Kondo F, Nagao T, Sato T, Tomizawa M, Kondo Y, Matsuzaki O, Wada K, Wakatsuki S, Nagao K, Tsubouchi H, Kobayashi H, Yasumi K, Tsukayama C, Suzuki M
Department of Pathology, Chiba University School of Medicine, Japan.
Pathol Res Pract. 1998;194(7):487-95. doi: 10.1016/S0344-0338(98)80117-9.
Pathological studies were performed on 23 cases of focal nodular hyperplasia (FNH) under the hypothesis that FNH is a hyperplastic lesion caused by abnormal vasculatures of portal tracts within the nodule. For a comparison of the histological features of portal tracts, nodular regenerative hyperplasia (NRH), idiopathic portal hypertension (IPH), chronic hepatitis and so-called normal liver were used as control tissues. Extranodular areas of FNH nodules 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 stenotic lumina, lymphocyte infiltration, and bile ductule proliferation. However, portal vein thrombi were not found. These findings were not thought to represent compensatory reaction to portal vein thrombosis. Similar abnormal features were also observed in extranodular areas of FNH although to a milder degree. These abnormal features resembled those of NRH and IPH. Moreover, the characteristic scar-like tissues within FNH nodules were proved to be abnormally large portal tracts including large feeding arteries, portal veins and bile ducts. It has been believed that septa and scar-like tissue within FNH nodules are not portal tracts and that arterial malformation independent of portal tracts are related to the development of FNH. In addition, venous structures within FNH modules have until now not been considered to be portal veins. However, this study revealed that severe anomaly of portal tracts including portal veins and hepatic arterial branches existed in FNH nodules. Moreover, portal tracts in extranodular areas were also abnormal. Clinically, only one patient had a history of oral contraceptives. Based on these findings, congenital anomaly of the portal tracts histologically resembling the abnormal portal tracts of NRH and IPH may be related to the pathogenesis of FNH.
在局灶性结节性增生（FNH）是由结节内门静脉分支异常血管导致的增生性病变这一假设下，对23例FNH进行了病理研究。为比较门静脉分支的组织学特征，将结节性再生性增生（NRH）、特发性门静脉高压（IPH）、慢性肝炎及所谓的正常肝脏作为对照组织。还检查了FNH结节的结节外区域。简要总结了临床资料。FNH结节内的大多数门静脉分支显示出各种异常表现，如门静脉扩张和/或狭窄、动脉壁肌肉增厚伴管腔扩张或狭窄、淋巴细胞浸润以及胆小管增生。然而，未发现门静脉血栓。这些表现不被认为是对门静脉血栓形成的代偿反应。在FNH的结节外区域也观察到类似的异常特征，不过程度较轻。这些异常特征类似于NRH和IPH。此外，FNH结节内特征性的瘢痕样组织被证实是异常增大的门静脉分支，包括粗大的供血动脉、门静脉和胆管。一直以来人们认为FNH结节内的间隔和瘢痕样组织不是门静脉分支，且与门静脉分支无关的动脉畸形与FNH的发生有关。此外，FNH结节内的静脉结构至今未被认为是门静脉。然而，本研究显示FNH结节内存在包括门静脉和肝动脉分支在内的门静脉分支严重异常。而且，结节外区域的门静脉分支也不正常。临床上，只有一名患者有口服避孕药史。基于这些发现，组织学上类似于NRH和IPH异常门静脉分支的门静脉分支先天性异常可能与FNH的发病机制有关。
