Management of an iatrogenic duodenal perforation with a helical tack system in a patient with pancreatic cancer complicated by gastric outlet obstruction.

Video 1Closure of an iatrogenic perforation with helical tack system and subsequent EUS-guided choledochoduodenostomy.

Use of helical tack system for management of a high-risk fibrotic peptic ulcer.

Background and Aims: GI bleeding because of peptic ulcer disease is a well-described entity in its diagnosis and management. Although hemostatic clips and thermal therapy have been the primary tools in bleeding from peptic ulcer disease, some bleeds remain refractory. New data have shown that obliteration of the underlying arterial blood flow is needed to control refractory peptic ulcer bleeding. Although this has been shown with over-the-scope clips, we present a case where GI bleeding is controlled via a helical tack system. Although there are several available tools that can be used for treatment of upper GI bleeds, there remains a need for devices that can be used when standard methods of closure, such as with clips, cannot be performed because of a challenging location or friable mucosa. The aim of this video case is to demonstrate the use of a novel helical tack system as a salvage technique in the treatment of challenging upper GI bleeds. Methods: One case of a bleeding GI ulcer that was refractory to standard endoscopic clips was identified. Results: In this case, the ulcer closure was achieved using the helical tack system. There were no adverse events. The patient did not require additional surgical or endoscopic interventions. Conclusions: The helical tack system is a novel device that may be useful as a salvage method for the cessation of GI bleeds refractory to standard clips. Additional comparative studies are needed to better understand the advantages and disadvantages of this system relative to other closure tools.

Morphine-potentiated cognitive deficits correlate to suppressed hippocampal iNOS RNA expression and an absent type 1 interferon response in LP-BM5 murine AIDS.

Opioid use accelerates neurocognitive impairment in HIV/AIDS patients. We assessed the effect of chronic morphine treatment and LP-BM5/murine AIDS (MAIDS) infection on cognition, cytokine production, and type 1 interferon (IFN) expression in the murine CNS. Morphine treatment decreased expression of pro-inflammatory factors (CCL5, iNOS) and reduced cognitive performance in LP-BM5-infected mice, correlating to increased hippocampal viral load and a blunted type 1 IFN response. In the striatum, morphine reduced viral load while increasing IFN-α RNA expression. Our results suggest that differentially regulated type 1 IFN responses may contribute to distinct regional outcomes in the hippocampus and striatum in LP-BM5/MAIDS.