Detecting intestinal metaplasia: Eight biopsies required


Am J Gastroenterol 2007; 102: 1154–1161

MedWire News: Clinicians should carry out eight biopsies per endoscopy to diagnose benign intestinal metaplasia in patients with long-segment Barrett’s esophagus (LSBE), suggests data from an observational study.

Rebecca Harrison (University Hospitals of Leicester, UK) and colleagues retrospectively analyzed the histological slides from 125 consecutive patients identified as having LSBE at endoscopy.

All endoscopic procedures were conducted at a single center over a 4-year period. A total of 296 endoscopies were performed in Barrett’s esophagus segments with a mean length of 4.9 cm (range 1-11 cm).

All biopsies were analyzed using conventional hematoxylin and eosin (H&E) staining. A subset of biopsies also underwent additional alcian blue/periodic-acid Schiff staining.

H&E staining showed a significant increase in the frequency of intestinal metaplasia in patients with five to eight biopsies per endoscopy, compared with those with one to four biopsies per endoscopy (mean 67.9% vs 34.6% of endoscopies).

Unless more than 16 biopsies were taken, which identified 100% of endoscopies with intestinal metaplasia, no additional significant detection was achieved beyond eight biopsies.

“Thus it appears that if eight or more biopsies are obtained and are negative for intestinal metaplasia, then intestinal metaplasia can reasonably be excluded,” say Harrison and team in the American Journal of Gastroenterology.

The use of additional alcian blue/periodic-acid Schiff staining demonstrated a marginal benefit, identifying 5.4% of new cases of intestinal metaplasia, compared with H&E staining alone.

“We would recommend that a minimum of eight random biopsies be taken at index endoscopy to confidently exclude intestinal metaplasia, and be assessed using H&E staining alone,” conclude the researchers.

Common Genetic Risk Factor For Colorectal And Prostate Cancer Identified By Study

A study led by researchers at the Keck School of Medicine of the University of Southern California (USC) has found that one of seven genetic risk factors previously identified as increasing the probability of developing prostate cancer also increases the probability of developing colorectal cancer. As in the previous prostate cancer study, which was also conducted by USC researchers and published in the April 2007 edition of Nature Genetics, the colorectal cancer risk factor is located in a region of the human genome devoid of known genes on chromosome 8. The study’s complete findings are published in the online edition of Nature Genetics.

“This is an important finding because, for the first time, a common genetic risk factor for multiple cancers has been identified,” says lead author Christopher Haiman, assistant professor of preventive medicine at the Keck School of Medicine of USC. Adding, “There appears to be something fundamental occurring in this region that influences not only colorectal and prostate cancer, but perhaps cancers in general.” (Another recently published study, in which USC researchers also were involved, identified variants in this same chromosomal region as playing a predictive role relative to the risk of developing breast cancer.)

For the current colorectal cancer study, the USC team genotyped six of the seven variants previously identified as increasing the risk of prostate cancer development. The samples analyzed totaled 1,807 invasive colorectal cancer cases and 5,511 controls. These samples were drawn from five populations (African Americans, Japanese Americans, Native Hawaiians, Latinos, and European Americans) included in the Multiethnic Cohort Study, an epidemiological study of more than 215,000 people from Los Angeles and Hawaii created in 1993 by Brian Henderson, dean, Keck School of Medicine of USC, and Laurence Kolonel of the University of Hawaii.

According to Henderson, co-author of the colorectal cancer study, “Having previously identified several genetic risk factors related to prostate cancer, and now having identified one of these same variants as predictive of colorectal cancer risk, brings us closer to our long-term goal of developing a model that more precisely pinpoints who is at greater risk for developing colorectal, prostate, and other cancers.” However, Henderson notes, “We still need to identify the biological mechanism through which these variants are influencing the development of various cancers.”

Article adapted by Medical News Today from original press release.

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