Primary intestinal tuberculosis is unusual in European and North American countries today. Its diagnosis is often surprising and differentiation from inflammatory bowel diseases is difficult. The authors present a rare case of severe stercoral peritonitis caused by multiple intestinal perforations in a patient with primary ileocecal tuberculosis. Initial clinical and laboratory investigations led to the suspicion of inflammatory bowel disease. The subsequent diagnostic workup included colonoscopic examination of the cecal and terminal region of the ileum with multiple biopsies. After the pathologist had assessed the specimen as indicating Crohn’s disease, appropriate therapy was initiated. Several days later, however, the patient was readmitted to a surgical intensive care unit with clinical signs of peritonitis and immediately operated on. The final diagnosis from a resection specimen confirmed the diagnosis of primary intestinal tuberculosis. The follow-up was complicated by a subhepatic abscess formation with the necessity for surgical drainage. The patient’s recovery was uneventful, she underwent intensive antituberculotic therapy and is asymptomatic at present. Surgeons caring for patients with acute abdomen should be aware of tuberculous perforation peritonitis even in non-risk groups of patients.

Carbon dioxide pneumoperitoneum causes alterations of the acid-base balance, mostly of respiratory or mixed type. Lowering of the insufflation pressure from 15 to 10 mmHg does not contribute to the elimination of acid-base balance alterations during laparoscopic cholecystectomy.

Background/Aim: Rectal cancer accounts for approximately one-third of all colorectal cancers. Currently, the standard treatment for locally advanced rectal cancer (LARC) is neoadjuvant chemoradiotherapy (CRT) with capecitabine or 5-fluorouracil followed by curative surgery. Unfortunately, only 20% of patients with LARC present complete pathological response after CRT, whereas in 20-40% cases the response is poor or absent. The aim of our study was to evaluate whether microRNAs (miRNAs) in tumor biopsy specimen have the potential to predict therapeutic response in LARC patients. Patients and Methods: In total 87 LARC patients treated by CRT were enrolled in our prospective study. To identify predictive miRNAs, we used small RNA sequencing in 40 tumor biopsy samples of LARC patients (20 responders, 20 non-responders) and qPCR validation of selected miRNA candidates. Results: In the discovery phase of the study, we identified 69 miRNAs to have significantly different expression between the group of responders (TRG 1,2) and a group of non-responders (TRG 4,5) to neoadjuvant CRT. Among these miRNAs, 48 showed a lower expression and 21 showed higher expression in tumor tissues from poorly responding LARC patients. Five miRNAs were selected for validation, but only miR-487a-3p was confirmed to have a significantly higher expression in the tumor biopsy specimens of non-responders to neoadjuvant CRT (p<0.0006, AUC=0.766). Gene Ontology (GO) clustering and pathway enrichment analysis of the miR-487a-3p mRNA targets, revealed potential mechanisms behind miR-487a-3p roles in chemoradioresistance (e.g. TGF-beta signaling pathway, protein kinase activity, double-stranded DNA binding, or microRNAs in cancer). Conclusion: By combination of miRNA expression profiling and integrative computational biology we identified miR-487a-3p as a potential predictive biomarker of CRT response in LARC patients. Colorectal cancer (CRC) is the third most common cancer worldwide and accounts for approximately 10% of all solid tumors. CRC is the second leading cause of cancer-related deaths, and its incidence is on the rise. Tumors of the rectum 249 This article is freely accessible online.

Long-term dysbiosis of the gut microbiome has a significant impact on colorectal cancer (CRC) progression and explains part of the observed heterogeneity of the disease. Even though the shifts in gut microbiome in the normal-adenoma-carcinoma sequence were described, the landscape of the microbiome within CRC and its associations with clinical variables remain under-explored. We performed 16S rRNA gene sequencing of paired tumour tissue, adjacent visually normal mucosa and stool swabs of 178 patients with stage 0–IV CRC to describe the tumour microbiome and its association with clinical variables. We identified new genera associated either with CRC tumour mucosa or CRC in general. The tumour mucosa was dominated by genera belonging to oral pathogens. Based on the tumour microbiome, we stratified CRC patients into three subtypes, significantly associated with prognostic factors such as tumour grade, sidedness and TNM staging, BRAF mutation and MSI status. We found that the CRC microbiome is strongly correlated with the grade, location and stage, but these associations are dependent on the microbial environment. Our study opens new research avenues in the microbiome CRC biomarker detection of disease progression while identifying its limitations, suggesting the need for combining several sampling sites (e.g., stool and tumour swabs).

Background: Myeloid-derived suppressor cells (MDSCs) contribute to tumor escape from host immune surveillance and to tumor progression by producing tumor-promoting factors. We focused on clinical and analytical MDSCs-related issues as potential bio markers and immune regulators involved in tumor progression. Patients and Methods: We analyzed 10 patients with advanced colorectal carcinoma (CRC) with (M1 subgroup) or without (M0 subgroup) distant metastases at dia gnosis. Peripheral blood was collected at dia gnosis prior to treatment and subsequently 12 months after therapy initiation. Using multicolor flow cytometry MDSC subsets were evaluated. Monocytic MDSCs (M-MDSCs) were detected as CD45 + CD11b + CD33 + HLA-DR low/ − CD14 + CD15-, granulocytic MDSCs (CD33 hi PMN-MDSC) were detected as CD45 + CD11b + CD33 hi HLA-DR low/ − CD14 − CD15 +. For analytical and preanalytical studies, random fresh blood specimens predominantly from cancer patients were analyzed. Results: Levels of circulating M-MDSCs were not associated with metastatic disease within advanced CRC patients. Levels of circulating CD33 hi PMN-MDSCs were elevated in patients with distant metastases compared to T3 M0 subgroup. Circulating M-MDSCs increased upon treatment initiation in 9 out of 10 patients. CD33 hi PMN-MDSCs substantially dropped upon treatment initiation in 5 out of 10 patients and substantially increased in 2 out of 10 patients. Analytical part showed that absolute and relative counts within each MDSC subset are correlated. Coefficient of variation (CV) for repeatability was 6-11% for M-MDSCs and 25-44% for CD33 hi PMN-MDSCs. CV for reproducibility was higher with 8-22% for M-MDSCs and 35-79% for CD33 hi PMN-MDSCs demonstrating that delay in measurement of MDSCs in whole blood specimen may distort quantification of circulating MDSC subsets. Conclusion: The quantification of MDSC subsets is substantially dependent on the type of specimen examined and its preanalytical processing. Exploratory analysis of M-MDSCs and CD33 hi PMN-MDSCs in CRC patients revealed different dynamics of M-MDSC and CD33 hi PMN-MDSC subsets in the context anti-cancer treatment.