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장기투석을 받은 만성 신부전 환자에서 발생한 종양에 관한 고찰
황정화,이혜경,홍현숙,박재성,김대호,권귀향,최득린,황승덕,이희발 순천향의학연구소 1996 Journal of Soonchunhyang Medical Science Vol.2 No.2
The authors tried to evaluate tumor occurrence in long-term dialysis patients with chronic renal failure. Among 359 patients, 20 patients (about 5.6%) were diagnosed with malignancy during long-term dialysis from the period of 1983 to 1995 at our nephrology department. The ultrasonographic and computed tomographic findings including the clinical features of 20 patients that were retrospectively reviewed. The mean age of the patients was 53 (37-75)years old and the ratio of male to female was 9:1. Among the 20 cases, 7 cases of hepatoma (35%) were developed. Among them, urinary tract tumors such as renal and bladder cancer were developed in 4 (20%) and 2 (10%) of the cases. Other malignant tumors were lymphoma, stomach cancer, uterine cervical cancer, cholangiocarcinoma, lung cancer, meningioma, and acoustic neuroma one case of each (each of 5.3%). The most common tumor in patients with chronic renal failure, who were receiving long-term dialysis, was hepatoma and the second most common tumor was cancer of the urinary tract such as kidney and bladder.
Hi Bahl Lee,하헌주 대한의학회 2007 Journal of Korean medical science Vol.22 No.6
A growing body of evidence indicates that epithelial-mesenchymal transition (EMT) of human peritoneal mesothelial cells (HPMC) may play an important role in the development and progression of peritoneal fibrosis during long-term peritoneal dialysis (PD) leading to failure of peritoneal membrane function. Here, we review our own observations and those of others on the mechanisms of EMT of HPMC and suggest potential therapeutic strategies to prevent EMT and peritoneal fibrosis during long-term PD. We found that high glucose and H2O2 as well as transforming growth factor- 1 (TGF- 1) induced EMT in HPMC and that high glucoseinduced EMT was blocked not only by inhibition of TGF- 1 but also by antioxidants or inhibitors of mitogen-activated protein kinases (MAPK). Since MAPKs are downstream target molecules of reactive oxygen species (ROS), these data suggest that high glucose-induced generation of ROS and subsequent MAPK activation mediate high glucose-induced EMT in HPMC. We and others also observed that bone morphogenetic protein-7 (BMP-7) prevented EMT in HPMC. Glucose degradation products (GDP) were shown to play a role in inducing EMT. Involvement of a mammalian target of rapamycin (mTOR) in TGF- 1-induced EMT has also been proposed in cultured HPMC. A better understanding of the precise mechanisms involved in EMT of HPMC may provide new therapeutic strategies for inhibiting peritoneal fibrosis in long-term PD patients.