Smoking Doubles Cancer Risk in Barrett's Esophagus



Smoking tobacco more than doubles the risk that Barrett’s esophagus will progress to adenocarcinoma or high-grade dysplasia, Dr. Helen G. Coleman and her colleagues wrote in the February issue of Gastroenterology.

The study also found that alcohol consumption – despite its known association with esophageal squamous cell carcinoma – was not linked to adenocarcinoma (Gastroenterology 2011 [Epub ahead of print, doi:10.1053/j.gastro.2011.10.034]).

Dr. Coleman of Queen’s University Belfast, United Kingdom, reviewed the medical records of patients in the population-based Northern Ireland BE register. The register includes all adults diagnosed with columnar-lined epithelium of the esophagus between 1993 and 2005 in that region, making it "one of the largest population-based cohorts of BE patients worldwide."

This cohort was then linked to the Northern Ireland Cancer Registry, and the researchers were able to identify patients in the former registry who subsequently developed adenocarcinomas or unspecified malignancies of the esophagus and gastric cardia adenocarcinomas.

Squamous cell esophageal carcinomas were not included as outcomes, and the results were tallied through Dec. 31, 2008.

Overall, 3,167 BE patients were included in the analysis, and were followed up for a total of 23,692 person-years up to 16 years, with a mean follow-up of 7.5 years.

In total, 117 patients developed high-grade dysplasia or cancer of the esophagus or gastric cardia, wrote the authors, including 70 adenocarcinomas or unspecified cancers of the esophagus, 10 adenocarcinomas of the gastric cardia and 37 cases of esophageal high-grade dysplasia.

The mean time from BE diagnosis to diagnosis of cancer or dysplasia was 4.5 years.

Those patients who progressed from BE were significantly more likely to be between 50 and 60 years old (P = .003), to be male (P = .001), and to have a Barrett’s segment length of 3 cm or greater (P = .006).

They were also much more likely (P less than .001) to have low-grade or indefinite dysplasia at their index BE diagnosis, wrote the authors.

Among the modifiable risk factors, smoking carried the greatest weight.

After researchers adjusted for demographics, presence of low-grade dysplasia, reflux symptoms, and Barrett’s segment length at diagnosis, current cigarette smokers had a more than twofold risk of BE progression, compared with patients who never smoked (hazard ratio, 2.02; 95% confidence interval, 1.13-3.11).

Pipe smokers had an even greater risk and were nearly three times as likely to have their BE progress, compared with patients who never smoked a pipe (HR, 2.95; 95% CI, 1.39-6.25).

Any current smoking status – be it pipe or cigarette – had a hazard ratio of 2.29, compared with nonsmokers (95% CI, 1.32-4.00).

Alcohol intake, in contrast, was not correlated with BE progression, even among patients who said they drank 10 units or more per week (HR, 0.82; 95% CI, 0.41-1.62).

That finding is in agreement with other studies, wrote the investigators, in which alcohol has been "consistently refuted as a risk factor for [esophageal adenocarcinoma], in contrast to its known direct association with esophageal squamous cell carcinoma," wrote the authors.

"Therefore we can only recommend that BE patients follow the advice of current public health guidelines for cancer prevention to consume alcohol in moderation, if taken," they added.

On the other hand, wrote Dr. Coleman, smoking has previously been "specifically demonstrated to inflict DNA damage on Barrett’s mucosa."

Additionally, she postulated that smoking may be "associated with an increased number of reflux episodes and that nicotine may reduce lower esophageal sphincter pressure, which would contribute to excess acid/bile exposure that may consequently increase neoplastic progression risk in BE."

The authors wrote that the study was funded by the Ulster Cancer Foundation and the Health and Social Care Research and Development Office. They added that they have no conflicts to declare.

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