Roux D, Bioulac-Sage P, Merlio J P, Lamouliatte H, Quinton A, Balabaud C
Laboratoire des Interactions Cellulaires, Université de Bordeaux II, France.
J Clin Gastroenterol. 1987 Aug;9(4):483-7. doi: 10.1097/00004836-198708000-00027.
The origin of sinusoidal portal hypertension often remains unknown in patients with agnogenic myeloid metaplasia. Four consecutive patients with agnogenic myeloid metaplasia had liver biopsies examined under light and electron microscopy. Two of the four had obvious clinical portal hypertension; of these two, only one had portal vein thrombosis. All four cases showed sinusoidal infiltration by myeloid cells (from very mild to obvious) and an increased perisinusoidal collagen network. Under electron microscopy we observed (a) the collagenization of the Disse space, (b) myeloid cells in the lumen and the Disse space, (c) the transformation of perisinusoidal cells into transitional cells, and (d) fragments of basement membrane-like material. It is possible that all these abnormalities, and not only sinusoidal infiltration, contribute to increase vascular resistance, even when there is no clinical evidence of portal hypertension unrelated to vascular thrombosis.
特发性骨髓化生患者的窦性门静脉高压的病因常常不明。连续4例特发性骨髓化生患者接受了肝脏活检,并进行了光镜和电镜检查。4例中有2例有明显的临床门静脉高压;在这2例中,只有1例有门静脉血栓形成。所有4例均显示髓样细胞的窦性浸润(从非常轻微到明显)以及窦周胶原网络增加。在电子显微镜下,我们观察到(a)狄氏间隙的胶原化,(b)管腔和狄氏间隙中的髓样细胞,(c)窦周细胞转化为过渡细胞,以及(d)基底膜样物质碎片。即使没有与血管血栓形成无关的门静脉高压的临床证据,所有这些异常,而不仅仅是窦性浸润,都有可能导致血管阻力增加。