Petersen's space hernia is caused by the herniation of intestinal loops through the defect between the small bowel limbs, the transverse mesocolon and the retroperitoneum, after any type of gastrojejunostomy. The laparoscopic approach facilitates the occurrence of this type of hernia, due to the lack of post-operative adhesions which prevent bowel motility and hence, herniation. We report the case of a 46 year-old male submitted to an open antrectomy and vagotomy with a Roux-en-Y reconstruction six-years before, for the treatment of bleeding gastric ulcer.He presented with epigastric abdominal pain radiating to the back and alimentary vomiting with a 3 days evolution, with an episode of hematemesis 2 h before admission. His abdomen was bloated and tender at the epigastric region. The laboratory exams revealed mild leucocytosis and CRP elevation with normal pancreatic tests. The abdominal CT scan revealed an intestinal occlusion. An exploratory laparotomy was performed, disclosing an incarcerated Petersen space hernia of the common limb, with obstruction and dilatation of the biliary limb. The knowledge of this anatomic post-operative defect and a low threshold for diagnosis are crucial to its management, since its nonspecific clinical and laboratory findings. Early operative intervention is warranted in order to avoid the severe complications of bowel necrosis.

Background. The tumor immune microenvironment exerts a pivotal influence in tumor initiation and progression. The aim of this study was to analyze the immune context of sporadic and familial adenomatous polyposis (FAP) lesions along the colorectal adenoma–carcinoma sequence (ACS). Methods. We analyzed immune cell counts (CD3+, CD4+, CD8+, Foxp3+, and CD57+), tumor mutation burden (TMB), MHC-I expression and PD-L1 expression of 59 FAP and 74 sporadic colorectal lesions, encompassing adenomas with low-grade dysplasia (LGD) (30 FAP; 30 sporadic), adenomas with high-grade dysplasia (22 FAP; 30 sporadic), and invasive adenocarcinomas (7 FAP; 14 sporadic). Results. The sporadic colorectal ACS was characterized by (1) a stepwise decrease in immune cell counts, (2) an increase in TMB and MHC-I expression, and (3) a lower PD-L1 expression. In FAP lesions, we observed the same patterns, except for an increase in TMB along the ACS. FAP LGD lesions harbored lower Foxp3+ T cell counts than sporadic LGD lesions. A decrease in PD-L1 expression occurred earlier in FAP lesions compared to sporadic ones. Conclusions. The colorectal ACS is characterized by a progressive loss of adaptive immune infiltrate and by the establishment of a progressively immune cold microenvironment. These changes do not appear to be related with the loss of immunogenicity of tumor cells, or to the onset of an immunosuppressive tumor microenvironment.