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We report our experience of the simultaneous occurrence of adenoma and focal nodular hyperplasia (FNH). Liver cell adenoma together with FNH was found in five out of 30 cases of "multiple benign hepatocytic nodules" collected in our files of the Department of Pathology of the University Hospital of Bordeaux, during the last 12 years. All five cases were women on oral contraceptives. In all cases, the reason for surgery was the discovery, by imaging techniques, of an adenoma (4 cases) or of an unidentified benign tumor, possibly an adenoma. Four cases of FNH were discovered by imaging techniques, prior to surgery. Additional small nodules were diagnosed either during surgery or during the slicing of the specimen in 3 cases. Adenoma and the FNH cases identified by imaging techniques were confirmed as such by light microscopy. Some small nodules could not be categorized with certainty because they contained biliary structures without ductular reaction. In one case, the non-nodular liver was abnormal around the area in which there were multiple nodules: there was approximation of portal tracts with portal and hepatic venous thromboses, and portal tract remnants with arteries surrounded with a rim of fibrosis. In two cases, some large hepatic veins had thickened walls. The association of FNH and adenoma could be coincidental or secondary to shared causal mechanisms: a) systemic and local angiogenic abnormalities induced by oral contraceptives; b) tumor-induced growth factors; c) thrombosis and local arterio-venous shunting. A better recognition of the association of adenoma and FNH, particularly in the context of multiple nodules, could be useful in clinical practice.

The typical lesion of focal nodular hyperplasia (FNH) is a benign tumor-like mass characterized by hepatocytic nodules separated by fibrous bands. The solitary central artery with high flow and the absent portal vein give the lesions their characteristic radiological appearance. The great majority of cases seen in daily practice conform to the above description. Additional small nodules (from 1-2 up to 15-20 mm in diameter) detected by imaging techniques or on macroscopic examination may be difficult to identify as representing FNH if they lack the key features of FNH as defined in larger lesions. The aim of this study was to characterize these small nodules, and to compare their characteristics with those of typical lesions of FNH present in the same specimens. Eight patients underwent hepatic resections for the removal of a mass lesion ("nodule") diagnosed as: FNH (1 patient); nodules of unknown nature (5 patients); or nodules thought to be adenoma or hepatocellular carcinoma (2 patients). Six nodules out of 9 discovered by imaging techniques met histopathological criteria for the diagnosis of typical FNH, at least in parts of the nodule; 2 nodules corresponded to a minor form of FNH ("subtle FNH") and one nodule to a steatotic area. Although FNH was thought to be found in a normal or nearly normal liver, this study revealed that, in addition, there were various types of small FNH-like nodules and vascular abnormalities in the liver with typical FNH nodule. The various types of small FNH-like nodules (n = 8, diameter 2 to 20 mm) consisted of the association to various degrees of numerous and/or enlarged arteries in portal tracts or in septa, with hyperplastic foci, slight ductular reaction, and regions of sinusoidal dilatation, accompanied by thin fibrous bands. Vascular abnormalities consisted of unpaired arteries, portal tracts with arteries larger than the associated bile duct, and regions of sinusoidal dilatation. Although these small nodules can be considered as insufficient type or abortive forms of FNH, or adenoma, they can be precursors of the large mass lesions in which FNH was recognized and defined.

Background In adult liver, the mesenchymal cells, portal fibroblasts and vascular smooth muscle cells can transdifferentiate into myofibroblasts, and are involved in portal fibrosis. Differential expression of markers, such as alpha-smooth muscle actin (ASMA), h-caldesmon and cellular retinol-binding protein-1 allows their phenotypic discrimination. The aim of our study was to explore the phenotypic evolution of the mesenchymal cells during fetal development in normal liver and in liver with portal fibrosis secondary to ductal plate malformation in a series of Meckel-Gruber syndrome, autosomal recessive polycystic kidney disease and Ivemark's syndrome. Results At the early steps of the portal tract maturation, portal mesenchymal cells expressed only ASMA. During the maturation process, these cells were found condensed around the biliary and vascular structures. At the end of maturation process, only cells around vessels expressed ASMA and cells of the artery tunica media also expressed h-caldesmon. In contrast, ASMA positive cells persisted around the abnormal biliary ducts in fibrous livers. Conclusion As in adult liver, there is a phenotypic heterogeneity of the mesenchymal cells during fetal liver development. During portal tract maturation, myofibroblastic cells disappear in normal development but persist in fibrosis following ductal plate malformation.