3). The nodule was slightly more whitish than the background liver. The border of the nodule was almost clear, but there was no

fibrous capsule. On histology, irregular sinusoidal dilatation and hemangioma-like dilated vessels around the portal tract-like area were seen (Fig. 3). Seliciclib There were no usual portal tracts with bile ducts in this nodular lesion (Fig. 3). Hepatocytes in the lesion showed a thickened cell layer and increased cellular density when compared with the background liver (Fig. 3). Focally, expanding growth into the background liver was seen (Fig. 3); however, there was no cellular atypia or loss of reticulin fibers around hepatic columns. The dilated sinusoid and vessels showed distinct immunoreactivity

for CD34 (Fig. 3). KU-60019 ic50 There were no abnormal thickened arteries or a central stellate scar. Immunostaining for SAA, GS and LFABP did not suggest any specific subtypes of a hepatocellular adenoma. Taken together, this nodular lesion was also diagnosed as hyperplastic hepatocellular lesion associated with localized hemangiomatosis. The background liver was almost normal. We surveyed the prevalence of similar hemangioma-like vessels in the background livers of 13 patients with hepatic cavernous hemangiomas. These hemangioma-like vessels appeared not to be continuous with cavernous hemangioma and it is not clear from what these vessels derived. Hemangioma-like vessels were seen in the background hepatic parenchyma in six patients

(46%) (Fig. 4). Immunoreactivity for CD34 was seen in endothelial cells lining sinusoids between hemangioma-like vessels in five patients: two to a moderate degree and three to a mild degree (Fig 4); however, hyperplastic hepatocellular lesions resembling the two nodules in the present cases were not observed in the background liver around hemangioma-like vessels in any patients. We reported unique hither-to unrecognized types of hyperplastic hepatocellular lesion associated with localized hemangiomatosis. The combination of dilated vessels and hyperplastic hepatocellular lesions resembled inflammatory hepatocellular adenoma, in which telangiectasia is frequently observed;[1] however, the immunoreactivity of SAA, a marker of inflammatory hepatocellular adenoma, was negative in the nodules. It is well this website known that FNH is usually associated with abnormal blood vessels such as unpaired arteries with a thickened wall and irregular capillarization of sinusoids showing CD34 expression.[1] Although findings of hyperplastic hepatocellular lesions and sinusoidal capillarization resembled FNH, abnormal unpaired arteries were not seen in the present nodules. Taken together, it is conceivable that the irregular blood flow due to hemangioma-like vessels may contribute to the formation of hyperplastic hepatocellular lesions, as well as FNH. Multiple hemangioma-like vessels were characteristically seen in the present nodules.