent at histopathologic analysis. CT and MR imaging seemed to demonstrate most but not all of the adenomas in liver adenomatosis; this was not surprising given the enormous number of small tumors and the distorted liver architecture that may be found in advanced cases of liver adenomatosis.
Other conditions may be associated with multiple solid, predominantly hypervascular hepatic masses. Hepatic epithelioid hemangioendothelioma also may manifest as multiple masses in the noncirrhotic liver of a young patient (25). However, the tumor nodules in hepatic epithelioid hemangioendothelioma tend to be coalescent, in a subcapsular location, and associated with capsular retraction, and to have a target appearance with abundant fibrous tissue in the core of the lesions and a hypervascular periphery. Neither focal fat nor calcifications are seen in hepatic epitheloid hemangioendothelioma.
As previously noted, both FNH and adenomas typically are hypervascular and nonencapsulated, occur predominantly in young women, and probably share a common predisposing factor of hepatic venous abnormality. FNH can often be distinguished from adenoma by the absence of fat, calcification, or hemorrhage and by the presence of a central scar and marked hypervascularity (9,26,27). We and others (9,18,19) have noted the coexistence of FNH and adenomas both in liver adenomatosis and in cases of sporadic liver adenomas. Other investigators (24) have reported cases of nodular regenerative hyperplasia demonstrating multiple hypervascular hepatic lesions, some of which contained fat components, in young patients without cirrhosis but with underlying portal venous abnormalities. Whether this constitutes a separate clinical entity or is identical to what we would regard as liver adenomatosis is unclear. Close surveillance and biopsy of several lesions are probably necessary for diagnosis.
Distinguishing liver adenomatosis from multifocal HCC might be impossible with imaging criteria alone, because HCC lesions are often hypervascular and partially encapsulated and may contain fat (28). In most cases of diffuse HCC, however, cirrhosis or clinical evidence of chronic liver disease is evident and serum tumor markers are elevated.
Hypervascular liver metastases may share some imaging features with liver adenomatosis. Most patients have a known primary malignancy (eg, medullary thyroid, neuroendocrine, or renal) (29,30). Such hepatic metastases almost never contain fat, and the diagnosis is usually easily confirmed by using percutaneous needle biopsy of a liver lesion.
In summary, liver adenomatosis is a rare condition that predominantly affects young to middle-aged women. The imaging and histopathologic features of individual adenomatous lesions are similar to those that are more commonly reported in young women who are taking oral contraceptives. However, the lesions in liver adenomatosis are not steroid dependent, but rather they are multiple, progressive, symptomatic, and more likely to lead to impaired liver function, hemorrhage, and perhaps malignant degeneration. Close surveillance is essential, and surgical therapy, with an end point of liver transplantation, may be necessary in some cases.
|
FOOTNOTES |
|---|
Author contributions: Guarantors of integrity of entire study, L.G., M.P.F.; study concepts and design, L.G., M.P.F., T.I.; definition of intellectual content, L.G., T.I.; literature research, L.G., T.I.; clinical studies, all authors; data acquisition, all authors; data analysis, L.G., M.P.F.; manuscript preparation, L.G., M.P.F.; manuscript editing and review, M.P.F.
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
This article has been cited by other articles:
|
|
 |
|
  S. W. Anderson, J. B. Kruskal, and R. A. Kane Benign Hepatic Tumors and Iatrogenic Pseudotumors RadioGraphics, January 1, 2009; 29(1): 211 - 229. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. Giovanoli, M. Heim, L. Terracciano, G. Bongartz, and H. P. Ledermann MRI of Hepatic Adenomatosis: Initial Observations with Gadoxetic Acid Contrast Agent in Three Patients Am. J. Roentgenol., May 1, 2008; 190(5): W290 - W293. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Svrcek, E. Jeannot, L. Arrive, R. Poupon, G. Fromont, J.-F. Flejou, J. Zucman-Rossi, P. Bouchard, and D. Wendum Regressive liver adenomatosis following androgenic progestin therapy withdrawal: a case report with a 10-year follow-up and a molecular analysis Eur. J. Endocrinol., June 1, 2007; 156(6): 617 - 621. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Lewin, A. Handra-Luca, L. Arrive, D. Wendum, V. Paradis, E. Bridel, J.-F. Flejou, J. Belghiti, J.-M. Tubiana, and V. Vilgrain Liver Adenomatosis: Classification of MR Imaging Features and Comparison with Pathologic Findings Radiology, November 1, 2006; 241(2): 433 - 440. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Grazioli, G. Morana, M. A. Kirchin, and G. Schneider Accurate Differentiation of Focal Nodular Hyperplasia from Hepatic Adenoma at Gadobenate Dimeglumine-enhanced MR Imaging: Prospective Study Radiology, July 1, 2005; 236(1): 166 - 177. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. V. Sahani and S. P. Kalva Imaging the Liver Oncologist, July 1, 2004; 9(4): 385 - 397. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Reznik, T. Dao, R. Coutant, L. Chiche, E. Jeannot, S. Clauin, P. Rousselot, M. Fabre, F. Oberti, A. Fatome, et al. Hepatocyte Nuclear Factor-1{alpha} Gene Inactivation: Cosegregation between Liver Adenomatosis and Diabetes Phenotypes in Two Maturity-Onset Diabetes of the Young (MODY)3 Families J. Clin. Endocrinol. Metab., March 1, 2004; 89(3): 1476 - 1480. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. Vilgrain, F. Uzan, G. Brancatelli, M. P. Federle, M. Zappa, and Y. Menu Prevalence of Hepatic Hemangioma in Patients with Focal Nodular Hyperplasia: MR Imaging Analysis Radiology, October 1, 2003; 229(1): 75 - 79. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Brancatelli, M. P. Federle, L. Grazioli, R. Golfieri, and R. Lencioni Benign Regenerative Nodules in Budd-Chiari Syndrome and Other Vascular Disorders of the Liver: Radiologic-Pathologic and Clinical Correlation RadioGraphics, July 1, 2002; 22(4): 847 - 862. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Grazioli, M. P. Federle, G. Brancatelli, T. Ichikawa, L. Olivetti, and A. Blachar Hepatic Adenomas: Imaging and Pathologic Findings RadioGraphics, July 1, 2001; 21(4): 877 - 892. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. D. Levy and P. R. Ros Invited Commentary RadioGraphics, July 1, 2001; 21(4): 892 - 894. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| RADIOLOGY | RADIOGRAPHICS | RSNA JOURNALS ONLINE |
