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Focal Nodular Hyperplasia (focal + nodular_hyperplasia)
Selected AbstractsMolecular characterization of the vascular features of focal nodular hyperplasia and hepatocellular adenoma: A role for angiopoietin-1,HEPATOLOGY, Issue 2 2010Annette S. H. Gouw Focal nodular hyperplasia (FNH) and hepatocellular adenoma (HCA) are two hepatic nodular lesions of different etiologies. FNH, a polyclonal lesion, is assumed to be a regenerative reaction following a vascular injury, whereas HCA is a monoclonal, benign neoplastic lesion. In addition to features that are predominantly found in either FNH or HCA (e.g., dystrophic vessels in FNH and single arteries in HCA), FNH and HCA share morphological vascular abnormalities such as dilated sinusoids. We hypothesized that these anomalous vascular features are associated with altered expression of growth factors involved in vascular remodeling. This was based on reports of morphologically abnormal hepatic vasculature and nodular lesions in transgenic models of hepatocytic overexpression of angiopoietin-1 (Ang-1), a member of the angiopoietin family, which is crucially involved in vascular morphogenesis and homeostasis. We investigated gene and protein expression of members of the angiopoietin system and vascular endothelial growth factor A (VEGF-A) and its receptors in 9 FNH samples, 13 HCA samples, and 9 histologically normal livers. In comparison with normal samples, a significant increase in Ang-1 was found in FNH (P < 0.01) and HCA (P < 0.05), whereas no significant changes in Ang-2, receptor tyrosine kinase with immunoglobulin-like and EGF-like domains 2, VEGF-A, or vascular endothelial growth factor receptor 2 (VEGFR-2) were observed. Conclusion: Because of the different etiological contexts of a preceding vascular injury in FNH and a neoplastic growth in HCA, Ang-1 might exert different effects on the vasculature in these lesions. In FNH, it could predominantly stimulate recruitment of myofibroblasts and result in dystrophic vessels, whereas in HCA, it may drive vascular remodeling that produces enlarged vessels and arterial sprouting that generates single arteries. Hepatology 2010 [source] Focal nodular hyperplasia: what are the indications for resection?HPB, Issue 4 2005Li Chun Hsee Focal nodular hyperplasia (FNH) is a benign condition of the liver that is often discovered incidentally on radiological investigation. FNH has no malignant potential, is rarely symptomatic and surgical intervention is almost never required. However, eight patients with a diagnosis of FNH associated with upper abdominal pain or rapid growth were referred for surgery. All patients had been extensively investigated for other causes of pain and had been observed for between 1 and 7 years prior to surgical referral. The FNH lesions were between 1 cm and 8 cm in diameter. One FNH lesion 7.5 cm in diameter lay in segment VII/VIII and was related to the right and middle hepatic veins. All patients were resected with immediate and lasting control of their symptoms. Based on this experience FNH should be managed in a manner similar to haemangiomas with most lesions being safe to observe. However, it should be recognized that symptomatic FNH does occur, as well as FNH behaving in an unusual fashion such as rapid growth. Both of these findings are indications for resection. [source] Focal nodular hyperplasia treated by Transcatheter arterial embolization using Lipiodol mixed with Gelfoam particlesJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 7 2001Shuda K No abstract is available for this article. [source] Focal nodular hyperplasia of the liver: Controversy over etiologyJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 11 2000Fukuo Kondo No abstract is available for this article. [source] Focal nodular hyperplasia: Central scar enhancement pattern using gadoxetate disodiumJOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 2 2010Adib R. Karam MD Abstract Purpose: To illustrate the unusual enhancement pattern of the focal nodular hyperplasia central scar using Gadoxetate Disodium. Materials and Methods: Over a 10-month period, six patients, with a total of seven focal nodular hyperplasia lesions with typical central scar, had MRI of the liver using Gadoxetate Disodium (Eovist, Bayer HealthCare Pharmaceuticals Inc., Wayne, NJ). Four of the six patients had a prior Gadobenate Dimeglumine (Multihance, Bracco Diagnostics Inc., Princeton, NJ) -enhanced MRI of the liver performed within the previous year. The dynamic