Abstract:Although low-grade dysplasia occurred at several colonic levels and at repeated colonoscopies in 73 percent of the patients, no progression to high-grade dysplasia was found during 10 years of follow-up, except in 2 cases with dysplasia-associated lesion or mass. Colectomy in cases with single or repeated low-grade dysplasia in flat mucosa does not appear to be justified.
“…Lynch et al [36] identified only 2.5% of patients with LGD who went on to develop cancer. Befrits et al [59] in a study of patients with extensive longstanding colitis who were found to have fLGD on index colonoscopy, found LGD on subsequent colonoscopy in 73% of cases but none progressed to HGD except in two patients with DALM during a 10-year follow-up period. Lim et al [66] in a retrospective cohort study of patients still alive with an intact colon who had LGD, HGD, or cancer developed 10% versus 4% in patients with no LGD after 10-year follow-up.…”
Section: Proctocolectomymentioning
confidence: 98%
“…Thus, these lesions represent sporadic adenomas developing in areas of inflammation. Other studies have showed that ''small polyploid dysplastic lesions,'' ''pedunculated polyps,'' and lesions that endoscopically and histologically resemble an adenoma can be safely treated endoscopically with no evidence of flat dysplasia or carcinoma on follow-up provided no other areas of flat dysplasia are recognized [41,51,[58][59][60]. Adenoma-like DALM has low risk for malignancy than flat LGD (fLGD) or flat HGD [11,32,41].…”
Section: Dysplasiamentioning
confidence: 99%
“…DALM is also a maker of increased cancer risk since cancer is found in 58-63% of patients with DALM [31,32]. The presence of HGD in flat or raised mucosa and any dysplasia with DALM is an indication for PC because of the high rate of synchronous CRC and progression to cancer [31,39,43,59,66]. The management of patients with fLGD varies from repeat colonoscopy to PC or watch and see.…”
Section: Proctocolectomymentioning
confidence: 99%
“…Some studies have found lower progression rate of LGD [36,44,59,66]. Lynch et al [36] identified only 2.5% of patients with LGD who went on to develop cancer.…”
Section: Proctocolectomymentioning
confidence: 99%
“…Some consider better outcomes are obtained if all patients with dysplasia undergo surgery [43]. Others favor continued surveillance, waiting for clinical deterioration or progression or persistence of LGD [36,47,58,59,80]. When recommending surgery for LGD the longterm outcome of PC must be considered: 50% minor pouchitis, 19-37% severe pouchitis, surgery for bowel obstruction (8-16%), pelvic sepsis (5%), multiple relaparotomies (17-20%), and mean frequency of bowel movements in 24 hr of 6-7 with incontinence 38-48% [81].…”
Patients with ulcerative colitis (UC) are at an increased risk for the development of colorectal cancer (CRC). Unlike sporadic CRC, the cancer in UC patients arises from a focal or multifocal dysplastic mucosa in areas of inflammation. The clinical features of UC-associated cancer are similar to those found in patients with hereditary non-polyposis colorectal cancer. As with other varieties of CRC, UC-associated cancer exhibits a variety of genetic and molecular changes/abnormalities. These abnormalities are however clustered in areas of mucosae with histological abnormalities. The magnitude and timing of these changes are however significantly different. Surveillance and identification of patients at risk for cancer are a challenging problem.
“…Lynch et al [36] identified only 2.5% of patients with LGD who went on to develop cancer. Befrits et al [59] in a study of patients with extensive longstanding colitis who were found to have fLGD on index colonoscopy, found LGD on subsequent colonoscopy in 73% of cases but none progressed to HGD except in two patients with DALM during a 10-year follow-up period. Lim et al [66] in a retrospective cohort study of patients still alive with an intact colon who had LGD, HGD, or cancer developed 10% versus 4% in patients with no LGD after 10-year follow-up.…”
Section: Proctocolectomymentioning
confidence: 98%
“…Thus, these lesions represent sporadic adenomas developing in areas of inflammation. Other studies have showed that ''small polyploid dysplastic lesions,'' ''pedunculated polyps,'' and lesions that endoscopically and histologically resemble an adenoma can be safely treated endoscopically with no evidence of flat dysplasia or carcinoma on follow-up provided no other areas of flat dysplasia are recognized [41,51,[58][59][60]. Adenoma-like DALM has low risk for malignancy than flat LGD (fLGD) or flat HGD [11,32,41].…”
Section: Dysplasiamentioning
confidence: 99%
“…DALM is also a maker of increased cancer risk since cancer is found in 58-63% of patients with DALM [31,32]. The presence of HGD in flat or raised mucosa and any dysplasia with DALM is an indication for PC because of the high rate of synchronous CRC and progression to cancer [31,39,43,59,66]. The management of patients with fLGD varies from repeat colonoscopy to PC or watch and see.…”
Section: Proctocolectomymentioning
confidence: 99%
“…Some studies have found lower progression rate of LGD [36,44,59,66]. Lynch et al [36] identified only 2.5% of patients with LGD who went on to develop cancer.…”
Section: Proctocolectomymentioning
confidence: 99%
“…Some consider better outcomes are obtained if all patients with dysplasia undergo surgery [43]. Others favor continued surveillance, waiting for clinical deterioration or progression or persistence of LGD [36,47,58,59,80]. When recommending surgery for LGD the longterm outcome of PC must be considered: 50% minor pouchitis, 19-37% severe pouchitis, surgery for bowel obstruction (8-16%), pelvic sepsis (5%), multiple relaparotomies (17-20%), and mean frequency of bowel movements in 24 hr of 6-7 with incontinence 38-48% [81].…”
Patients with ulcerative colitis (UC) are at an increased risk for the development of colorectal cancer (CRC). Unlike sporadic CRC, the cancer in UC patients arises from a focal or multifocal dysplastic mucosa in areas of inflammation. The clinical features of UC-associated cancer are similar to those found in patients with hereditary non-polyposis colorectal cancer. As with other varieties of CRC, UC-associated cancer exhibits a variety of genetic and molecular changes/abnormalities. These abnormalities are however clustered in areas of mucosae with histological abnormalities. The magnitude and timing of these changes are however significantly different. Surveillance and identification of patients at risk for cancer are a challenging problem.
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