For patients with hepatocellular carcinoma and cirrhosis, the rupture of thin lymphatic vessel walls leads to a profuse outflow of lymph fluid. Typically, chyloperitoneum tends to precede the development of chylothorax in patients with cancer. The present study describes the case of a male patient with hepatocellular carcinoma who developed chylothorax without chyloperitoneum. Computed tomography showed lymphatic system developmental abnormalities with a large volume of leaked lymph fluid. Multiple thoracic duct ligations (TDLs) failed, but a side-to-end lymphatic venous anastomosis (LVA) surgery resolved the symptoms. To the best of our knowledge, there are no reports of chylothorax occurrence after cirrhosis further complicated by congenital lymphatic abnormalities in the English-language literature. In conclusion, LVA could be appropriate to treat chylothorax when TDL is ineffective as a remedial or even prophylactic intervention.
Polycystic ovary syndrome (PCOS) is an endocrine disorder and metabolic syndrome. Ovarian fibrosis pathological change in PCOS has gradually attracted people's attention. In this study, we constructed a PCOS mouse model through the use of dehydroepiandrosterone. Sirius red staining showed that the ovarian tissues in PCOS mice had obvious fibrosis. Prolyl oligopeptidase (POP) is a serine protease and N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is its catalytic product. Studies show that abnormal expression and activity of POP and Ac-SDKP are closely related to tissue fibrosis. It was found that the expression of POP and Ac-SDKP was decreased in the ovaries of PCOS mice. Further studies showed that POP and Ac-SDKP promoted the expression of matrix metalloproteinases 2 (MMP-2) expression and decreased the expression of transforming growth factor beta 1 (TGF-ß1) in granulosa cells. Hyperandrogenemia is a typical symptom of PCOS. We found that testosterone induced the low expression of POP and MMP2 and high expression of TGF-ß1 in granulosa cells. POP overexpression and Ac-SDKP treatment inhibited the effect of testosterone on TGF-ß1 and MMP2 in vitro and inhibited ovarian fibrosis in the PCOS mouse model. In conclusion, PCOS ovarian tissue showed obvious fibrosis. Low expression of POP and Ac-SDKP and changes in fibrotic factors contribute to the ovarian pathological fibrosis induced by androgen.