enhancement pattern of the central scar on the 10 liver MRIs was independently analyzed by two abdominal imaging radiologists who were blinded to the contrast agent used. Results: On the Gadoxetate Disodium-enhanced MRIs and during the arterial phase, 1-min, 2-min, and 3-min delay, none of the central scars demonstrated enhancement. However, all four of the lesions that were previously scanned using Gadobenate Dimeglumine demonstrated typical enhancement after a 3-min delay. Conclusion: On Gadoxetate Disodium-enhanced MRIs of the liver, the central scar of focal nodular hyperplasia lesions does not typically demonstrate delayed enhancement. J. Magn. Reson. Imaging 2010;32:341,344. © 2010 Wiley-Liss, Inc. [source] Analysis of somatic APC mutations in rare extracolonic tumors of patients with familial adenomatous polyposis coliGENES, CHROMOSOMES AND CANCER, Issue 2 2004Hendrik Bläker Patients with familial adenomatous polyposis coli (FAP) carry heterozygous mutations of the APC gene. At a young age, these patients develop multiple colorectal adenomas that consistently display a second somatic mutation in the remaining APC wild-type allele. Inactivation of APC leads to impaired degradation of ,-catenin, thereby promoting continuous cell-cycle progression. The role of APC inactivation in rare extracolonic tumors of FAP patients has not been characterized sufficiently. Among tissue specimen from 174 patients with known APC germ-line mutations, we identified 8 tumors infrequently seen in FAP. To investigate the pathogenic role of APC pathway deregulation in these lesions, they were analyzed for second-hit somatic mutations in the mutational cluster region of the APC gene. Immunohistochemistry was performed to compare the expression pattern of ,-catenin to the mutational status of the APC gene. Exon 3 of the ,-catenin gene (CTNNB1) was analyzed for activating mutations to investigate alternative mechanisms of elevated ,-catenin concentration. Although CTNNB1 mutations were not observed, second somatic APC mutations were found in 4 of the 8 tumors: a uterine adenocarcinoma, a hepatocellular adenoma, an adrenocortical adenoma, and an epidermal cyst. These tumors showed an elevated concentration of ,-catenin. No APC mutations were seen in focal nodular hyperplasia of the liver, angiofibrolipoma, and seborrheic wart. This is the first study reporting second somatic APC mutations in FAP-associated uterine adenocarcinoma and epidermal cysts. Furthermore, our data strengthen a role for impaired APC function in the pathogenesis of adrenal and hepatic neoplasms in FAP patients. © 2004 Wiley-Liss, Inc. [source] Molecular characterization of the vascular features of focal nodular hyperplasia and hepatocellular adenoma: A role for angiopoietin-1,HEPATOLOGY, Issue 2 2010Annette S. H. Gouw Focal nodular hyperplasia (FNH) and hepatocellular adenoma (HCA) are two hepatic nodular lesions of different etiologies. FNH, a polyclonal lesion, is assumed to be a regenerative reaction following a vascular injury, whereas HCA is a monoclonal, benign neoplastic lesion. In addition to features that are predominantly found in either FNH or HCA (e.g., dystrophic vessels in FNH and single arteries in HCA), FNH and HCA share morphological vascular abnormalities such as dilated sinusoids. We hypothesized that these anomalous vascular features are associated with altered expression of growth factors involved in vascular remodeling. This was based on reports of morphologically abnormal hepatic vasculature and nodular lesions in transgenic models of hepatocytic overexpression of angiopoietin-1 (Ang-1), a member of the angiopoietin family, which is crucially involved in vascular morphogenesis and homeostasis. We investigated gene and protein expression of members of the angiopoietin system and vascular endothelial growth factor A (VEGF-A) and its receptors in 9 FNH samples, 13 HCA samples, and 9 histologically normal livers. In comparison with normal samples, a significant increase in Ang-1 was found in FNH (P < 0.01) and HCA (P < 0.05), whereas no significant changes in Ang-2, receptor tyrosine kinase with immunoglobulin-like and EGF-like domains 2, VEGF-A, or vascular endothelial growth factor receptor 2 (VEGFR-2) were observed. Conclusion: Because of the different etiological contexts of a preceding vascular injury in FNH and a neoplastic growth in HCA, Ang-1 might exert different effects on the vasculature in these lesions. In FNH, it could predominantly stimulate recruitment of myofibroblasts and result in dystrophic