Rapid Responses to:
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Rapid Responses: Rapid Responses published:
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Dosage of omeprazole
- Vogt Bruno (2 November 2001)
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H. pylori in dental plaque biofilms
- Trevor Watts (2 November 2001)
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Chronic infections: to treat or not to treat? That's the problem.
- Giovanni Cammarota (3 November 2001)
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Wrong Omeprazole dose stated in treatment regimen
- Jasbir Nahal (5 November 2001)
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Triple therapy with furazolidone is a cost-effective alternative in developing countries
- Walter H Curioso (7 November 2001)
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Treatment of ulcer patients can be improved and over-reliance on PPI-based therapies reduced
- Ian L P Beales (7 November 2001)
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Is there still room for a good H.pylori?
- Filippo Cremonini, Antonio Gasbarrini (8 November 2001)
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H pylori eradication therapy in patients undergoing endoscopy can be individually tailored
- Helena Parsons (21 November 2001)
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Vogt Bruno, Associate Professor Nephrology/Hypertension Inselspital Bern, Switzerland
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Dear Dr. Adam Harris and Dr. J J Misiewicz, concerning your excellent clinical review article "Management of Helicobacter pylori infection" in BMJ 2001;323:1047-1050, I wonder about the high dose of omeprazole of 400 mg/daily for eradication therapy of H. pylori on page 1050, flow sheet for choosing a treatment regimen for H pylori eradication. Do you recommend such a high doses or should it be 40 mg/daily? Sincerely yours, B. Vogt, MD
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Trevor Watts, Senior Lecturer and Consultant in Periodontology Guy's, King's and St Thomas' Dental Institute
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I was a little surprised to see no mention at all, in this review paper on management of H. pylori infection, of the potential reservoir of H. pylori in dental plaque on teeth. Because this is a biofilm, no antibiotic will penetrate it and if it carries the organism, it is essential to remove it mechanically with oral hygiene, scaling and root planing, exactly as for periodontal diseases caused by plaque microorganisms (1). The effect of removal and control of dental plaque on the plaque reservoir of H. pylori was shown clearly in a short study published this year (2). Triple therapy alone (omeprazole, clarithromycin + 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 mouthrinse is useless without the scaling. Biofilms like dental plaque provide a ready source for re-infection. They are complex communities of many bacterial species with powerful defences against chemical and pharmacological threats (3), but some organisms may not gain a foothold in them because of bacterial antagonisms. 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. Re-infection from plaque will also be subject to variable host defences, and therefore not occur consistently in all cases where conventional H. pylori therapy is used. 1. Watts TLP. Periodontitis for medical practitioners. BMJ 1998; 316: 993-996. 2. Butt AK, Khan AA, Suleman BA, Bedi R. Randomized clinical trial of Helicobacter pylori from dental plaque. Br J Surg 2001; 88: 206. 3. Watts TLP. Periodontics in Practice. London: Martin Dunitz, 2000, p 47-52. |
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Giovanni Cammarota, Medical Doctor - Investigator of Internal Medicine Dept. of Internal Medicine and Gastroenterology, Catholic University of Rome - Italy
