Management of Staple Line Leaks after Laparoscopic Sleeve Gastrectomy.

Background and Objectives: Laparoscopic sleeve gastrectomy has become one of the most popular bariatric surgeries in the United States with a low rate of morbidity and effective weight loss. However, staple line leak remains a feared complication requiring a lengthy and difficult treatment course until resolution. This study outlines the various treatment methods used within a high-volume bariatric practice for successful leak resolution without necessitating a conversion procedure. Methods: A retrospective review was conducted on all patients with staple line leak after laparoscopic sleeve gastrectomy in a three-surgeon bariatric practice from January 1, 2010 to December 31, 2019. Results: A total of 10 staple line leaks were identified with a leak rate of 0.9%. Patients presented on average 29.3 days postoperatively and were all diagnosed on computed tomography. Three patients were initially managed operatively with washout and drainage procedure. Six patients were managed endoscopically initially with either stent or over-the-scope clip placement. Most patients required multiple interventions with an average of 2.4 interventions per patient. Average time to leak resolution was 48.2 days (15-95 days). Conclusion: Management of staple line leaks after laparoscopic sleeve gastrectomy requires a multimodal approach usually requiring multiple interventions before leak resolution. We demonstrate effective utilization of varying interventions that lead to effective leak resolution and avoid conversion operations.

IGPR-1 Is Required for Endothelial Cell-Cell Adhesion and Barrier Function.

Endothelial cell (EC) barrier function plays a prevalent regulatory mechanism for the integrity and homeostasis of blood vessels and modulates angiogenesis and immune responses. Cell adhesion molecules (CAMs) play a central role in the barrier function of ECs. Although Ig-containing and proline-rich receptor-1(IGPR-1) was recently identified as a novel CAM expressed in ECs, the molecular mechanisms underlying the function of IGPR-1 in ECs remain uncharacterized. In this report, we investigated the role of IGPR-1 in EC barrier function and the molecular mechanism of its activation in ECs. We demonstrate that IGPR-1 is localized to endothelial adherens junctions and, through trans-homophilic dimerization, regulates endothelial cell-cell adhesion and barrier function. Trans-homophilic dimerization of IGPR-1 stimulates the phosphorylation of serine 220 (Ser220), which is required for IGPR-1 to regulate endothelial barrier function and angiogenesis. Moreover, IGPR-1 chimera, which mimics the trans-homophilic dimerization of IGPR-1, induced a sustained phosphorylation of Ser220 upon stimulation with a ligand. Coordinated dimerization of IGPR-1 and its homophilic interaction modulates its adhesive function and Ser220 phosphorylation. This adhesive function of IGPR-1 contributes to the barrier function of ECs.