Background: Ureteroarterial fistula is a rare life-threatening complication of indwelling ureteral stents. The mechanism has not yet been fully evaluated using intravascular imaging. Case presentation: An-84-year-old female was referred to our unit because of large volume pulsatile bleeding from the left ureter during routine stent exchange in the urology department. The hematuria was initially managed by rapidly exchanging for a new stent; however, the patient went into hypovolemic shock due to acute blood loss. The patient underwent implantation of the bilateral ureteral stents due to urinary retention caused by retroperitoneal fibrosis 2 years ago. To prevent ureteral infection, occlusion of the stents and stone formation, the stents were exchanged every 6 months. Computed tomography revealed contact between the left ureter and the common iliac artery. Therefore, ureteroarterial fistula was suspected and endovascular therapy was performed. Although angiography did not show definite blood flow into the ureter, a soft guidewire was advanced from the subintima of the external iliac artery to the left ureter. The diagnosis of ureteroarterial fistula was confirmed. Intravascular ultrasound identified the stent in the ureter and its connection to the subintima of the external iliac artery. The ureter did not contact directly to the inner lumen of the iliac arteries according to the ultrasound findings; therefore, we considered that the risk of stent-graft infection might not be high. After coil embolization of the ipsilateral internal iliac artery, a covered stent was implanted in the external iliac artery to seal the subintimal entry. The patient had no further episodes of any gross hematuria on dual anti-platelet therapy, when the ureteral stent was exchanged three time during 1 year after the endovascular therapy. Conclusions: We demonstrated a case of ureteroarterial fistula, in which intravascular ultrasound allowed to visualize the communication between the ureter and the subintimal lumen in the external iliac artery.

Abstract. Transforming growth factor (TGF) β is a pro-fibrotic cytokine. While three isoforms (TGF-β1, 2 and 3) are known, the functional differences between them are obscure. To investigate the roles of TGF-β isoforms during liver fibrogenesis, male Wistar rats were administrated carbon tetrachloride (CCl 4 ) subcutaneously twice a week for two months. Livers were excised and sectioned for histochemical examinations. These livers were also used to quantitate the expression of genes associated with fibrogenesis, including TGF-β isoforms, as well as those associated with retinoid metabolism. Expression levels of Tgfb1 and Tgfb3 were up-regulated in CCl 4 -treated rat livers while that of Tgfb2 was not changed. The mRNAs for lecithin-retinol acyltransferase (Lrat) and retinoic acid hydroxylase, Cyp26a1, were also elevated. By immunohistochemical staining, TGF-β3 protein was found to be localized mainly in liver parenchymal cells (hepatocytes). These results indicate that retinoid mobilization likely takes place within the rat's liver following CCl 4 treatment, and suggest the possibility that the expression of Tgfb mRNA is regulated by retinoic acid receptors. Reporter analyses of a region of the Tgfb3 gene were performed using the rat liver parenchymal cell line, RLC-16, and a positively responsive region was identified within its intron.

No abstract

No abstract

No abstract