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Editor-We read with great interest the excellent clinical review article by Harris and Misiewicz (3 November issue) concerning the management of Helicobacter pylori infection (1). Nevertheless, in our opinion, a great question we would underline is whether to treat the majority of infected individuals when they are asymptomatic. Some literature data suggest that chronic diseases may have an infectious component (2). For example, even is contradictory, several lines of research indicate that common chronic infections (including cytomegalovirus, herpesviruses, Chlamydia pneumoniae, dental infections, and ultimately Helicobacter pylori) are plausible candidate for triggering and perpetuating inflammatory changes that may contribute to the development of atherosclerosis through the generation of a persistent low- grade inflammatory stimulus. Now, the discovery that transmissible agents may play roles in diseases non suspected of being infectious in origin may have important implications for treatment. There is a simple strategy that states: testing an infection in the individual patient for any reason and with any method should always be followed up with treatment. Therefore, in our opinion, the major priority in the future could become not whom to treat but rather whom to test. Giovanni Cammarota, MD, Investigator Massimo Montalto, MD, Fellow of Internal Medicine Giovanni GAsbarrini, MD, Director, Professor of Internal Medicine References. 1. Harris A, Misiewicz JJ. BMJ 2001;323:1047-1050. 2. Libby P, Egan D, Skarlatos S. Roles of infectious agents in atherosclerosis and restenosis: an assessment of the evidence and need for future research. Circulation 1997;96:4095-103. |
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Jasbir Nahal, Gastroenterology Nurse Specialist Walsall Manor Hospital, West Midlands UK
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Dear Sirs, Having followed and enjoyed your G.I. series with great interest, I was rather alarmed to find an incorrect drug dosage ten times higher than the intended amount which is stated in the final table of your article, surely this should be Omeprazole 40mgs. once daily rather than Omeprazole 400mgs! Whilst it may be an obvious typing error it may lead to a grave clinical error occuring. |
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Walter H Curioso, Medical Student Universidad Peruana Cayetano Heredia
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To the editor, Helicobacter pylori (HP) infection is very prevalent worldwide and triple drug schemes have been shown to be the most effective approach to erradicate HP infection. Nevertheless, high rates of resistance against some antibiotics as well as high costs affect the effectiveness of these therapies.(1) The Latin-American Consensus Conference on Helicobacter pylori infection (2) suggest the use of furazolidone, an old but cheap antibiotic, as a good alternative to metronidazole in triple therapy for Helicobacter pylori eradication in areas where metronidazole resistant bacteria are common. We report a cost-effective alternative for the therapy of HP infection in low income populations with a high prevalence of infection with this bacteria. In a prospective, open, simple blind study De Idiaquez et al (3) included 59 peruvians patients with diagnosis of HP infection. They received the following scheme for 10 days: tetracycline 500 mg qid., furazolidone 100 mg qid., and colloidal bismuth subcitrate 120 mg qid. HP erradication was achieved in 54 patients (91.5%). Control biopsies showed improvement in the following parameters: presence and density of HP (p<0.001); presence, depth and grade of chronic gastritis (p<0.001); presence and grade of inflammatory activity (p<0.001); presence, grade and extent of mucinous damage (p<0.001); and presence of lymphoid follicles (p<0.001). Also in Peru Ramirez-Ramos A et al (4) in a study involved three randomized trials show that furazolidone combined with bismuth subsalicylate and amoxicillin, erradicated infection in 82% of patients. Another authors as Segura et al (5) evaluate the combination of subcitrate 240 mg b.d., furazolidone 100 mg q.d.s. and amoxycillin 500 mg q.d.s. for 14 days in 30 patients for the treatment of H. pylori infection in Colombia. 25 patients were cured (86%, 95% CI: 65-94%). Mild, well- tolerated side-effects were reported by six patients (20%). This evidence suggest furazolidone-containing therapies may become especially useful in developing countries as an effective, simple and inexpensive non-metronidazole therapy for H. pylori infection. Walter H. Curioso, medical student
Walter I. Curioso, MD., Chief of gastrointestrinal endoscopy