vessels, whereas in HCA, it may drive vascular remodeling that produces enlarged vessels and arterial sprouting that generates single arteries. Hepatology 2010 [source] Diagnosis of hepatic nodules 20 mm or smaller in cirrhosis: Prospective validation of the noninvasive diagnostic criteria for hepatocellular carcinoma,HEPATOLOGY, Issue 1 2008Alejandro Forner This study prospectively evaluates the accuracy of contrast-enhanced ultrasound (CEUS) and dynamic magnetic resonance imaging (MRI) for the diagnosis of nodules 20 mm or smaller detected during ultrasound (US) surveillance. We included 89 patients with cirrhosis [median age, 65 years; male 53, hepatitis C virus 68, Child-Pugh A 80] without prior hepatocellular carcinoma (HCC) in whom US detected a small solitary nodule (mean diameter, 14 mm). Hepatic MRI, CEUS, and fine-needle biopsy (gold standard) (FNB) were performed at baseline. Non-HCC cases were followed (median 23 months) by CEUS/3 months and MRI/6 months. FNB was repeated up to 3 times and on detection of change in aspect/size. Intense arterial contrast uptake followed by washout in the delayed/venous phase was registered as conclusive for HCC. Final diagnoses were: HCC (n = 60), cholangiocarcinoma (n = 1), and benign lesions (regenerative/dysplastic nodule, hemangioma, focal nodular hyperplasia) (n = 28). Sex, cirrhosis cause, liver function, and alpha-fetoprotein (AFP) levels were similar between HCC and non-HCC groups. HCC patients were older and their nodules significantly larger (P < 0.0001). First biopsy was positive in 42 of 60 HCC patients. Sensitivity, specificity, and positive and negative predictive values of conclusive profile were 61.7%, 96.6%, 97.4%, and 54.9%, for MRI, 51.7%, 93.1%, 93.9%, and 50.9%, for CEUS. Values for coincidental conclusive findings in both techniques were 33.3%, 100%, 100%, and 42%. Thus, diagnosis of HCC 20 mm or smaller can be established without a positive biopsy if both CEUS and MRI are conclusive. However, sensitivity of these noninvasive criteria is 33% and, as occurs with biopsy, absence of a conclusive pattern does not rule out malignancy. These results validate the American Association for the Study of Liver Disease (AASLD) guidelines. (HEPATOLOGY 2007.) [source] Case report of a focal nodular hyperplasia-like nodule present in cirrhotic liverHEPATOLOGY RESEARCH, Issue 5 2008Sho Takahashi An 81-year-old female was referred to Sapporo Medical University Hospital because of a nodular lesion 20 mm in diameter found in the liver S8 during follow-up for type C liver cirrhosis. Abdominal ultrasonography showed a capsule-like structure, and contrast computed tomography revealed hypervascularity at the early phase and inner pooling of the contrast medium with ring enhancement at the late phase. Magnetic resonance T2-weighted imaging (T2WI) demonstrated a hyperintensity nodule with further hyperintensity signals in some parts of the nodule, and the signal pattern differed from that of typical fibrosis. SPIO-magnetic resonance imaging showed partial hypointensity signals by T2WI, which indicated the presence of Kupffer cells. Angiography did not show a spoke-wheel pattern. The results by imaging modalities indicated that the nodule was atypical for hepatocellular carcinoma (HCC) and focal nodular hyperplasia (FNH), and liver nodule biopsy was performed for histological diagnosis. Compared with the background liver, the nodule revealed high cellular density, cellular dysplasia at the periphery, a pseudo-crypt structure and irregular hepatic cord arrangement in some parts of the nodule. Among them, there was immature fibrous tissue containing arterioles with muscular hypertrophy. There has been no report of well-differentiated HCC with a central scar, and this case was presumed to be an FNH-like nodule with dysplasia physically associated with cirrhotic tissue. [source] Natural course of hepatic focal nodular hyperplasia: A long-term follow-up study with sonographyJOURNAL OF CLINICAL ULTRASOUND, Issue 3 2009Yuan-Hung Kuo MD Abstract Purpose. We aimed to investigate the natural course of hepatic focal nodular hyperplasia (FNH) in a long-term follow-up study with sonography. Method. This study comprised 30 patients (24 women and 6 men) with 34 FNHs. Diagnosis of FNH was made using color Doppler sonography, contrast-enhanced CT, or MRI in combination with needle biopsy. Patients were followed every 3 to 6 months with sonography. Regression or progression of tumor was defined as a change of over 30% in maximal diameter. Disappearance was defined as