Laparoscopic Paraesophageal Hernia Repair With Nissen Fundoplication in a Patient With Ancient Schwannoma of the Gastroesophageal Junction.

Schwannomas are mostly benign tumors that originate from Schwann cells and are rarely seen in the gastrointestinal tract. Our patient is a 65-year-old female who was found to have a 1.5 cm lesion at the gastroesophageal junction, which was clipped and excised on endoscopy. Histologic examination demonstrated an ancient schwannoma. Two years afterward, she presented to our clinic for a large type III paraesophageal hernia. We took her to the operating room for a laparoscopic paraesophageal hernia repair and Nissen fundoplication. We performed an upper endoscopy during the case and found no recurrence of the ancient schwannoma. The case progressed well without complications. She was discharged on postoperative day 1 after tolerating a pureed diet and reported no issues in follow-up. In summary, we demonstrate a successful surgical outcome in a patient who had undergone resection of this rare tumor 2 years prior to her surgery.

Efficacy and Safety of Recurrent Paraesophageal Hernia Repair with Roux-en-Y Gastric Bypass.

Roux-en-Y gastric bypass (RYGB) has been explored as a revisional option to failed paraesophageal hernia (PEH) repair with fundoplication, particularly in patients suffering from obesity. However, few studies have assessed long-term outcomes of RYGB with revisional PEH repair in regard to acid-suppressing medication use. We retrospectively identified 19 patients who underwent revisional PEH repair with RYGB between 2011 and 2018. The median operative time was 232 minutes with a median hospital length of stay of two days. The median length of follow-up was 24 months. Two patients (10.5%) had complications in the first 30 days, and five patients (26.3%) had complications within one year. Of the 12 patients on preoperative acid suppression, 6 (50%) were either off medication or on reduced dose at 12 months. The median BMI decrease was 14.4 kg/m² at 12 months and did not change significantly afterward. Although rates of acid-suppression medication use did not change overall after revisional PEH repair with RYGB, patients experienced successful long-term management of morbid obesity and sustained weight loss. Revisional PEH repair with RYGB is a safe and effective option, with a complication rate comparable with the reported rates after revisional foregut procedures such as revisional Nissen fundoplication.

The indoleamine 2,3-dioxygenase pathway controls complement-dependent enhancement of chemo-radiation therapy against murine glioblastoma.

BACKGROUND: Indoleamine 2,3-dioxygenase (IDO) is an enzyme with immune-suppressive properties that is commonly exploited by tumors to evade immune destruction. Anti-tumor T cell responses can be initiated in solid tumors, but are immediately suppressed by compensatory upregulation of immunological checkpoints, including IDO. In addition to these known effects on the adaptive immune system, we previously showed widespread, T cell-dependent complement deposition during allogeneic fetal rejection upon maternal treatment with IDO-blockade. We hypothesized that IDO protects glioblastoma from the full effects of chemo-radiation therapy by preventing vascular activation and complement-dependent tumor destruction. METHODS: To test this hypothesis, we utilized a syngeneic orthotopic glioblastoma model in which GL261 glioblastoma tumor cells were stereotactically implanted into the right frontal lobes of syngeneic mice. These mice were treated with IDO-blocking drugs in combination with chemotherapy and radiation therapy. RESULTS: Pharmacologic inhibition of IDO synergized with chemo-radiation therapy to prolong survival in mice bearing intracranial glioblastoma tumors. We now show that pharmacologic or genetic inhibition of IDO allowed chemo-radiation to trigger widespread complement deposition at sites of tumor growth. Chemotherapy treatment alone resulted in collections of perivascular leukocytes within tumors, but no complement deposition. Adding IDO-blockade led to upregulation of VCAM-1 on vascular endothelium within the tumor microenvironment, and further adding radiation in the presence of IDO-blockade led to widespread deposition of complement. Mice genetically deficient in complement component C3 lost all of the synergistic effects of IDO-blockade on chemo-radiation-induced survival. CONCLUSIONS: Together these findings identify a novel mechanistic link between IDO and complement, and implicate complement as a major downstream effector mechanism for the beneficial effect of IDO-blockade after chemo-radiation therapy. We speculate that this represents a fundamental pathway by which the tumor regulates intratumoral vascular activation and protects itself from immune-mediated tumor destruction.