Rapid Responses to:
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Rapid Responses: Rapid Responses published:
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H pylori doesn't live only in the stomach!
- Dr Trevor Watts (5 July 2002)
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Re: H pylori doesn't live only in the stomach!
- VH Chong (9 July 2002)
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Re: Re: H pylori doesn't live only in the stomach!
- Jamie S Wilson (11 July 2002)
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Re: Re: H pylori doesn't live only in the stomach!
- Dr Trevor Watts (11 July 2002)
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Reduction of Helicobacter pylori and Lactobacilli.
- Mahantayya V. Math (14 July 2002)
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Excellent results can be achieved without sensitivity testing
- Ian L. P. Beales (17 July 2002)
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Dr Trevor Watts, Senior Lecturer and Consultant in Periodontology Guy's, King's and St Thomas' Dental Institute, London Bridge, SE1 9RT
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I find it totally perplexing that this editorial does not mention the increasing literature implicating H pylori reinfection from the dental plaque biofilm. To treat patients as though this organism were only in their stomach is to risk reinfection from the mouth. Furthermore, as I have already pointed out in the BMJ (1), organisms in a biofilm cannot be removed with systemic antibiotics. 1. Watts T. Dental plaque is a potential reservoir of Helicobacter pylori. BMJ 2002; 324: 614-615. |
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VH Chong, clinical fellow Tan Tock Seng Hospital, Singapore.
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I understand that H pylori organism can actually be recovered from dental plague but has not been consistent. What i would like to enquire is how does the H pylori survive in an enviroment which is completely different from that of stomach (this is assuming that H pylori Survive best in the stomach)? What might be the mechanism? Thanks. |
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Jamie S Wilson, Medical Student Ninewells Hospital
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Is the environment of the mouth necessarily different to the stomach? Is the environment of the mouth necessarily different to the stomach in people infected with H Pylori infection? Could it not be that people discovered to have H Pylori are already receiving acid suppression therapy? Could bile presence in the stomach predispose to H Pylori infection. Alternatively, in Gastro-Oesophageal Reflux Disease (GORD), it is emerging that susceptibility is conferred by derrangement of defence mechanisms such as those provided by EGF which may act on the Oesophageal epithelium and carbonic anhydrase (CA). CA is present in secretory cells of the salivary gland and helps bring about the high pH of saliva. In addition, isoforms of CA may be secreted themselves be secreted in saliva. It may be that people are susceptible to H Pylori because of a reduced or absent CA. Alternatively, it may be the other way round. H Pylori may prefer a genuinely normal stomach pH. In which case, is it possible that such acidic environments are not produced in the mouth as a function of the consumption of sugary foods? |
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Dr Trevor Watts, Senior Lecturer and Consultant in Periodontology Guy's, King's and St Thomas' Dental Institute, London SE1 9RT.
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In response to Dr Chong's query, dental plaque is a complex biofilm which may have as many as 200-300 identifiable taxa, as shown by Virginia Polytechnic Institute workers in the late 1970s-1980s by culture techniques. These organisms live in a matrix of extracellular polysaccharides and other substances derived from bacteria, saliva and gingival crevicular fluid. There are clearly many possible niches for all types of organism from streptococci, which occur all over the mouth, to spirochaetes, which are quite fastidious and live mainly in the depths of subgingival plaque. Taxonomy is often a problem, and organisms have been reclassified. Helicobacter was originally classified as Campylobacter, and species of the latter are also found in dental plaque. Some microbiologists think there are as many unidentified organisms in dental plaque as there are organisms already identified. Clearly, there may be a problem in identifying organisms which may not be present in all dental plaque samples. There is a lot of dental plaque in the average mouth! Also, see my earlier letter (1) to BMJ, along with its refs. I think the clearest evidence so far of the oral link of H pylori to gastrointestinal disease comes in a Turkish study (2) where oral hygiene effectiveness was related to both plaque positivity and gastric recurrence. 1. Watts T. Dental plaque is a potential reservoir of Helicobacter pylori. BMJ 2002; 324: 614-615. 2. Avcu N et al. The relationship between gastric-oral Helicobacter pylori and oral hygiene in patients with vitamin B12 deficiency anemia. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001; 92: 166-169 |
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Mahantayya V. Math, Assistant Lecturer in Physiology MGM Medical College, Kamothe, Navi Mumbai-410209.
