The role of smoking and alcohol in metaplasia and cancer risk in Barrett's columnar lined oesophagus.

Smoking and alcohol consumption predispose to oesophageal mucosal damage and exacerbates gastro-oesophageal reflux. The alcohol and smoking habits of patients with severe oesophagitis (n = 24), Barrett's columnar lined oesophagus (CLO) (n = 58), and adenocarcinoma arising in CLO (n = 23) were studied. There was no significant difference between the age (median 67, 64, and 65 years respectively) or duration of symptoms (median 10 years) in each group. Patients with benign CLO were significantly more likely to be non-smokers and non-drinkers, or both than patients with both severe oesophagitis and adenocarcinoma (p < 0.001). Of those who smoked or drank, patients with CLO had a smoking history of a median 15 pack years (range 2-60 pack years), which was less than both the severe oesophagitis (median 45.5, range 5-150 pack years) (p < 0.01), and adenocarcinoma groups (median 55.25, range 4-200 pack years) (p < 0.001). Patients with adenocarcinoma had smoked for more years in total (median 38.5, range 4-54 years) than patients with CLO (median 29.5, range 6-55 years) (p < 0.01). Patients with severe oesophagitis (median 38.5, range 27-55 years) and adenocarcinoma patients had a similar long history of smoking both of which were greater than CLO patients (p < 0.003). Half of the severe oesophagitis group drank more than 40 units/week and six more than 100 units/week (median 40, range 1-->100 units/week), whereas CLO patients who drank did so more moderately (median 10, 1-100 units/week) (p < 0.02). Adenocarcinoma patients also had a somewhat greater alcohol intake than CLO patients, median 15 (1-100 units/week) (p<0.02). Smoking and alcohol consumption do not predispose to the development od metaplastic columnar lined oesophagus in patients with severe gastro-oesophageal reflux but are strongly associated with the development of adenocarcinoma in patients with established Barrett's oesophagus.