Regular aspirin use cuts Barrett’s oesophagus risk in women
Aspirin may exert a protective effect on the risk of Barrett’s oesophagus (BE) in women, with the effect being evident in regular aspirin users who take higher doses and who have longer duration of exposure, a recent study has found.
“These results may provide further insight into the earliest mechanisms of BE pathogenesis, suggest the possibility that aspirin prevents EAC [oesophageal adenocarcinoma] by influencing the initiation as well as progression of oesophageal neoplasia, and provide the rationale for future prevention trials in high-risk patients,” the authors said.
The study used data from the Nurses’ Health Study and included 27,881 women (mean age 66 years; 97.6 percent Caucasian) who had undergone upper GI endoscopy. There were 667 cases of BE recorded over 18 years of follow-up.
In a multivariable unconditional logistic regression model, the risk of BE was 15-percent lower in regular aspirin users (≥2 times/week; n=13,462) than in nonregular users (<2 times/week; n=14,419; adjusted odds ratio [aOR], 0.85; 95 percent CI, 0.72–0.99). The corresponding aOR for developing BE ≥1 cm long was 0.73 (0.56–0.96). [Clin Transl Gastroenterol 2017;doi:10.1038/ctg.2017.57]
On further analysis, the risk appeared to drop with increasing dose and duration of aspirin use. The aOR for any BE was 0.91 (0.69–1.20) with intake of 0.5–1.5 tablets/week, 0.92 (0.76–1.11) with intake of 2–5 tablets/week and 0.71 (0.55–0.92) with intake of ≥6 tablets/week as compared with nonuse (p=0.01 for trend). The corresponding aORs with regular aspirin use for 1–5 years, 6–10 years, and >10 years were 0.90 (0.67–1.20), 0.84 (0.65–1.09) and 0.81 (0.67–0.97) relative to nonregular use (p=0.03 for trend).
The authors pointed out that the current data, when taken together with those from other studies demonstrating aspirin to be inversely associated with EAC and dysplasia development among patients with BE, suggest that the drug may be a chemopreventive agent for the earliest stages of the inflammation>metaplasia>adenocarcinoma sequence in women.
Aspirin may prevent the onset of BE and its progression to EAC by inhibiting prostaglandin-endoperoxide synthase (also known as cyclo-oxygenase) 1 and 2–enzymes that mediate inflammation and regulate epithelial cell growth, and are believed to play a role in the development of BE as they are overexpressed early in metaplastic tissue–thus indirectly reducing cellular proliferation and angiogenesis. [Histopathology 2003;42:457–465; Gastroenterology 2012;142:442–452; Cancer Res 2006;66:4975–4982]
Despite having a large sample size and being prospective in nature, the study was limited by the lack of information on BE length in a number of endoscopy records, as well as the possibility of a secular effect due to an increase in both aspirin use and endoscopy utilization over time, the authors noted.
“[Also,] our findings may not be generalizable to other populations, since our participants were all female nurses and primarily Caucasian,” they added.
“Additional research into a potential role for aspirin in the chemoprevention of EAC is [thus] warranted,” the authors said.