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To The editor British Medical Journal London, UK. Sub: Response to your editorial “causes of failure of eradication of Helicobacter pylori” (BMJ 2002; 325: 3-4, 6 July). Dear Sir, I have read with interest the editorial “causes of failure of eradication of Helicobacter pylori” (BMJ 2002; 325: 3-4, 6 July) by Dr. Jenks. It is difficult to eradicate Helicobacter pylori (H.pylori) from the gastric and duodenal mucosa and effective treatment requires multiple drug regiments(1). Antibiotic resistance to H. pylori is increasing due to widespread use of antibiotics(1). H.pylori organisms have been noted under the finger nails, between gums and teeth, dental plaque and over the tongue(2,3). In Vitro studies have shown that Lactic acid and Lactobacilli inhibit the growth of H.pylori(4). H. pylori has cytoplasmic urease which converts urea into carbon dioxide and ammonia(5). Lactic acid and Lactobacilli may prevent or suppress the production of ammonia which can inhibit the colonisation of H. pylori. Fermented milk products (curd, buttermilk and yoghurt) have lactic acid, Lactobacilli and nutrients. Intake of these fermented milk products will cause slower gastric emptying, and this will give enough time for local action of lactic acid and Lactobacilli to act on H. pylori organisms in the stomach. In addition to the use of antibiotics, proper washing of hands before meal and consumption of buttermilk(200-300 ml) twice a day before meal may help in reduction of H. pylori organisms. References: 1. Jenks P.J. Causes of failure of eradication of Helicobacter pylori. BMJ 2002; 325: 3-4. 2. Larkin M. Hands could be key to spread of Helicobacter pylori Lancet 1999: 354(9179): 654 3. Watts T. H. pylori doesn’t live only in the stomach. bmj.com, 5 Jul 2002 (electronic response) 4. Midolo P.D., Lambert J.R., Hull R., Luo F., Grayson M.L. In Vitro inhibition of Helicobacter pylori NCTC 11637 by organic acids and lactic acid bacteria. J Appl Bacteriol 1995; 79(4): 475-9. 5. Weeks D.L., Eskandari S., Scott D.R., Sachs G. A H+gated urea channel: the link between Helicobacter pylori urease and gastric colonization. Science 2000;287(5452): 482-5. Dr. Mahantayya V. Math Department of Physiology MGM Medical College, Kamothe, Navi Mumbai-410209. Email: mgmmc@vsnl.com | |||
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Ian L. P. Beales, Senior Lecturer School of Medicine, Health Policy and Practice, University of East Anglia, Norwich, NR4 7TJ, UK
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Jenks has provided an interesting microbiolgical perspective of H. pylori eradication (1) but has failed to either appreciate the realities of current gastroenterological practice or provide a convincing argument to change said practice. Meta-analyses of per protocol first-line eradication rates show failure in 7-9% and antibiotic resistance is indeed probably the main cause (2), However in everyday practice (the “real world” of Editor’s choice) results are significantly poorer with first-line success of only about 73% (3). This is partly due to choice of poor regimens, specialists seem to get better results; not only by choosing better combinations but they also get better results with the same regimes. This probably reflects better counselling and compliance (4). Despite such indifferent first-line results, ultimate H. pylori eradication rates of 94% after a second course and 98.7% after a third can be achieved in real-world practice (3). These results can be produced by choosing logical, complimentary, subsequent regimens without recourse to sensitivity testing (3, 5). This is possible as long as clarithromycin-nitroimidazole regimens are avoided as a first- line, as there is no logical follow-on regime without sensitivity testing. It is unclear how more use of routine sensitivity testing as advocated by Jenks would be able to improve these results without a huge increase in costs. Jenks has also mistakenly used eradication rates after a single first line course as the arbiter of success. It is more appropriate to judge the success and costs on the basis of a whole strategy involving multiple courses and as described above excellent results can already be achieved with this approach (3, 5). Sensitivity-guided therapy may be slightly better as a first-line than empirical therapy but the overall results within a multi-step strategy have not been demonstrated and would seem unlikely to better those of logically chosen but empirical treatments, without prohibitive cost. A significant proportion of patients receive eradication therapy after non-invasive testing and an empirical sequence of regimes are necessary and to insist on unnecessary sensitivity testing will increase costs and waiting lists. The exact place of sensitivity testing within an overall strategy for H. pylori eradication remains to be determined. Certainly two complimentary sequential treatments can be used successfully without sensitivity-testing and although determination of resistance patterns may be useful before third-line therapy, the costs and benefits of this need to be fully investigated (3, 5). References 1. Jenks PJ. Causes of failure of eradication of Helicobacter pylori. BMJ 2002; 325: 3-4 2. Van Oijen AH, Verbeek AL, Jansen JB, De Boer WA. Review article: treatment of Helicobacter pylori infection with ranitidine bismuth citrate - or proton pump inhibitor-based triple therapies. Aliment Pharmacol Ther 2000; 14:991-9 3. Beales ILP. Efficacy of Helicobacter pylori eradication therapies: a single centre observational study. BMC Gastroenterology 2001; 1:7 4. Lee M, Kemp JA, Canning A, Egan C, Tataronis G, Farraye FA. A randomized controlled trial of an enhanced patient compliance program for Helicobacter pylori therapy. Arch Intern Med. 1999; 159:2312-6. Gisbert JP, Pajares JM. Review article: Helicobater pylori “recue” regimen when proton pump inhibitor-based triple therapies fail. Aliment Pharmacol Ther 2002; 16: 1047-1058 |
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