[Severe cholecystitis during the COVID-19 pandemic : Influence of the COVID-19 pandemic on the frequency of surgery and outcome for elective and emergency cholecystectomy: a monocentric retrospective cohort analysis]. / Schwerere Cholezystitiden während der COVID-19-Pandemie : Einfluss der COVID-19-Pandemie auf OP-Frequenz und Outcome bei elektiven und notfälligen Cholezystektomien: eine monozentrische retrospektive Kohortenanalyse.

BACKGROUND: With the outbreak of the COVID-19 pandemic medical care focused on management of the infectious event. Elective interventions were cancelled and the general advice was to stay at home. How this impacted urgent and elective cholecystectomies is the subject of this work. METHOD: Urgent and elective cholecystectomy patients during the first year of the pandemic were compared with those of the previous year. The primary endpoint was the frequency of surgery. Furthermore, the American Society of Anesthesiologists (ASA) score, symptom duration until presentation as well as until surgery, preoperative inflammatory parameters, imaging, positive Murphy's sign, type and duration of surgery, intraoperative drain placement, intraoperative and histological severity, need for and duration of postoperative antibiotic therapy, intensive care stay, length of stay and occurrence of postoperative complications were recorded. RESULTS: During the pandemic patients were sicker (ASA 2.13 vs. 2.31; p = 0.039), the operating time was prolonged (64.4 min vs. 74.9 min; p = 0.001) and patients were more likely to have concomitant peritonitis (15.4% vs. 29.1%: p = 0.007). Furthermore, there was a trend in the presence of leukocytosis, a positive Murphy's sign, intraoperative drain placement, intraoperative severity of inflammation, duration of postoperative antibiotic therapy and complication rate. CONCLUSION: During the COVID-19 pandemic cholecystitis presented with more pronounced inflammation, the surgical conditions were more difficult and postoperative recovery was prolonged.

Impact of defunctioning loop ileostomy on outcome after restorative proctocolectomy for ulcerative colitis.

PURPOSE: This study analyzes the impact of a temporary loop ileostomy on postoperative outcome after restorative proctocolectomy for ulcerative colitis in terms of complications and reoperations including ileostomy closure. METHODS: The records of 122 consecutive patients undergoing restorative proctocolectomy for ulcerative colitis during a 12-year period were reviewed. In 89 patients, a defunctioning ileostomy was created, while 33 patients had no ileostomy. Statistics were done with Chi-square test and Mann-Whitney U test, p < 0.05 considered significant. RESULTS: Both study groups were comparable concerning age, colitis activity, previous diseases, previous surgery, use of steroids, and immunosuppressives. Pouch-related septic complications (anastomotic dehiscence, pouch leakage, pelvic abscess) were significantly lower in the ileostomy group (5.6% vs. 18.2%, p = 0.031), resulting in a lower rate of emergency laparotomies following restorative proctocolectomy (4.5% vs. 30.3%, p < 0.001). Including all complications associated with scheduled closure of ileostomy, the cumulative frequency of emergency laparotomies was significantly lower in the ileostomy group (13.5% vs. 30.3%, p = 0.032). The cumulative duration of hospitalization, including all hospital stays for complications or closure of the ileostomy, was significantly longer in the ileostomy group [median 22 days (11-92) vs. 14 days (9-109), p < 0.001]. During long-term follow-up, a stricture at the pouch-anal anastomosis was more common in the ileostomy group (24.7% vs. 6.1%, p = 0.021), whereas only one stricture necessitated surgical therapy. CONCLUSIONS: Creation of a defunctioning loop ileostomy reduces pouch-related septic complications and the frequency of emergency second laparotomies after restorative proctocolectomy for ulcerative colitis.

Diagnostic evaluation, surgical technique, and perioperative management after esophagectomy: consensus statement of the German Advanced Surgical Treatment Study Group.

PURPOSE: Correct diagnosis, surgical treatment, and perioperative management of patients with esophageal carcinoma remain crucial for prognosis within multimodal treatment procedures. This study aims to achieve a consensus regarding current management strategies in esophageal cancer by questioning a panel of experts from the German Advanced Surgical Treatment Study (GAST) group, comprised of 9 centers specialized in esophageal surgery, with a combined total of >220 esophagectomies per year. MATERIALS AND METHODS: The Delphi method, a systematic and interactive, evidence-based approach, was used to obtain consensus statements from the GAST group regarding ambiguities and disparities in diagnosis, patient selection, surgical technique, and perioperative management of patients with esophageal carcinoma. After four rounds of surveys, agreement was measured by Likert scales and defined as full (100% agreement), near (≥66.6% agreement), or no consensus (<66.6% agreement). RESULTS: Full or near consensus was obtained for essential aspects of esophageal cancer staging, proper surgical technique, perioperative management and indication for primary surgery, and neoadjuvant treatment or palliative treatment. No consensus was achieved regarding acceptability of minimally invasive technique and postoperative nutrition after esophagectomy. CONCLUSION: The GAST consensus statement represents a position paper for treatment of patients with esophageal carcinoma which both contributes to the development of clinical treatment guidelines and outlines topics in need of further clinical studies.

