Treatment of ulcers can be improved and over-reliance on proton pump inhibitors reduced

EDITOR—Harris and Misiewicz in their review of managing Helicobacter pylori infection take a balanced view of the contentious issues surrounding treatment in patients without ulcers.1 But several inconsistencies are apparent in their approach to patients with ulcers, for whom solid evidence for treatment is available.

Harris and Misiewicz advocate only two attempts at eradication in patients with duodenal and gastric ulcers; failure of the second attempt is followed by maintenance treatment with antisecretory drugs. Although the 90% success rate for one course of eradication treatment is ideal, combined data from randomised controlled trials suggest that eradication rates of 73-87% are more usual.2 In everyday practice, rates of 64% or lower may be expected, depending on the regimen and interest of the clinician.3

After two courses of treatment, potentially one in eight patients may still be infected, and failure to persevere with eradication denies these patients a treatment that alters the natural history of the disease by preventing recurrence and haemorrhage of ulcers. Continuous antisecretory treatment is less convenient, less effective, and more costly; strategies must therefore be constructed to improve overall eradication rates.

In the light of this need to optimise success, Harris and Misiewicz's bias towards treatments based on using proton pump inhibitors and reluctance to endorse ranitidine bismuth citrate is surprising. Ranitidine based triple treatments are at least equivalent, and in some cases significantly superior, to regimens based on proton pump inhibitors as initial treatment.2 Bismuth based regimens (either ranitidine bismuth citrate or colloidal bismuth) seem superior to others after an initial failure. 3 4 In this situation, triple therapy with ranitidine bismuth citrate, tetracycline, and metronidazole produced significantly better eradication rates than the quadruple therapy with proton pump inhibitors and bismuth advocated by Harris and Misiewicz.5 Treatments based on ranitidine bismuth citrate are effective and equivalent in cost to those using proton pump inhibitors, but Harris and Misiewicz did not recommend their wider use.

Few data are available concerning third line treatments. After using regimens containing clarithromycin and nitroimidazole, there is no logical combination. Although a combination regimen using proton pump inhibitors, rifabutin, and amoxicillin seems promising in this situation, treatment directed by endoscopy, culture, and sensitivity testing seems better than empirical choice.3 More than 98% of patients requiring H pylori eradication can be successfully treated using a three step algorithm, removing the need for continued drug treatment.3 Strategies for H pylori eradication should not be based merely on first line eradication rates but include further steps to maximise success in those who will definitely benefit from treatment.

Eradication treatment can be tailored in patients undergoing endoscopy

EDITOR—In their review of the management of Helicobacter pylori infection Harris and Misiewicz suggest that patients likely to have metronidazole resistant H pylori infection should be treated with non-nitroimidazole containing eradication regimens.1 But prediction of resistance to antimicrobials in H pylori infection relies on the availability of resistance data in the given geographic area of practice. Few hospitals carry out sensitivity testing of H pylori, therefore local data are seldom available. In addition, although Harris and Misiewicz point out that metronidazole resistance is commoner in women and patients from developing countries, translation of this knowledge into prescribing practice is difficult in treating individual patients.

Our study of 1064 consecutive patients in Sheffield found to be H pylori culture positive at endoscopy showed metronidazole resistance rates to be 45% for women compared with 37% for men (odds ratio 1.48; 95% confidence interval 1.15 to 1.91). For patients >60 years resistance was 34% compared with 44% for patients <60 years (odds ratio 0.62; 0.48 to 0.8).2 A pragmatic approach to H. pylori eradication may be to exclude nitroimidazoles from regimens. This would not be advised, as metronidazole is a cheap and effective antibiotic when used in regimes to treat metronidazole sensitive strains. Also, increased use of clarithromycin, as a replacement for metronidazole, is likely to result in more disruption and induction of resistance in host microflora and thereby reduce the efficacy of macrolides in the treatment of other infectious conditions.3

Culture and sensitivity testing of H pylori is well established and requires few special facilities. As Harris and Misiewicz discuss management of H pylori after endoscopy, it seems appropriate to recommend taking an additional biopsy at the time of procedure for microbiological culture. The patients could be treated with proton pump inhibitors if indicated, while sensitivity results are obtained (about one week), and then prescribed a specific, effective eradication regimen. In this era of increasing resistance to antimicrobials optimisation of treatment is of paramount importance in clinical practice.

Dental plaque is a potential reservoir of Helicobacter pylori

EDITOR—In their review of the management of Helicobacter pylori infection Harris and Misiewicz do not mention the potential reservoir of H pylori in dental plaque on teeth.1 Because this is a biofilm, no antibiotic will penetrate it, and if it carries the organism, it must be removed mechanically with oral hygiene, scaling, and root planing—exactly as for periodontal diseases caused by plaque micro-organisms.2

The effect of removal and control of dental plaque on the plaque reservoir of H pylori was shown clearly in a short study.3 Triple therapy alone (omeprazole, clarithromycin, and metronidazole) was wholly ineffective, but scaling followed by chlorhexidine mouthrinse eradicated H pylori in 80-90% of patients. Everyone dealing with bacterial diseases should remember that if biofilms are involved, antibiotics alone are unlikely to be sufficient treatment. Similarly, the mouth rinse is useless without the scaling.

Biofilm, like dental plaque, is a ready source for reinfection. They are complex communities of many bacterial species with powerful defences against chemical and pharmacological threats, but some organisms may not gain a foothold in them because of bacterial antagonisms.4 This means that not all patients with H pylori infection will necessarily have the organism in their dental plaque, which may have misled some investigators in the past. Reinfection from plaque will also be subject to variable host defences and therefore not occur consistently in all cases in which conventional H pylori treatment is used.