Predictors of colorectal neoplasia after polypectomy: based on initial and consecutive findings.

BACKGROUND: Colorectal adenoma patients are kept under surveillance because of the risk of developing metachronous neoplasia. The aim is to determine predictors of neoplasia development after polypectomy. METHODS: It is an observational cohort study. 433 Patients who had ≥1 adenoma removed between 1988 and 2004 were included, with follow-up until 2010. Multivariate analysis of patient and adenoma characteristics was performed at initial colonoscopy and at consecutive positive examinations. The main outcome measured was the development of metachronous (advanced) adenomas during follow-up. RESULTS: Median follow-up was 85 months. Multivariate analysis identified male sex, ≥3 adenomas, high-grade dysplasia and age ≥55 years as risk factors for metachronous lesions at first surveillance. Analysis using life expectancy as a timescale showed ≥3 adenomas to be the only predictive factor. The time to second or third metachronous adenoma did not depend on the number of adenomas. Patients with ≥3 adenomas were five years older at the time of their first polypectomy compared with those with fewer adenomas, but of the same age at the first recurrence. Prevalence of high-grade dysplasia was associated with age and high-grade dysplasia in the prior adenoma independent of time interval. CONCLUSIONS: Adenoma development after polypectomy occurs in a regular and repetitive way. Our data suggest that only the interval between the initial colonoscopy and the first follow-up colonoscopy should be based on initial findings, i.e. number of adenomas, and that subsequent colonoscopies can be planned at predetermined intervals.

N-acetylcysteine and hemodialysis treatment of a severe case of methyl ethyl ketone peroxide intoxication.

The plastic hardener methyl ethyl ketone peroxide (MEKP) is an unstable peroxide that releases free oxygen radicals. Ingestion of this compound induces widespread liver necrosis that is often fatal, extensive ulceration with subsequent scarring, and stenosis of the proximal digestive tract in survivors. Severe metabolic acidosis occurs due to the accumulation of formic acid and other organic acids inducing neurologic damage, such as optic nerve lesions. A 53-year-old man unintentionally ingested approximately 120 ml of a 33% solution of this compound in dimethylphtalate. The patient was treated with the free radical scavenger N-acetylcysteine to counteract free radical-mediated damage and with hemodialysis to remove accumulated organic acids. Although our patient demonstrated considerable edema and ulceration of the distal esophagus, stomach and duodenum in the acute phase, there was never any sign of liver damage or neurological damage, nor were there any demonstrable lesions in the proximal digestive tract three weeks after the event. Treatment with a combination of N-acetylcysteine and haemodialysis may be a promising therapy for this severe and potentially life-threatening intoxication.