Tight junctions and cell-cell interactions.

Chronic inflammation in mucosal tissues can influence epithelial barrier function via pro-inflammatory cytokines such as interferon (IFN)-gamma and tumor necrosis factor-alpha. Increased mucosal levels of these cytokines have been observed in mucosal biopsies from patients with a chronic inflammatory condition referred to as inflammatory bowel disease. Paracellular permeability across epithelial cells is regulated by tight junctions (TJs), which are the apical most junctions in epithelial cells. Given that pro-inflammatory cytokines modulate the epithelial barrier and that TJs regulate epithelial permeability, we analyzed the influence of IFN-gamma on U function/structure. Our results suggest that IFN-gamma induced a time-dependent increase in paracellular permeability that was associated with internalization of TJ transmembrane proteins, occludin, junction adhesion molecule A, and claudin-1. In this chapter, we focus on selected methods used to investigate the influence of IFN-gamma on epithelial barrier function.

Expression of IL-12-related molecules in human intestinal microvascular endothelial cells is regulated by TLR3.

Members of the interleukin (IL)-12 family constitute subunits of IL-12, -23, and -27. These ILs represent pivotal mediators in the regulation of cell-mediated immune responses and in animal models of human inflammatory bowel disease. Recent work has suggested that intestinal endothelial cells might serve as a second line of defense in bacterial sensing of invading pathogens. The purpose of this study was to examine the production of IL-12 family members in intestinal endothelial cells (HIMEC). HIMEC were stimulated with proinflammatory agents (TNF-alpha, IFN-gamma, IL-1beta) and microbial antigens [LPS, lipoteichoic acid, peptidoglycan, CpG-DNA, flagellin, poly(I:C)]. Expression of IL-12 family members and of Toll-like receptor (TLR)3 in HIMEC was assessed by real-time RT-PCR, immunostaining, flow cytometry, and immunoblot analysis. HIMEC display an induction of Epstein-Barr virus-induced gene 3 (EBI3), IL-12p35, and IL-23p19, whereas no expression of IL-12p40 and IL-27p28 was detectable. The strongest induction was induced by proinflammatory factors known to utilize the NF-kappaB pathway, and expression of EBI3 and IL-23p19 was diminished by an NF-kappaB inhibitor. HIMEC display regulated expression of TLR3. Adhesion and transmigration assays showed proinflammatory responses after HIMEC stimulation. HIMEC are capable of producing IL-12 family members as a response to microbial stimuli. The TLR3 agonist, poly(I:C), was shown to enhance leukocyte adhesion in vitro in HIMEC. Our data suggest that the intestinal microvasculature is responsive to ligands of TLR3 expressed on intestinal endothelial cells, thereby adding to the regulation of adaptive immunity and leukocyte recruitment.

Ischaemic colitis mimicking inflammatory bowel disease in a young adult receiving oral anticoagulation.

Ischaemic colitis (IC) is the most frequent form of gastrointestinal ischaemia. Discrepancy between non-specific symptoms and objective findings is a hallmark of IC. Thus delay of diagnosis is common due to its often subtle and unpredictable presentation. In particular, the clinical symptoms and signs of IC can overlap with those of inflammatory bowel disease. We present a case of a young man with known factor-V-Leiden mutation in whom IC developed during effective therapy with oral anticoagulants, presenting with symptoms and endoscopic findings suggestive of inflammatory bowel disease.

Immunohistochemical expression of P53 and oncogenes in ulcerative colitis-associated colorectal carcinoma.

The role of the tumor suppressor gene p53 and proto-oncogenes mdm-2, waf-1,and bcl-2 in sporadic colorectal carcinoma (CRC) has been well investigated. However, little is known about the role of these genes in the development of ulcerative colitis-associated colorectal carcinoma (CAC). Colectomy specimens from patients with CAC, patients with ulcerative colitis (UC) and dysplasia, patients with long-standing UC without carcinoma or dysplasia, and patients with CRC were investigated in comparison to normal colon (NC) specimens from patients with diverticulosis without histologic signs of inflammation. Immunohistochemistry was performed with antibodies against p53, mdm-2, waf-1, and bcl-2; and staining was evaluated semiquantitatively with an expression of more than 20% of tumor cell nuclei or epithelial cell nuclei in nontumor specimens considered "positive." Statistical analysis was performed using Fisher's exact test. In carcinomas, p53 was positive in 50% of CRC tissues and 60% of CAC tissues without statistical difference. Positive expression of p53 was found in most high-grade dysplasia but not in low-grade dysplasia (p < 0.01). Whereas mdm-2 and bcl-2 were only sporadically expressed, waf-1 was observed in most specimens, with a high prevalence in UC without carcinoma or dysplasia (11/15). NC specimens were always negative for all antibodies. Immunohistochemical expression of p53, mdm-2, waf-1, and bcl-2 is similar for CAC and CRC. The malignant potential of dysplasia in UC is partially confirmed by a high prevalence of p53 and waf-1 expression, suggesting that CAC may develop along pathways that are different from CRC. High expression of waf-1 in nonmalignant long-standing UC has to be proved over a long-term course in its role as an independent cancer risk factor in UC patients.