PDF(Pubmed)
Abstract：
Hepatocellular adenomas are benign endothelial tumors of the liver, mostly associated with female individual users of estrogen-containing medications. However, the precise factors underlying the selective development of hepatic adenomas in certain females remain elusive. Additionally, the conventional profile of individuals prone to hepatic adenoma is changing. Notably, male patients exhibit a higher risk of malignant progression of hepatocellular adenomas, and there are instances where hepatic adenomas have no identifiable cause. In this paper, we theorize the role of the human gastrointestinal microbiota, specifically, of bacterial species producing β-glucuronidase enzymes, in the development of hepatic adenomas through the estrogen recycling pathway. Furthermore, we aim to address some of the existing gaps in our knowledge of pathophysiological pathways which are not yet subject to research or need to be studied further. As microbial β-glucuronidases proteins recycle estrogen and facilitate the conversion of inactive estrogen into its active form, this process results in elevated levels of unbound plasmatic estrogen, leading to extended exposure to estrogen. We suggest that an imbalance in the estrobolome could contribute to sex hormone disease evolution and, consequently, to the advancement of hepatocellular adenomas, which are estrogen related.
摘要：
肝细胞腺瘤是肝脏的良性内皮肿瘤，主要与女性个体使用含雌激素药物有关。然而,某些女性肝腺瘤选择性发展的确切因素仍然难以捉摸。此外,容易患肝腺瘤的个体的常规特征正在发生变化。值得注意的是,男性患者表现出肝细胞腺瘤恶性进展的风险较高，有些情况下，肝腺瘤没有明确的原因。在本文中,我们对人类胃肠道微生物群的作用进行了理论分析，具体来说,产生β-葡糖醛酸糖苷酶的细菌种类，通过雌激素循环途径在肝腺瘤的发展中。此外，我们的目标是解决我们在病理生理途径知识方面存在的一些空白，这些空白尚未经过研究或需要进一步研究。由于微生物β-葡糖醛酸酶蛋白质回收雌激素并促进无活性雌激素转化为其活性形式，这个过程导致未结合的血浆雌激素水平升高，导致长期接触雌激素。我们认为，雌激素的失衡可能会导致性激素疾病的演变，因此,肝细胞腺瘤的进展，与雌激素有关。
