Kővári, Bence

Various subtypes of nonconventional dysplasia have been recently described in inflammatory bowel disease (IBD). We hypothesized that goblet cell deficient dysplasia and serrated dysplasia may be the primary precursor lesions for goblet cell deficient (GCDAC) and serrated (SAC) variants of colonic adenocarcinoma, respectively. Clinicopathologic features of 23 GCDAC and 10 SAC colectomy cases were analyzed. All dysplastic lesions found adjacent to the colorectal cancers (n = 22 for GCDACs and n = 10 for SACs) were subtyped as conventional, nonconventional, or mixed-type dysplasia. As controls, 12 IBD colectomy cases with well to moderately differentiated adenocarcinoma that lacked any mucinous, signet ring cell, low-grade tubuloglandular, or serrated features while retaining goblet cells throughout the tumor (at least 50% of the tumor) were evaluated. The cohort consisted of 19 (58%) men and 14 (42%) women, with a mean age of 53 years and a long history of IBD (mean duration: 18 y). Twenty-seven (82%) patients had ulcerative colitis. GCDACs (57%) were more often flat or invisible than SACs (10%) and controls (25%; P = 0.023). The GCDAC and SAC groups were more likely to show lymphovascular invasion (GCDAC group: 52%, SAC group: 50%, control group: 0%, P = 0.001) and lymph node metastasis (GCDAC group: 39%, SAC group: 50%, control group: 0%, P = 0.009) than the control group. Notably, GCDACs and SACs were more frequently associated with nonconventional dysplasia than controls (GCDAC group: 77%, SAC group: 40%, control group: 0%, P < 0.001). Goblet cell deficient dysplasia (73%) was the most prevalent dysplastic subtype associated with GCDACs (P = 0.049), whereas dysplasias featuring a serrated component (60%) were most often associated with SACs (P = 0.001). The GCDAC group (75%) had a higher rate of macroscopically flat or invisible synchronous dysplasia compared with the SAC (20%) and control (33%) groups (P = 0.045). Synchronous dysplasia demonstrated nonconventional dysplastic features more frequently in the GCDAC (69%) and SAC (40%) groups compared with the control group (0%; P = 0.016). In conclusion, goblet cell deficient dysplasia and dysplasias featuring a serrated component could potentially serve as high-risk markers for GCDACs and SACs, respectively.

Aims There is limited information regarding the clinicopathological features of low‐grade tubuloglandular (LGTGA) and mucinous (MAC) adenocarcinomas occurring in inflammatory bowel disease (IBD), especially with regard to their precursor lesions. Methods and results Forty‐six IBD colectomy specimens with LGTGA ( n = 17) or MAC ( n = 29) with adjacent precursor lesions were analysed. As controls, 12 IBD colectomy specimens with well‐ to moderately differentiated adenocarcinoma that lacked any mucinous, signet ring cell, low‐grade tubuloglandular or serrated features were also analysed. Compared with MACs and controls, LGTGAs more often had a flat/invisible macroscopic appearance (LGTGAs = 88%, MACs = 34%, controls = 25%, P < 0.001). MACs were more likely to have high‐grade differentiation (MACs = 31%, LGTGAs = 0%, controls = 0%, P = 0.002) and a higher pathological stage (pT3 and pT4 MACs = 76%, LGTGAs = 35%, controls = 33%, P = 0.007) than LGTGAs and controls. LGTGAs (70%) and MACs (53%) were more frequently associated with non‐conventional dysplasia than controls (0%) ( P < 0.001). Crypt cell (40%) and hypermucinous (34%) dysplasias were the most common non‐conventional subtypes associated with LGTGAs and MACs, respectively. Synchronous dysplasia often demonstrated non‐conventional features in the LGTGA (33%) and MAC (47%) groups (versus 0% for the control group, P = 0.074). Synchronous cancer frequently showed similar histological features as the main tumour (LGTGA group = 60%, MAC group = 38%, control group = 100%). Conclusions Crypt cell and hypermucinous dysplasias are the most common precursor lesions associated with LGTGAs and MACs, respectively, and may serve as a marker of increased risk for these cancer subtypes.

The upper gastrointestinal (UGI) manifestations of inflammatory bowel diseases (IBDs) are frequently obscured by classic ileal and colonic symptoms and are reported to involve only 0.5% to 4% of adult patients. However, because of the improvement of endoscopic techniques and the growing use of esophagogastroduodenososcopy with biopsy, both asymptomatic and clinically significant esophageal, gastric, and duodenal manifestations are increasingly recognized. The UGI involvement in IBD was historically synonymous with Crohn’s disease (CD), but the doctrine of ulcerative colitis (UC) being limited to the colon has been challenged, and UC-related gastroduodenal lesions have been reported. The diagnosis of UGI IBD should ideally rely on a combination of the clinical history, endoscopic picture, and histologic features. Although endoscopic changes such as aphthoid or longitudinal ulcers and bamboo-joint-like pattern are suggestive of CD, histologic evaluation increases the sensitivity of the IBD diagnosis since histologic alterations may be present in endoscopically unremarkable mucosa. Conversely, in many cases, the histologic findings are nonspecific, and the knowledge of clinical history is vital for reaching an accurate diagnosis. The presence of epithelioid granuloma is highly suggestive of CD but is present in a minority of CD cases; thus, pathologists should be aware of how to diagnose UGI IBD in the absence of granulomata. This article reviews the most important clinical, endoscopic, and histologic features of IBD-associated esophagitis, gastritis, and duodenitis, as well as the IBD-related manifestations in the biliary tract and the postcolectomy setting.

The increasing use of gastrointestinal endoscopic procedures has led to the recognition by histopathologists of non‐conventional (or special‐type) dysplasias of the gastrointestinal tract. These lesions can be recognised in association with prevalent underlying gastrointestinal conditions, such as Barrett oesophagus, chronic atrophic gastritis, and inflammatory bowel disease. The diagnosis of these special types can be challenging, and their biological behaviours are not fully characterised. The aim of this review is to provide a global view of non‐conventional dysplastic lesions observed in the various segments of the tubular gastrointestinal tract and describe their salient features. Furthermore, as the clinical implications of these various subtypes have not been broadly tested in practice and are not represented in most management guidelines, we offer guidance on the best management practices for these lesions.