no vizualization of the tumor on at least 3 follow-up sonographic examinations. Results. Thirty-four FNHs were followed over a mean period of 42 months (range, 7,95 months). Twenty-four lesions (70.6%) were stable in size, 1 (2.9%) progressed, and 9 (26.5%) regressed. Of those that regressed, 6 (17.6%) disappeared over a mean period of 59 ± 30 months (range, 20,95 months). Older age (OR 1.26, 95% CI 1.02,1.56; p < 0.05) and longer follow-up time (OR 1.11, 95% CI 1.01,1.21; p < 0.05) were the independent factors associated with complete regression of FNH. Conclusion. Most FNHs were stable or regressed/disappeared after a long follow-up period. Based on the benign course, conservative treatment for asymptomatic FNH should be advocated. © 2008 Wiley Periodicals, Inc. J Clin Ultrasound 2009. [source] Is there a common cause of adenoma, focal nodular hyperplasia, and hemangioma of the liver?JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 4 2003FUKUO KONDO No abstract is available for this article. [source] Focal nodular hyperplasia-like lesion of the liver in a child previously treated for nephroblastomaPATHOLOGY INTERNATIONAL, Issue 9 2008Junji Takeyama Described herein is the case of an 8-year-old boy who developed a hepatic nodular lesion after having received anti-neoplastic therapy for nephroblastoma. Histological examination of the excised specimen indicated a disordered arrangement of hepatic components with hemangioma-like features. This case was diagnosed as a variant of focal nodular hyperplasia. It is speculated that this hepatic lesion is a late complication of treatment for nephroblastoma and might develop from congenital malformative area of the liver. [source] Diagnostic and pathogenetic implications of the expression of hepatic transporters in focal lesions occurring in normal liverTHE JOURNAL OF PATHOLOGY, Issue 4 2005Sara Vander Borght Abstract Hepatocellular adenoma and focal nodular hyperplasia (FNH) are benign liver tumours. The differential diagnosis of these lesions and of well- to moderately differentiated hepatocellular carcinomas is often difficult but is very important in view of their different treatment. Although neither type of lesion is connected to the biliary tree, FNHs are cholestatic, whereas this is rarely the case for hepatocellular adenomas. This suggests that hepatocellular uptake and secretion of bile constituents is different in FNHs compared to adenomas. We therefore evaluated the expression and localization of hepatic transporters in hepatocellular adenomas, different types of FNH and well- to moderately differentiated hepatocellular carcinomas in non-cirrhotic liver and compared them with normal liver, using real-time RT-PCR and (semi-)quantitative immunohistochemistry. The parenchymal expression of the uptake transporter OATP2/8 (OATP1B1/3) was minimal or absent in adenoma, while there was strong and diffuse expression in FNH. We observed diffuse parenchymal expression of the basolateral export pump MRP3 in adenomas, while only reactive bile ductules and adjacent cholestatic hepatocytes were MRP3-positive in FNH. The MRP3/OATP2/8 expression pattern of atypical FNHs resembled that of adenomas, suggesting that both types of lesion are related. Most hepatocellular carcinomas showed decreased expression of one or more of the canalicular transporters (MDR1, MDR3, BSEP). The differences in transporter expression profile between FNHs and adenomas are most likely pathogenetically important and may explain why only FNHs are cholestatic. The finding that each type of focal lesion in non-cirrhotic liver has a specific transporter expression pattern may be useful in the establishment of a correct diagnosis by imaging or on needle biopsy. Copyright © 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source] Congenital absence of the portal vein,Case report and a review of literatureCLINICAL ANATOMY, Issue 7 2010Jana Mistinova Abstract Congenital absence of the portal vein (CAPV) is a rare anomaly in which the intestinal and the splenic venous drainage bypass the liver and drain into systemic veins through various venous shunts. To our knowledge, we have reviewed all 83 cases of CAPV, since first described in 1793. This equates to a rate of almost 2.5 cases per year over the last 30 years. Morgan and Superina (1994, J. Pediatr. Surg. 29:1239,1241) proposed the following classification of portosystemic anomalies; either the liver is not perfused with portal blood because of a complete shunt (Type I) or the liver is perfused with portal blood due to