Endometriotic disease: the role of peritoneal fluid
Endometriotic disease: the role of peritoneal fluid
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DOI：
10.1093/humupd/4.5.741
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发表时间：
1998-09-01
影响因子：
13.3
通讯作者：
Barlow, DH
中科院分区：
文献类型：
--
作者：
Koninckx, PR;Kennedy, SH;Barlow, DH
腹腔液和卵巢内环境是一个特殊的微环境。腹腔液主要起源于血管通透性增加引起的卵巢渗出产物，其体积和类固醇激素的周期性变化总是高于血浆中的水平，它含有大量的巨噬细胞及其分泌产物，并通过腹膜与血浆有较大的交换面积？扩散对小分子具有高度的渗透性，分子扩散几乎为零，分子质量为100000 Da。在黄素化未破裂卵泡(LUF)综合征患者中，黄体期雌激素和孕酮浓度要低得多。子宫内膜异位症与无菌低度炎症、激活的巨噬细胞及其许多分泌物浓度增加有关，如细胞因子、生长因子和血管生成因子。子宫内膜细胞局部分泌CA-125和糖蛋白，自然杀伤(NK)细胞功能下降，可能是由糖蛋白或局部细胞间黏附分子(ICAM)-1脱落介导的；卵巢也是一个特殊的微环境，卵泡中的类固醇激素浓度是血浆的1000倍；子宫内膜和浅着床细胞受腹腔液浓度的影响，因此，局部环境，而不是固有的细胞差异，可以解释浅表子宫内膜异位症与在位内膜之间的差异。因此，浅层种植体与子宫内膜异位症、深层浸润性或囊性卵巢子宫内膜异位症之间的差异可能通过不同的内分泌环境而产生。浅层子宫内膜植入受腹腔液因素的影响，而深层子宫内膜异位症和囊性卵巢子宫内膜异位症则受血液或卵巢因素的影响。子宫内膜异位症理论认为大多数女性的浅表异位内膜植入和改建是一个生理过程，并集中在严重的内异症的原因上，例如患有和不患有内异症的妇女在位内膜的差异(这可能表明存在遗传差异)，一些子宫内膜异位细胞的体外侵袭，粘连对子宫内膜异位灶的局部屏蔽，以及ICAM-1和糖蛋白对NK活性的抑制。因此，子宫内膜异位症被认为是一种良性肿瘤，细胞病变的类型、遗传和免疫环境以及卵巢和腹腔液中的局部激素浓度将决定其表现为囊性卵巢子宫内膜异位症、深部子宫内膜异位症或外部子宫腺肌症，以及后者是否与粘连有关。
Peritoneal fluid and the intraovarian milieu are a specific microenvironment. Peritoneal fluid originates mainly as an ovarian exudation product caused by increased vascular permeability, with cyclic variation in volume and steroid hormones which are always higher than in plasma, It contains large amounts of macrophages and their secretion products, and has a large exchange area with plasma through the peritoneum? which is highly permeable for small molecules, Diffusion becomes virtually zero for molecules,vith a molecular weight of >100 000 Da, In women with the luteinized unruptured follicle (LUF) syndrome, concentrations of oestrogens and progesterone are much lower in the luteal phase. Endometriosis is associated with sterile low-grade inflammation, increased concentrations of activated macrophages and many of their secretions, such as cytokines, growth factors and angiogenic factors. Concentrations of CA-125 and of glycodelins are also increased, secreted locally by the endometrial cells, Natural killer (NK) cell function declines, possibly mediated by glycodelins or local intercellular adhesion molecule (ICAM)-1 shedding, The ovary is also a specific microenvironment, with steroid hormone concentrations 1000-fold higher in follicles than in plasma, Endometrial and superficially implanted cells are influenced by peritoneal fluid concentrations so that local environment, rather than inherent cellular differences could explain differences between superficial endometriosis and eutopic endometrium. Differences between superficial implants and endometriotic disease, deep infiltrating or cystic ovarian endometriosis, may thus arise via different endocrine environments. Superficial endometrial implants are regulated by peritoneal fluid factors, whereas deep endometriosis and cystic ovarian endometriosis are influenced by blood or ovarian factors. The endometriotic disease theory considers superficial endometriotic implants and their remodelling as a physiological process in most women, and concentrates on the causes of severe endometriosis such as differences in the eutopic endometrium from women with and without endometriosis (which may indicate hereditary differences), the invasiveness of some endometriotic cells irt vitro, focal 'shielding' of endometriotic foci by adhesions, and inhibition of NK activity by ICAM-1 and glycodelins. Endometriotic disease is thus seen as a benign tumour, The type of cellular lesion, hereditary and immunological environments and local hormone concentrations in the ovary and in peritoneal fluid, will decide expression as cystic ovarian endometriosis, deep endometriosis or adenomyosis externa, and whether the latter is associated with adhesions.