Background
Although self‐expandable metal stent (SEMS) placement as bridge to surgery (BTS) in patients with left‐sided obstructing colonic cancer has shown promising short‐term results, it is used infrequently owing to uncertainty about its oncological safety. This population study compared long‐term oncological outcomes between emergency resection and SEMS placement as BTS.
Methods
Through a national collaborative research project, long‐term outcome data were collected for all patients who underwent resection for left‐sided obstructing colonic cancer between 2009 and 2016 in 75 Dutch hospitals. Patients were identified from the Dutch Colorectal Audit database. SEMS as BTS was compared with emergency resection in the curative setting after 1 : 2 propensity score matching.
Results
Some 222 patients who had a stent placed were matched to 444 who underwent emergency resection. The overall SEMS‐related perforation rate was 7·7 per cent (17 of 222). Three‐year locoregional recurrence rates after SEMS insertion and emergency resection were 11·4 and 13·6 per cent (P = 0·457), disease‐free survival rates were 58·8 and 52·6 per cent (P = 0·175), and overall survival rates were 74·0 and 68·3 per cent (P = 0·231), respectively. SEMS placement resulted in significantly fewer permanent stomas (23·9 versus 45·3 per cent; P < 0·001), especially in elderly patients (29·0 versus 57·9 per cent; P < 0·001). For patients in the SEMS group with or without perforation, 3‐year locoregional recurrence rates were 18 and 11·0 per cent (P = 0·432), disease‐free survival rates were 49 and 59·6 per cent (P = 0·717), and overall survival rates 61 and 75·1 per cent (P = 0·529), respectively.
Conclusion
Overall, SEMS as BTS seems an oncologically safe alternative to emergency resection with fewer permanent stomas. Nevertheless, the risk of SEMS‐related perforation, as well as permanent stoma, might influence shared decision‐making for individual patients.
Unless colonoscopy is regarded for screening in individuals aged 50 years and older, routine colonoscopy in the absence of other clinical signs of CRC is not required.
BackgroundDectin-1 is a pattern recognition receptor (PRR) expressed by myeloid cells that specifically recognizes β-1,3 glucan, a polysaccharide and major component of the fungal cell wall. Upon activation, dectin-1 signaling converges, similar to NOD2, on the adaptor molecule CARD9 which is associated with inflammatory bowel disease (IBD). An early stop codon polymorphism (c.714T>G) in DECTIN-1 results in a loss-of-function (p.Y238X) and impaired cytokine responses, including TNF-α, interleukin (IL)-1β and IL-17 upon in vitro stimulation with Candida albicans or β-glucan. The aim of the present study was to test the hypothesis that the DECTIN-1 c.714T>G (p.Y238X) polymorphism is associated with lower disease susceptibility or severity in IBD and to investigate the level of dectin-1 expression in inflamed and non-inflamed colon tissue of IBD patients.MethodologyParaffin embedded tissue samples from non-inflamed and inflamed colon of IBD patients and from diverticulitis patients were immunohistochemically stained for dectin-1 and related to CD68 macrophage staining. Genomic DNA of IBD patients (778 patients with Crohn's disease and 759 patients with ulcerative colitis) and healthy controls (n = 772) was genotyped for the c.714T>G polymorphism and genotype-phenotype interactions were investigated.Principal FindingsIncreased expression of dectin-1 was observed in actively inflamed colon tissue, as compared to non-inflamed tissue of the same patients. Also an increase in dectin-1 expression was apparent in diverticulitis tissue. No statistically significant difference in DECTIN-1 c.714T>G allele frequencies was observed between IBD patients and healthy controls. Furthermore, no differences in clinical characteristics could be observed related to DECTIN-1 genotype, neither alone, nor stratified for NOD2 genotype.ConclusionsOur data demonstrate that dectin-1 expression is elevated on macrophages, neutrophils, and other immune cells involved in the inflammatory reaction in IBD. The DECTIN-1 c.714T>G polymorphism however, is not a major susceptibility factor for developing IBD.
The homozygous state of the UGT1A1*28 polymorphism, associated with higher serum bilirubin levels, may be protective for the development of Crohn's disease, suggesting that the anti-oxidant capacity of bilirubin may play a part.
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