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Copyright of Der Gastroenterologe is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Der Gastroenterologe is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objectives: To evaluate the impact of CT scans on diagnosis or change of therapy in patients with systemic inflammatory response syndrome (SIRS) or sepsis and obscure clinical infection.Methods: CT records of patients with obscure clinical infection and SIRS or sepsis were retrospectively evaluated. Both confirmation of and changes in the diagnosis or therapy based on CT findings were analysed by means of the hospital information system and radiological information system. A sub-group analysis included differences with regard to anatomical region, medical history and referring department.Results: Of 525 consecutive patients evaluated, 59% had been referred from internal medicine and 41% from surgery. CT examination had confirmed the suspected diagnosis in 26% and had resulted in a different diagnosis in 33% and a change of therapy in 32%. Abdominal scans yielded a significantly higher (p=0.013) change of therapy rate (42%) than thoracic scans (22%). Therapy was changed significantly more often (p=0.016) in surgical patients (38%) than in patients referred from internal medicine (28%).Conclusions: CT examination for detecting an unknown infection focus in patients with SIRS or sepsis is highly beneficial and should be conducted in patients with obscure clinical infection.Key Points: • Evaluation of patients with obscure clinical infection is a challenging task. • CT examination of patients with SIRS or sepsis seems to be beneficial. • CT examination confirmed suspected diagnosis in 26% of patients. • CT examination yielded a new infection focus in 33% of patients. • CT examination changed therapy in up to 32% of patients. [ABSTRACT FROM AUTHOR]

Background:Aberrant activation of the canonical WNT signaling is a feature of colorectal cancer (CRC). Van-Gogh-like 2 (VANGL2) belongs to the non-canonical WNT pathway whose activation inhibits canonical WNT signaling. In this study, we investigated the role of VANGL2 and its epigenetic regulation in CRC.Methods:Van-Gogh-like 2 expression and promoter methylation after 5-aza-2′-deoxycytidine (5-aza) treatment were evaluated in CRC cells. DNA samples from 418 sporadic CRCs were tested for VANGL2 promoter methylation and microsatellite instability (MSI). Proliferation, colony formation and activation of the WNT pathway were tested in cells after VANGL2 overexpression.Results:Van-Gogh-like 2 mRNA was significantly higher in 5-aza-treated RKO, LOVO and SW48, whereas no differences were found in SW480. Van-Gogh-like 2 was fully methylated in RKO, SW48, HCT116, DLD1 and Caco2; partially methylated in LOVO, LS174T and SW837; and unmethylated in SW480, SW620 and HT29. Higher expression of VANGL2 mRNA was found in the unmethylated cell lines. In CRC specimens (8.93% MSI), methylated VANGL2 was associated with MSI, higher grade, proximal colon location and BRAF mutation. Van-Gogh-like 2 overexpression in SW480 significantly decreased proliferation, colony formation and β-catenin levels.Conclusion:Van-Gogh-like 2 is frequently methylated in MSI-CRCs with BRAF mutation and may act as a tumour suppressor gene, counteracting WNT/β-catenin signaling. [ABSTRACT FROM AUTHOR]