CLINICAL REVIEW SECTION – Helicobacter pylori and gastric diseases. Blaser, M.J. Division of Infectious Diseases, University School of Medicine, Nashville, TN, USA. BMJ, 316(7143): 1507-1510, 16 May 1998.
Helicobacter pylori is part of a large family of related bacteria. Its strains are enormously diverse and are likely to have existed for many thousands of years. They can be regarded as normal flora, which are acquired during childhood. However, colonization rates of Helicobacter pylori seem to be decreasing, which may reflect environmental circumstances, e.g. better living conditions.
• Carriers of Helicobacter pylori have a 3-10-fold risk of developing a peptic ulcer and a similar risk of developing adenocarcinoma of the antrum and body of the stomach. Carriers also have an increased risk of developing non-Hodgkin’s lymphomas of the stomach.
• Non-ulcer dyspepsia occurs as often in Helicobacter pylori carriers as non carriers. It is likely that for some carriers of Helicobacter pylori, treatment may be effective but, as yet, a firm relationship has not been established. Hence indiscriminate treatment of non-ulcer dyspepsia is likely to produce mixed results.
• As Helicobacter pylori colonization declines, so does ulcer disease and the associated gastric adenocarcinoma. However, in Western countries, this decline is associated with an increase in oesophageal reflux and adenocarcinoma of the distal oesophagus. A protective effect of Helicobacter pylori against these diseases has been proposed. Hence some have argued against the widespread elimination of all types of Helicobacter pylori, particularly in asymptomatic individuals. It is suggested that asymptomatic individuals should be left untreated unless they have a first-degree relative with gastric cancer.
Commentary: Helicobacfer pylori – the story so far. Thomson, M. Department of Paediatric Gastroenterology, Royal Free Hospital, London, UK. BMJ, 319(7209): 537-541, 28 Aug. 1999.
• Helicobacter pylori is the main cause of gastritis, responsible for 80% of gastric and 95% of duodenal ulcers.
• Helicobacter pylori is also implicated in the pathogenesis of gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma.
• Infection is now accepted to occur in childhood, most rapidly under 5 years of age.
• Low socioeconomic status and overcrowding are associated with a higher prevalence.
• The probable route of transmission is via intra-familial faeco-oral or oro-oral contamination.
• Helicobacter pylori‘s antibiotic resistance is an increasing problem.
• Helicobacter pylori has a high genetic variability. Some strains are more pathogenic than others.
• Vaccination research remains active. So far, the mucosal routes of vaccination have not produced a serological response.
Helicobacfer pylori and childhood recurrent abdominal pain: community based case-control study. Macarthur, C, Sounders, N., Feldman, W. et al. Department of Paediatrics, Hospital for Sick Children, Toronto, Ont., Canada. BMJ, 319(7213): 822-823, 25 Sept. 1999.
The 100 ‘cases’ were 5-15-year-old children presenting with at least three episodes of abdominal pain of sufficient severity to interrupt normal activities. The 100 ‘controls’ were children attending for routine check-up or vaccinations to six primary care paediatricians in Toronto.
• Children with recurrent abdominal pain were more likely to be girls, to have symptoms of chronic headache or limb pain, and to have more frequent school absences.
• With both serology and breath testing, there was no evidence to suggest an association between recurrent abdominal pain and Helicobacter pylori infection.