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At least 829 records · Page 46Linked to original sources
PubMed2006

Flat polyps of the colon: detection with 16-MDCT colonography--preliminary results.

OBJECTIVE: This study evaluates the ability of contrast-enhanced, 16-MDCT colonography to display flat colonic lesions when a very narrow slice thickness (1 mm) is used. CONCLUSION: Less than 50% of flat lesions in our population could be visualized by blinded and unblinded review. Before they could be visualized, flat lesions were 2 mm or greater in height and 7 mm or greater in diameter. Lesions with a height of 1 mm or less were not seen on CT colonography. Contrast enhancement, location on a haustral fold, and abnormal 2D and 3D morphology contributed to lesion conspicuity.

Aged↗
PubMed2026

Analysis of APC promoter 1B deletions in Russian families with familial adenomatous polyposis.

OBJECTIVE: Familial adenomatous polyposis (FAP) is a severe autosomal dominant hereditary cancer syndrome. Patients develop hundreds of adenomatous polyps throughout the colon with the risk of colorectal cancer, if untreated, approaching 100%. FAP is caused by pathogenic germline variants in the APC gene. Deletions in the APC 1B promoter cause FAP in a small subgroup of patients. Previous studies suggested that the APC promoter deletions in unrelated FAP patients from the US and Italy are identical and may thus have spread from a single founder. The aim of this study was to investigate whether a similar founder effect can be detected in the Russian population. PATIENTS AND METHODS: We performed whole-genome sequencing on five unrelated patients (three males and two females) with extensive (over 100) colon polyps, family history of FAP, and germline APC 1B promoter deletions previously detected by the multiplex ligation-dependent probe amplification (MLPA) and detected precise deletion boundaries. RESULTS: The patients carried deletions in the APC 1B promoter ranging from ~3 to ~122 kbp. We found no association between the deletion size and either the age of the onset or severity of the disease. All deletions were unique and no identical deletion boundaries were observed. However, in four patients, the right deletion breakpoints fell into a 1 kbp region downstream of the 1B promoter. The right breakpoints of several deletions detected in FAP patients from other countries also fell into this narrow region. CONCLUSION: The APC 1B promoter deletions analyzed in this study had arisen independently and there is thus no evidence of a founder effect. Therefore, at least for the cohort of FAP patients with APC 1B promoter deletions studied here, WGS did not provide an added diagnostic benefit to MLPA aside from precisely determining the deletion breakpoints.

APC promoter 1B deletion↗
PubMed1995

The forms and the levels of fecal PMN-elastase in patients with colorectal diseases.

OBJECTIVES: To compare the form of polymorphonuclear leukocyte (PMN)-elastase in feces with that in plasma and to investigate the usefulness of measuring fecal PMN-elastase levels in patients with colorectal diseases. METHODS: We examined PMN-elastase complexed with alpha 1-antitrypsin (alpha 1-AT), chymotrypsin, and alpha 2-macroglobulin by ELISA in feces and plasma. Fecal levels of total PMN-elastase were determined in patients with colonic polyp (N = 19), colonic cancer (N = 20), ulcerative colitis (UC; N = 36), colonic Crohn's disease (CD; N = 26), and in control subjects (N = 20). RESULTS: Most PMN-elastase was not complexed with alpha 1-AT, chymotrypsin, or alpha 2-macroglobulin in feces, whereas most plasma PMN-elastase was complexed with alpha 1-AT. Fecal concentrations and daily fecal excretion of PMN-elastase were significantly increased in patients with active UC (medians 54.8 micrograms/g, 15.14 mg/day) and active CD (41.5 micrograms/g, 10.24 mg/day) compared to those values in control subjects (0.6 micrograms/g, 0.11 mg/day) and in patients with colonic cancer (2.5 micrograms/g, 0.33 mg/day). In inactive UC and CD, these values (3.4 micrograms/g, 0.52 mg/day and 5.2 micrograms/g, 0.59 mg/day, respectively) were significantly lower than in active UC and CD, respectively. In UC, all patients whose rectal biopsies showed infiltration of PMN had high fecal PMN-elastase levels. CONCLUSIONS: Our results suggest that the measurement of fecal PMN-elastase concentrations are useful for monitoring the disease activity of UC and CD, especially when evaluating whether intestinal inflammation has disappeared completely.

Adult↗
PubMed1996

Angioimmunoblastic lymphadenopathy: an etiology for gastrointestinal lymphomatous polyposis.

We describe a case of angioimmunoblastic lymphadenopathy with multiple polyps of the gastrointestinal tract. The patient presented with fever, abdominal mass, ascites, diarrhea, generalized lymphadenopathy, anemia, and marked peripheral eosinophilia. She had multiple polyps in the colon, as well as in the stomach and duodenum. Histology of a colonic polyp showed involvement by angioimmunoblastic lymphadenopathy. The patient responded initially to combination chemotherapy, with total disappearance of polyps. However, she succumbed later to infections. Angioimmunoblastic lymphadenopathy, although rare, should be included as a cause of lymphomatous polyposis of the gastrointestinal tract.

Adult↗
PubMed1996

The role of laparoscopic colectomy and laparotomy with resection in the management of complex polyps of the colon.

Surgical options available to patients with endoscopically unresectable lesions include laparoscopic assisted colonscopy, colonscopic assisted laparoscopy, laparotomy with segmental resection, and laparoscopic colon resection. The choice of modality depends on the nature of the lesion as well as the choice of both the patient and the surgeon. The surgeon should be fluent in all available therapeutic modalities.

Colectomy↗