Background: Anastomotic leakage (AL) still remains a common complication after colorectal anastomosis that leads to increased morbidity and mortality. The gut microbiota has been hypothesized as one of the risk factors associated with anastomotic leakage. The aim of the present study was to summarize all existing clinical and experimental studies that evaluate the impact of intestinal microbiota on anastomotic leakage after colorectal resection. Methods: The present scoping review was designed according to PRISMA recommendations and a systematic search in Medline, Scopus, EMBASE, Clinicaltrials.gov, Google Scholar, and CENTRAL was conducted until September 2024. Results: Overall, 7 clinical and 5 experimental studies were included. A diminished α-diversity of the gut microbiota in patients suffering from AL was demonstrated. Specific microbe genera, such as Lachnospiraceae, Bacteroidaceae, Bifidobacterium, Acinetobacter, Fusobacterium, Dielma, Elusimicronium, Prevotella, and Faecalibacterium, seem to be associated with AL. However, specific genera, like Prevotella, Streptococcus, Eubacterium, Enterobacteriaceae, Klebsiella, Actinobacteria, Gordonibacter, Phocaeicola, and Ruminococcus2, seem to be protective against AL. Experimental studies highlighted that the Western diet seems to affect microbiota diversity and increases the AL rate, whereas anastomotic healing seems to be impaired by high metalloproteinase production and increased collagenase activity. Conclusions: The intestinal microbiota seems to play an important role in anastomotic leakage after colorectal resection. Specific interventions targeting the microbiota’s composition and the pathophysiological mechanisms by which it impairs anastomotic healing could diminish the risk for anastomotic leakage and improve clinical outcomes. However, future studies should be based on prospective design and eliminate heterogeneity.

Neutrophil extracellular traps (NETs) are a neutrophil-generated extracellular network of chromatin and chromatin-bound molecules with antimicrobial potency. Recent data suggest that NETs are associated with cancer progression and cancer-associated hypercoagulability. Pancreatic adenocarcinoma (PDAC) is a lethal type of cancer in which hypercoagulability and cancer-related thrombosis are among the main complications. In the current report, we summarize the available data on the interplay between NET formation and PDAC development. We conclude that NETs support a dual role during PDAC progression and metastasis. Their formation is on the one hand an important event that shapes the cancer microenvironment to support cancer cell proliferation, invasion and metastasis. On the other hand, NETs may lead to cancer-associated thrombosis. Both mechanisms seem to be dependent on distinct molecular mechanisms that link inflammation to cancer progression. Collectively, NET formation may contribute to the pathogenesis of PDAC, while during cancer development, the proinflammatory environment enables the induction of new NETs and thrombi, forming a vicious cycle. We suggest that targeting NET formation may be an effective mechanism to inhibit both PDAC development and the accompanying hypercoagulability.

INTRODUCTION: A rare case of hemorrhagic gastritis induced by radiation is presented, which was resistant to conservative treatment and required subtotal gastrectomy. PRESENTATION OF CASE: A 56-year-old male was initially undergone right hepatectomy, resection of the extrahepatic biliary tree, hilar lymph node dissection and hepatico-jejunostomy due to advanced hilar cholangiocarcinoma. Because of the extent of the disease, chemo-radiotherapy was administered. The patient received a total radiotherapy dose of 57.6 Gy in 32 sessions. Unfortunately, diffused hemorrhagic gastritis induced by radiation was developed, which was resistant to conservative treatment (endoscopic hemostasis, transfusion). A subtotal gastrectomy was performed. The patient is in good condition 45 months after the liver resection, but with local recurrence. CONCLUSION: In resistant situations to conservative treatment and recurred bleeding of diffused hemorrhagic gastritis induced by radiation, surgical management may have a role. Highlights:

The role of immune system components in the development of myocardial remodeling in chronic kidney disease (CKD) and kidney transplantation remains an open question. Our aim was to investigate the associations between immune cell subpopulations in the circulation of CKD patients and kidney transplant recipients (KTRs) with subclinical indices of myocardial performance. We enrolled 44 CKD patients and 38 KTRs without established cardiovascular disease. A selected panel of immune cells was measured by flow cytometry. Classical and novel strain-related indices of ventricular function were measured by speckle-tracking echocardiography at baseline and following dipyridamole infusion. In CKD patients, the left ventricular (LV) relative wall thickness correlated with the CD14++CD16− monocytes (β = 0.447, p = 0.004), while the CD14++CD16+ monocytes were independent correlates of the global radial strain (β = 0.351, p = 0.04). In KTRs, dipyridamole induced changes in global longitudinal strain correlated with CD14++CD16+ monocytes (β = 0.423, p = 0.009) and CD4+ T-cells (β = 0.403, p = 0.01). LV twist and untwist were independently correlated with the CD8+ T-cells (β = 0.405, p = 0.02 and β = −0.367, p = 0.03, respectively) in CKD patients, whereas the CD14++CD16+ monocytes were independent correlates of LV twist and untwist in KTRs (β = 0.405, p = 0.02 and β = −0.367, p = 0.03, respectively). Immune cell subsets independently correlate with left ventricular strain and torsion-related indices in CKD patients and KTRs without established CVD.