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[肝细胞结节性增生、腺瘤和癌]

[Hepatocellular nodular hyperplasias, adenomas and carcinomas].

作者信息

Altmann H W

机构信息

Pathologisches Institut, Universität Würzburg.

出版信息

Verh Dtsch Ges Pathol. 1995;79:84-108.

PMID:8600698
Abstract

Nodular hyperplasias ("hyperplasiomas") are new formations whose development as a required and regulated response can be traced either to compensatory reactions to the loss of cells (regeneration in a narrow sense) and to decreased cellular performance, or to primary growth impulses. Included in this group are: the "macroregenerative nodules" after extensive cell losses; solitary nodules of uncertain etiology; and the minute foci of "micronodular transformation" whose origin can be traced to a particular disturbance of the hepatic blood supply. The so-called "adenomatous hyperplasias" of the cirrhotic liver that have a tendency towards carcinomatous change are not included in this group and are perhaps better considered as "hyperplasiogenic adenomas". The so-called "focal nodular hyperplasia" too, it must be stressed, should be separated from the simple hyperplasias, for it is more closely related to the adenomas, but represents a new formation of limited growth potential. Morphologically it is conspicuously subdivided by multiple connective tissue bands and scars, but it is above all characterized by metaplastically derived neoductuli, and hence it is appropriately designated as a "combined nodule". Among the true uninodular adenomas there are several variants differing in their morphology,--the so-called "atypical" or "intermediate" forms, that can give rise to carcinomas. The hepatocellular carcinoma, that may arise in a variety of ways, presents multiple cytological and histological variants, but only the so-called "fibrolamellar carcinoma" presents also a clinical peculiarity. "Hepatoblastomas" differ from the common hepatocellular carcinomas by their origin in early childhood from immature early precursor cells and, in the later phases of life, from redifferentiated cells that can even give rise to mesenchymal elements. There is no evidence of the existence of particular pluripotential stem cells.

摘要

结节性增生(“增生瘤”)是新形成的组织,其作为一种必要且受调控的反应而发展,要么可追溯到对细胞丢失的代偿反应(狭义的再生)和细胞功能下降,要么可追溯到原发性生长冲动。这一组包括:广泛细胞丢失后的“大再生结节”;病因不明的孤立结节;以及“微结节转化”的微小病灶,其起源可追溯到肝脏血液供应的特定紊乱。肝硬化肝脏中具有癌变倾向的所谓“腺瘤样增生”不包括在这一组中,或许更好地应被视为“增生性腺瘤”。必须强调的是,所谓的“局灶性结节性增生”也应与单纯增生区分开来,因为它与腺瘤关系更密切,但代表一种生长潜力有限的新形成组织。从形态学上看,它明显被多条结缔组织带和瘢痕分割,但首先其特征是化生衍生的新小胆管,因此它被恰当地称为“复合结节”。在真正的单结节腺瘤中,有几种形态不同的变体,即所谓的“非典型”或“中间”形式,它们可引发癌变。肝细胞癌可能以多种方式出现,呈现多种细胞学和组织学变体,但只有所谓的“纤维板层癌”也具有临床特殊性。“肝母细胞瘤”与常见的肝细胞癌不同,其起源于儿童早期的未成熟早期前体细胞,在生命后期起源于甚至可产生间充质成分的再分化细胞。没有证据表明存在特定的多能干细胞。

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