References 1) Harris A, Misiewicz JJ. Management of Helicobacter pylori infection. BMJ. 2001 Nov 3;323(7320):1047-1050. 2) Coelho LG, Leon-Barua R, Quigley EM. Latin-American Consensus Conference on Helicobacter pylori infection. Latin-American National Gastroenterological Societies affiliated with the Inter-American Association of Gastroenterology (AIGE). Am J Gastroenterol. 2000 Oct;95(10):2688-91. 3) De ldiáquez D, Bussalleu A, Rodrigo I, et al. Erradicación de la infección por Helicobacter pylori utilizando Tetraciclina, Furazolidona y Bismuto en pacientes dispépticos con y sin úlcera péptica. Rev Gastroenterol Peru 1999;19(3):179-94. Full-text available (in spanish): http://200.10.68.58/bibvirtual/revistas/gastro/vol_19n3/trabajos01.htm 4) Ramirez-Ramos A, Gilman RH, Leon-Barua R, et al. Rapid recurrence of Helicobacter pylori infection in Peruvian patients after successful eradication. Clin Infect Dis 1997 Nov;25(5):1027-31 5) Segura AM, Gutierrez O, Otero W, et al. Furazolidone, amoxycillin, bismuth triple therapy for Helicobacter pylori infection. Aliment Pharmacol Ther 1997 Jun;11(3):529- 32 |
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Ian L P Beales, Clinical Senior Lecturer in Cell Biology School of Medicine, Health Policy and Practice, University of East Anglia, Norwich, NR4 7TJ, UK
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Editor- I enjoyed Harris and Misiewicz’s paper on management of H. pylori infection(1). They are congratulated for taking a balanced view of the contentious issues surrounding treatment in non-ulcer patients. However, several inconsistencies are apparent in their approach to ulcer patients, for whom solid evidence for treatment is available. The authors advocate only two attempts at eradication in duodenal and gastric ulcer patients: failure of the second being followed by maintenance anti-secretory therapy. Although the 90% success rate for one course of eradication therapy is ideal, as quoted by the authors, combined data from randomised controlled trials suggest eradication rates of 73-87% are more usual(2). In everyday practice, without trialist enthusiasm, rates of 64% or lower may be expected, depending on the regimen and interest of the clinician(3). Thus after two courses of therapy, potentially 1 in 8 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 ulcer recurrence and haemorrhage. Continuous anti-secretory therapy is less convenient, less effective and more costly, thus strategies must be constructed to improve overall eradication rates. In the light of this need to optimise success, the authors’ bias towards proton pump inhibitor (PPI)-based therapies and obvious reluctance to endorse ranitidine bismuth citrate (RBC)is surprising. RBC-based triple therapies are at least equivalent to, and in some cases significantly superior to PPI-based regimens as initial therapy(2). Bismuth-based regimens (either RBC or colloidal bismuth) appear superior to others following an initial failure(3,4). In this situation, RBC-tetracycline- metronidazole triple therapy produced significantly better eradication rates than the PPI-bismuth quadruple therapy advocated by the authors(5). RBC-based therapies are effective and equivalent in cost to PPI-therapies, it is unfortunate that the authors did not recommend their wider use. There are relatively few data concerning 3rd line therapies. After using both clarithromycin-, and nitroimidazole-containing regimes, there is no logical combination. Although a PPI-rifabutin-amoxicillin combination regimen appears promising in this situation, therapy directed by endoscopy, culture and sensitivity testing seems better than empirical choice(3). Using a 3-step algorithm >98% of patients requiring H. pylori eradication can be successfully treated, removing the need for continued drug therapy(3). It is important that strategies for H. pylori eradication are not based merely on first-line eradication rates but include appropriate further steps to maximise success in those who will definitely benefit from therapy. References 1 Harris A, Misiewicz JJ. Management of Helicobacter pylori infection. BMJ 2001;323:1047-1050. 2 Gisbert JP, Gonzalez L, Calvet X, Roque M, Gabriel R, Pajares JM. Helicobacter pylori eradication: proton pump inhibitor vs. ranitidine bismuth citrate plus two antibiotics for 1 week-a meta-analysis of efficacy. Aliment Pharmacol Ther 2000;14:1141-50. 3 Beales IL. Efficacy of Helicobacter pylori eradication therapies: a single centre observational study. BMC Gastroenterol 2001;1:7 4 Kearney DJ. Retreatment of Helicobacter pylori infection after initial treatment failure. Am J Gastroenterol 2001;96:1335-9. 5 Gisbert JP, Gisbert JL, Marcos S, Gravalos RG, Carpio D, Pajares JM. Seven-day 'rescue' therapy after Helicobacter pylori treatment failure: omeprazole, bismuth, tetracycline and metronidazole vs. ranitidine bismuth citrate, tetracycline and metronidazole. Aliment Pharmacol Ther 1999;13:1311-1316. Competing Interests Dr Beales has received research funding from AstraZeneca and financial support and sponsorship for educational activities from AstraZeneca, Jannssen-Cilag and Wyeth. Dr Beales has investments in a number of unit trusts which have holdings in a number of pharmaceutical companies including AstraZeneca and GlaxoSmithKline. |
