• Oesophageal Cancer
• Helicobacter Pylori

Two consensus reports on Helicobacter pylori (Hp), published recently in Gut, summarise the role of Hp gastritis in upper GI diseases, including gastric cancer (GCA).1 2 Although Hp gastritis definitely increases the risk of GCA as suggested in both reports, Hp is, on the other hand, also associated with a notable low incidence of oesophageal cancer (EC), of both adenomatous and squamous type.

In our earlier 15-year follow-up of a large population-based sample of males aged 50–65 years (n=12 016) from two Finnish cities, with or without Hp, diagnosed in 1994–1996 by serological (IgG) Hp test (Biohit HealthCare, Helsinki, Finland), 57 GCA cases were recorded in the study population by the nationwide Cancer Registry during the follow-up.3 Of these cancers, 50 were in men and seven in those with and without Hp, respectively. The relative standardised incidence ratio (RR) of GCA incidence in Hp positive compared with that in Hp-negative men, calculated with the Altman’s procedure, was 6.0 (95%CI 2.3 to 19.0).

In a 20-year follow-up of the same population sample, 39 ECs appeared during the follow-up. Of these, 29 were in the Hp-negative subgroup (6625 men) and 10 in the Hp-positive subgroup (5391 men) (table 1). Of the cancers in Hp-negative and in Hp-positive subgroups, 11 and three were ECs of adenocarcinoma type and 14 and six of squamous cell type, respectively. In five cases, the histological type was unknown. All estimates of RR of EC in the Hp-positive men compared with EC in the Hp-negative men were very low, as shown in table 1, indicating that the Hp gastritis associates strongly with reduced EC risk. In addition to ECs of adenocarcinoma type also, the RR of squamous cell EC was notably low (table 1). Serum level of pepsinogen I did not markedly alter any of the RR estimates.

The prevented fraction of EC due to Hp positivity was very high, 78%. In comparison, the corresponding attributable percentage of GCA in Hp-positive men was 84%.3 Thus, relatively, the Hp gastritis reduces EC incidence roughly similarly as it increases GCA incidence. However, the incidence rate of GCA in the present study population was nearly twice as high as the incidence of EC. Therefore, the numbers of GCA caused by Hp positivity were nearly twice the numbers of EC prevented by Hp positivity.

Lower than the expected risk of oesophageal cancer in men with Hp gastritis has been presented in several other studies (see, eg, Nie et al, Rokkas et al, Islami and Kamangar, Xie et al, Ye et al, de Martel et al, Whiteman et al 4–10) The reason of this low risk is unknown. So far, the most plausible explanation is the intragastric acidity that tends to be lower in patients with Hp gastritis than in those without it. In people with ‘healthy’ stomach, a highly acid gastro-oesophageal refluxate, in persons prone and liable to GERD, may promote cascades that result in acid-related erosive and finally cancerous lesions in the oesophageal epithelium. In this context, in contrast to alkaline reflux, the acid reflux into the oesophagus is likely the key factor that associates with the increased risk and incidence of EC.