ETIOLOGIC ANALYSIS OF FOCAL NODULAR HYPERPLASIA OF THE LIVER, WITH EMPHASIS ON SIMILAR ABNORMAL VASCULATURES TO NODULAR REGENERATIVE HYPERPLASIA AND IDIOPATHIC PORTAL-HYPERTENSION

Citation
F. Kondo et al., ETIOLOGIC ANALYSIS OF FOCAL NODULAR HYPERPLASIA OF THE LIVER, WITH EMPHASIS ON SIMILAR ABNORMAL VASCULATURES TO NODULAR REGENERATIVE HYPERPLASIA AND IDIOPATHIC PORTAL-HYPERTENSION, Pathology research and practice, 194(7), 1998, pp. 487-495
Citations number
34
Categorie Soggetti
Pathology
ISSN journal
03440338
Volume
194
Issue
7
Year of publication
1998
Pages
487 - 495
Database
ISI
SICI code
0344-0338(1998)194:7<487:EAOFNH>2.0.ZU;2-0
Abstract
Pathological studies were performed on 23 cases of focal nodular hyper plasia (FNH) under the hypothesis that FNH is a hyperplastic lesion ca used by abnormal vasculatures of portal tracts within the nodule. For a comparison of the histological features of portal tracts, nodular re generative hyperplasia (NRH), idiopathic portal hypertension (IPH), ch ronic hepatitis and so-called normal liver were used as control tissue s. Extranodular areas of FNH modules were also examined. Clinical data were briefly summarized. Most of the portal tracts within FNH nodules showed various abnormal findings, such as dilatation and/or stenosis of portal vein, muscular thickening of arterial wall with dilated or s tenotic lumina, lymphocyte infiltration, and bile ductule proliferatio n. However, portal vein thrombi were not found. These findings were no t thought to represent compensatory reaction to portal vein thrombosis . Similar abnormal features were also observed in extranodular areas o f FNH although to a milder degree. These abnormal features resembled t hose of NRH and IPH. Moreover, the characteristic scar-like tissues wi thin FNH nodules were proved to be abnormally large portal tracts incl uding large feeding arteries, portal veins and bile ducts.It has been believed that septa and scar-like tissue within FNH nodules are not po rtal tracts and that arterial malformation independent of portal tract s are related to the development of FNH. In addition, venous structure s within FNH modules have until now not been considered to be portal v eins. However, this study revealed that severe anomaly of portal tract s including portal veins and hepatic arterial branches existed in FNH nodules. Moreover, portal tracts in extranodular areas were also abnor mal. Clinically, only one patient had a history of oral contraceptives . Based on these findings, congenital anomaly of the portal tracts his tologically resembling the abnormal portal tracts of NRH and IPH may b e related to the pathogenesis of FNH.