Two cases of local nodular hyperplasia (FNH), in which ultrasound (US), computed tomography (CT), and magnetic resonance imaging (MR) studies detected an atypical hemorrhagic pattern associated with an intrahepatic arterio venous malformation (AVM) around the growths, are presented. In both cases, histology demonstrated a very early regenerative stage - without central scar or fibrosis - and necrotichemorrhagic areas within the lesions. In these cases, the analysis of radiological findings, surgical specimens and histology seemed to confirm the pathogenetic hypothesis suggested by Wanless [1]: in normal liver parenchyma, a "blood steal" phenomenon due to congenital or acquired intrahepatic AVM - arterio portal or porto systemic shunt - could cause ischemic damaged, appering as a hemorrhagic necrotic area, the extent of which depends on the degree of residual portal supply (maintained in Case 1, and markedly reduced in Case 2 due to arterio portal shunting). The subsequent phase of repair could activate the regenerative-hyperplastic process, evolving into final fibrosis, which represents the "mature" pattern of FHN. © 1994 Springer-Verlag.
Golfieri, R., Giampalma, E., Berardi, R., Caputo, M., Lalli, A., Grazi, G., et al. (1994). Early-stage focal nodular hyperplasia: US/CT/MR features correlated with histology. EUROPEAN RADIOLOGY, 4(1), 65-70 [10.1007/BF00177391].
Early-stage focal nodular hyperplasia: US/CT/MR features correlated with histology
Golfieri R.;Giampalma E.;Mazziotti A.;Gozzetti G.;D'Errico A.;Grigioni W.;
1994
Abstract
Two cases of local nodular hyperplasia (FNH), in which ultrasound (US), computed tomography (CT), and magnetic resonance imaging (MR) studies detected an atypical hemorrhagic pattern associated with an intrahepatic arterio venous malformation (AVM) around the growths, are presented. In both cases, histology demonstrated a very early regenerative stage - without central scar or fibrosis - and necrotichemorrhagic areas within the lesions. In these cases, the analysis of radiological findings, surgical specimens and histology seemed to confirm the pathogenetic hypothesis suggested by Wanless [1]: in normal liver parenchyma, a "blood steal" phenomenon due to congenital or acquired intrahepatic AVM - arterio portal or porto systemic shunt - could cause ischemic damaged, appering as a hemorrhagic necrotic area, the extent of which depends on the degree of residual portal supply (maintained in Case 1, and markedly reduced in Case 2 due to arterio portal shunting). The subsequent phase of repair could activate the regenerative-hyperplastic process, evolving into final fibrosis, which represents the "mature" pattern of FHN. © 1994 Springer-Verlag.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