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Filippo Cremonini, Clinical Research Fellow, Associate Professor UCSC Rome, Italy, Antonio Gasbarrini
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Dear Sir, after reading the brief, but comprehensive review by Harris and Misiewicz (1), I noticed that Authors seem not to take into account the evidence coming from a recent Japanese large-scale prospective, randomized study.(2) Uemira et al., studying dyspeptic patients for 7.8 years mean follow-up, found incidence of gastric cancer in almost 3 percent of the H.pylori infected versus none in the non-infected. High cancer incidence was found, when subgrouping, even in patients with nonulcer dyspepsia, for whom eradication has remained until now an unsolved issue. From these results, the role of H.pylori as a gastric carcinogen seems undeniable now more than ever.I wonder if the Authors will be willing to change the approach to the controversy, and if giving raise to campaign of testing (and treating) H.pylori on a population basis, even in absence of megatrials, is our next (best) thing. 1. Harris A, Misiewicz JJ. ABC of the upper gastrointestinal tract: Management of Helicobacter pylori infection. BMJ 2001;323:1042-1046 2. Uemura N, Okamoto S, Yamamoto S, Matsumura N, Yamaguchi S, Yamakido M, Taniyama K, Sasaki N, Schlemper RJ. Helicobacter pylori Infection and the Development of Gastric Cancer. N Engl J Med 2001;345:784 -789 |
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Helena Parsons, research fellow in infection and immunity Royal Hallamshire Hospital, Sheffield S10 2JF
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Helicobacter pylori eradication therapy in patients undergoing endoscopy can be individually tailored to avoid resistance and treatment failure. Editor--In their review on the management of Helicobacter pylori infection Harris and Misiewicz1 suggest that patients "likely" to have metronidazole resistant H pylori infection should be treated with non- nitroimidazole containing eradication regimens. However, 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 is seldom available. In addition, although the authors rightly point out that metronidazole resistance is commoner in women and patients from developing countries, translation of this knowledge into prescribing practice is difficult in the treatment of 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 to 37% for men (odds ratio 1.48; 95% confidence interval 1.15-1.91) and for patients 60 years or over resistance was 34% compared to 44% for patients <60 years (OR 0.62; 95%CI 0.48-0.8)2. A pragmatic approach to H pylori eradication treatment may be to exclude nitroimidazoles from eradication regimens. In our view 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 significantly more disruption and induction of resistance in host microflora3 and thereby reduce the efficacy of macrolides in the treatment of other infectious conditions. Culture and sensitivity testing of H pylori is well established and requires few special facilities. As the authors discuss management of H pylori following endoscopy, it would seem 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 (approximately one week) and then prescribed a specific, effective eradication regime. In this era of increasing resistance to antimicrobials optimisation of therapy is of paramount importance in our clinical practice. Helena K Parsons David S Sanders Martyn J Carter Alan J Lobo Gastroenterology and Liver Unit, Royal Hallamshire Hospital, Sheffield S10 2JF 1 Harris A, Misiewicz JJ. Management of Helicobacter pylori infection. BMJ 2001; 323: 1047-1050. 2 Parsons HK, Carter MJ, Sanders DS, Winstanley T, Lobo AJ. Rates of Helicobacter pylori antimicrobial resistance in the United Kingdom and the effect of age, sex and socio-economic status. Aliment Pharmacol Ther 2001; 3 Adamsson I, Nord CE, Ludquist P, et al. Comparative effects of omeprazole, amoxycillin plus metronidazole versus omeprazole, clarithromycin plus metronidazole on the oral, gastric and intestinal microflora of Helicobacter pylori-infected patients. J Antimicrob Chemother 1999; 44: 629-40. |
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