Initial experience using N-butyl cyanoacrylate for embolization of lower gastrointestinal hemorrhage.

PURPOSE: To report initial experience using N-butyl cyanoacrylate (n-BCA) to control lower gastrointestinal hemorrhage (LGIH). MATERIALS AND METHODS: From May 2005 to March 2009, 14 patients with LGIH underwent mesenteric angiography and transcatheter arterial embolization using n-BCA. Candidacy was primarily based on the patient's hemodynamic stability and the risk for future LGIH, determined by the presence of at least one of the following risk factors: more than one arterial feeder supplying the bleeding vessel, underlying coagulopathy, or need to resume anticoagulation after embolization. Outcome measures included technical success (immediate postembolic hemostasis confirmed with completion angiography showing no further extravasation of contrast medium), clinical success (postembolic hemostasis in the absence of complications 30 days after the procedure), and clinical failure (recurrence of LGIH necessitating repeat embolization or surgical treatment). RESULTS: Fourteen patients with active LGIH were treated with n-BCA, with 100% technical success. Two patients had rebleeds resulting in bowel resection. One patient experienced a minor rebleed that spontaneously resolved. One patient died secondary to multiorgan failure in the setting of multiple medical problems. The remaining 10 patients had complete clinical success, experiencing no signs of rebleeding or infarction. CONCLUSIONS: The results suggest that n-BCA can be a useful alternative embolic agent for the treatment of hemodynamically unstable patients with LGIH when standard microcoiling techniques fail or are not feasible and in patients with coagulopathy.

Cyclic AMP stimulates fructose transport in neonatal rat small intestine.

Intestinal fructose transporter (GLUT5) expression normally increases significantly after completion of weaning in neonatal rats. Increases in GLUT5 mRNA, protein, and activity can be induced in early weaning pups by precocious consumption of dietary fructose or by perfusion of the small intestine with fructose solutions. Little is known about the signal transduction pathway of the dietary fructose-mediated increase in GLUT5 expression during early intestinal development. Recent microarray results indicate that key gluconeogenic enzymes modulated by cAMP are markedly upregulated by fructose perfusion; hence, we tested the hypothesis that cAMP plays an important role in regulating intestinal fructose absorption by simultaneously perfusing adenylyl cyclase, phosphodiesterase, or protein kinase A (PKA) inhibitors along with fructose. Intestinal fructose uptake rates increased by 100% in rat pups perfused with 8-bromo-cAMP. Simultaneous fructose and dideoxyadenosine (DDA; inhibitor of adenylyl cyclase) perfusion completely inhibited increases in fructose uptake rate induced by perfusion with fructose alone. Fructose perfusion increased intestinal mucosal cAMP concentrations by 27%, but simultaneous perfusion of fructose and DDA inhibited the fructose-induced increase in cAMP. However, GLUT5 and sodium-glucose cotransporter (SGLT1) mRNA abundance and glucose transport rates were each not significantly affected by 8-bromo-cAMP and DDA. Moreover, simultaneous perfusion of the small intestine with fructose and PKA inhibitor or N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamid. 2HCl, both inhibitors of PKA, did not prevent the fructose-induced increases in GLUT5 mRNA abundance and fructose uptake rate. Cyclic AMP appears to modulate fructose transport without affecting GLUT5 mRNA abundance, and without involving PKA.