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Background and Aim The feasibility of endoscopic submucosal dissection (ESD) as a treatment option for dysplasia in ulcerative colitis (UC) has been reported, but the associated therapeutic decision‐making and clinical outcomes have not been extensively investigated. Methods We retrospectively reviewed 25 UC patients who were referred for potential ESD of non‐polypoid or sessile dysplasia. We analyzed the treatment decisions and the ESD and colectomy outcomes for this patient group. Results All lesions were located at the colitic segments. The median UC duration was 13.4 years. A colectomy was recommended for 10 patients because of ulceration with indistinct borders (one patient), non‐ulceration with indistinct borders (two patients), and non‐lifting signs (seven patients). The remaining 15 patients underwent ESD. The en bloc and R0 resection rates were 93.3% and 80%, respectively. The median hospitalization periods were 1 (range, 1–2) day after ESD and 7 (range, 5–30) days after colectomy. No procedure‐related complications occurred after ESD, but early and late postoperative complications occurred in two (22.2%) and six (66.7%) of the colectomized patients, respectively. Fourteen ESD cases were followed endoscopically for a median period of 24.7 (range, 5.2–64.8) months. Local recurrence occurred in 2 (14.3%) patients, and metachronous recurrence was identified in two separate patients (14.3%). Conclusions Endoscopic submucosal dissection is a feasible endoscopic treatment option for UC‐associated dysplasia showing noninvasive pit or vascular patterns, no surface ulceration, distinct borders, and appropriate lifting after submucosal injection. Meticulous endoscopic surveillance is essential to monitor for local or metachronous recurrence of dysplasia after ESD.

There were changes in the profiles of fecal fatty acid metabolomes in CRC patients compared to healthy controls, implying that fecal fatty acids could be used as a novel screening tool for CRC.

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BackgroundWe aimed to evaluate the role of fecal calprotectin (FC) as a noninvasive marker for the disease activity of ulcerative colitis (UC) in a Korean cohort.MethodsA total of 181 fecal samples were collected from 181 consecutive UC patients between April 2015 and September 2016. FC levels were measured using the Quantum Blue® Calprotectin rapid test. The laboratory test results, partial Mayo Score (pMS), and colonoscopic imaging findings at FC level measurement were retrospectively reviewed. The Mayo endoscopic subscore (MES) and UC endoscopic index of severity (UCEIS) were graded by 2 certified endoscopists after training with 50 other cases.ResultsThe FC levels were significantly correlated with pMS (Spearman correlation coefficient r = 0.428, p < 0.001), MES (r = 0.304, p < 0.001), UCEIS (r = 0.430, p < 0.001), and CRP (r = 0.379, p < 0.001). FC levels exhibited a significantly better correlation with UCEIS than with MES (Meng’s z = − 2.457, p = 0.01). The FC cut-off level of 187.0 mg/kg indicated complete mucosal healing (MES = 0; UCEIS =0) with a sensitivity and specificity of 0.857 and 0.891, respectively (area under the curve, 0.883; 95% confidence interval, 0.772–1.000).ConclusionThe FC level is significantly correlated with the clinical disease activity index, endoscopic indices, and serum inflammatory biomarkers in a Korean UC cohort. FC is highly predictive of complete mucosal healing in UC. UCEIS exhibits a stronger correlation with the FC level, as compared to MES. Thus, FC could be used as a reliable noninvasive indicator for evaluating disease activity and mucosal healing in UC.

Although early treatment of Crohn’s disease (CD) patients with anti-tumor necrosis factor (TNF) agents or immunomodulators (IMs) may improve long-term outcomes, especially those with poor prognostic factors, their effectiveness in Asians remains unclear. In this study, Korean patients with CD naïve to both intestinal surgery and intestinal complications, and with at least two risk factors for progression (diagnosis at age <40 years, systemic corticosteroid treatment <3 months after diagnosis, and perianal fistula at diagnosis) were retrospectively analyzed. Patients were classified into those who started anti-TNFs, or IMs but not anti-TNFs, within 2 years of diagnosis, and those who started anti-TNFs and/or IMs later. Their probabilities of intestinal surgery and intestinal complications were compared. A total of 670 patients were enrolled, 79 in the early anti-TNF, 286 in the early IM, and 305 in the late treatment group. Kaplan-Meier analysis with the log-rank test showed that from starting anti-TNFs/IMs, times to intestinal surgery (P < 0.001), stricturing complications (P = 0.002), and penetrating complications (P < 0.001) were significantly longer in the early anti-TNF/IM groups than in the late treatment group. Multivariate Cox regression analysis showed that, from starting anti-TNFs/IMs, late anti-TNF/IM treatment was independently associated with higher risks of intestinal surgery (adjusted hazard ratio [aHR] 2.321, 95% confidence interval [CI] 1.503–3.584, P < 0.001), behavioral progression (aHR 2.001, 95% CI 1.449–2.763, P < 0.001), stricturing complications (aHR 1.736, 95% CI 1.209–2.493, P = 0.003), and penetrating complications (aHR 3.315, 95% CI 2.094–5.249, P < 0.001) than early treatment. In conclusion, treatment of Asian CD patients having poor prognostic factors with anti-TNFs/IMs within 2 years of diagnosis is associated with better clinical outcomes than later treatment.

Aortic regurgitation caused by leaflet perforation is most frequently seen in association with infective endocarditis that involves the aortic valve. There have been occasional reports of iatrogenic aortic regurgitation caused by aortic valve injury after cardiac surgery with the use of the transaortic approach or invasive cardiac procedures. Suture-related aortic valve injury can develop during periaortic cardiac surgery, but this has been very rarely reported. Inadvertent injury to an aortic valve leaflet caused by a stitching needle or surgical forceps can produce leaflet perforation with aortic regurgitation. This report describes a case of aortic regurgitation that was caused by iatrogenic aortic valve leaflet perforation, and this occurred in a 22-year-old woman who underwent repair of a ventricular septal defect (VSD) 15 years previously. Transthoracic echocardiography (TTE) showed a defect located at the aortic annulus close to the infundibular septum on a two-dimensional echocardiographic study and we observed an eccentric jet flow into the left ventricle in early diastole on the continuous wave and color flow Doppler studies. A small perforation in the body of the right aortic cusp and mild to moderate aortic regurgitation were confirmed by the use of transesophageal echocardiography (TEE) and ascending aortography.

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