the presence of a partial shunt (Type II). In our case, abdominal venous blood drained into the suprarenal inferior vena cava via the left renal vein and dilated left gastric veins. After analyzing all reported cases, we recognize that more than 65% of patients are females and more than 30% of all published cases had been diagnosed by the age of 5 years. Additional anomalies are common in CAPV. In the reported cases, more then 22% of patients had congenital heart disease. Other commonly found anomalies include abnormalities of the spleen, urinary and male genital tract, brain as well as skeletal anomalies. Hepatic changes such as focal nodular hyperplasia, hepatocellular carcinoma, and hepatoblastoma are diagnosed in more then 40% of patients. This article also illustrates the radiological findings of CAPV. Radiological evaluation by ultrasound, CT, and MRI is helpful to detect coexisting abnormalities. Clin. Anat. 23:750,758, 2010. © 2010 Wiley-Liss, Inc. [source] Telangiectatic adenoma: An entity associated with increased body mass index and inflammation,HEPATOLOGY, Issue 1 2007Valérie Paradis What were previously called telangiectatic focal nodular hyperplasias are in fact true adenomas with telangiectatic features (TAs) without overt characterized genetic abnormalities. The aim of our study was to review a surgical series of TAs in order to describe clinical, biological, and radiological findings of these lesions and to evaluate their outcomes. From January 1996 to November 2005, 284 patients with benign hepatocellular nodules underwent surgical resection at Beaujon Hospital. Among them, 32 TAs from 27 patients were diagnosed. Ninety-two percent of the patients were women. Mean age was 38 years (range 17,63). Mean body mass index was 28 (range 18,49), with 16 patients being overweight. Symptoms revealed lesions in 10 patients. In 13 patients, TA was associated with another benign liver lesion. Mean size of the TAs was 5 cm (range 1,17 cm). Histological analysis showed cellular atypias in 6 cases (19%), steatosis in 17 cases (53%), vascular changes in 19 cases (59%), and significant inflammatory infiltrate in 29 cases (91%). In 1 case, the TA had foci of well-differentiated hepatocellular carcinoma. In 18 of the 26 cases (69%), adjacent liver showed significant steatosis. Serum biomarkers of inflammation were increased in 90% of patients (19 of 22). After surgical resection, inflammatory marker levels returned to normal values in all patients tested. Conclusion: This study has shown that TAs occur in a characteristic background of overweight patients and are often associated with a biological inflammatory syndrome. Moreover, a TA may progress to malignancy. (HEPATOLOGY 2007;46:140,146.) [source] Resovist enhanced MR imaging of the liver: Does quantitative assessment help in focal lesion classification and characterization?JOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 5 2009Lucia Santoro MD Abstract Purpose: To improve characterization of focal liver lesions by a prospective quantitative analysis of percentage signal intensity change, in dynamic and late phases after slow (0.5 mL/s) Resovist administration. Materials and Methods: Seventy-three patients were submitted on clinical indication to MR examination with Resovist. Signal intensity of 92 detected focal lesions (5,80 mm) were measured with regions of interest and normalized to paravertebral muscle in arterial, portal, equilibrium and T1/T2 late phases, by two observers in conference. Five values of percentage variations per patient were obtained and statistically evaluated. Results: The enhancement obtained on dynamic study is more suitable in hemangiomas and focal nodular hyperplasias than in adenomas and hepatocellular carcinomas. To discriminate benign versus malignant lesions on late-phase-T2-weighted images, a cutoff = ,26%, allowed sensitivity and specificity values of 97.4% and 97.7%, respectively. Area under the receiver operating characteristic (ROC) curve was 0.99. To differentiate hemangioma versus all other focal liver lesions, on late-phase-T1-weighted images, a cutoff = +40% permitted sensitivity and specificity values of 90.5% and 98.0%, respectively. Area under the ROC curve was 0.98. Conclusion: Late phase quantitative evaluation after slow Resovist administration, allows to differentiate malignant from benign hepatic masses and hemangiomas from all the others focal liver lesions, on T2-/T1-weighted acquisitions, respectively. J. Magn. Reson. Imaging 2009;30:1012,1020. © 2009 Wiley-Liss, Inc. [source] |