Rapid Responses to:
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the story so far
Rapid Responses: Rapid Responses published:
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Response to Helicobacter pylori article
- Susan Abraham (10 September 1999)
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Familial clustering of Helicobacter pylori infection
- Filippo Cremonini (24 September 1999)
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H.pylori eradication in NUD
- Derek Gillen (9 October 1999)
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Susan Abraham, Stage 3 medical student Department of Epidemiology and Public Health
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Dear Editor, Dominici et al found that Helicobacter Pylori infection tends to cluster within families belonging to the same population (1). The study was original in it’s use of family units and the population based approach used avoided potential selection bias. In contrast, previous studies have been based on parents and siblings of children referred for symptoms, and not on the general population. However, 56.4% of the study population were excluded from the study by the definition of a family unit used by the investigators. It is important to include units such as single parent families, cohabiting parents, as well as families with a husband, wife and children to be truly representative of the population. We feel that valuable information could be obtained by including such groups. It is possible, for example, that being a single parent is a risk factor in itself. In addition, the authors suggest that social status may be a risk factor for infection. We as a group feel that the categories used (white collar, blue collar and farmers) were too broad to capture the necessary information. If socio-economic status is to be defined by occupation, then it is important to include unemployment as a sub group. The unemployed are more likely to be in a lower socio-economic group and therefore to exclude them is to exclude a high risk population which will adversely influence results, and any conclusions drawn from them. We therefore question the appropriateness of socio-economic status to observe trends in H.Pylori infection. We suggest that alternative variables such as parental income, housing, dietary factors and sanitation would be more relevant measures as these factors are more likely to be directly implicated in transmission of H.Pylori infection. Overall, we thought that this study addressed important issues, as little is known about H.Pylori transmission. Yours sincerely, Susan Abraham (S.M.Abraham@ncl.ac.uk), Will Chong, Anita Kundu, Clare Parker and Lauren Turner. Stage Three (Year Four) medical students, Department of Epidemiology and Public Health, The Medical School, University of Newcastle upon Tyne. 1. Dominici P, Bellentani S et al. Familial clustering of Helicobacter Pylori infection: population based study. BMJ August 1999 319:537-540 |
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Filippo Cremonini
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EDITOR-In their paper appearing in the August 28th issue of BMJ, Dominici and colleagues investigated the rate of intrafamilial transmission of Helicobacter pylori (H.pylori) in a population of 3289 subjects accounting for 416 families in Northern Italy. 1 They found a familiar clustering of infection within families and a definite role for social status as a risk factor for acquiring infectious status. Infection was serologically defined as anti H.pylori IgG positivity. Since immigration is a concrete reality in Northern Italy, geographic provenience of the families should be taken into account when adjusting for risk factors, considering that dietary habits and sociohygienic standards notably differ between Northern and Southern Italy.2 In fact, families immigrating towards Northern Italy very frequently perform "blue collar" jobs and a seroepidemiological analysis should preherably not be blind about their environmental background. Migration from an area with higher risk of infection cannot be underestimated. In such case, the hypothesis of a common source of exposure for parents and children would not represent a serious alternative to the model of direct (mother/father- son) transmission. Moreover, in addition to IgG measurements, testing subjects for markers of pathogenicity of H.pylori, such as anti cagA (citotoxin associated gene A) antibodies, would have eventually revealed which familial clusters have more commonly come in contact with virulent H.pylori strains. These strains could possibly represent the quote of "bad" helicobacters in the picture of a worldwide diffuse, often harmless, infection.3,4 This would possibly bring more clues to determine why the wide diffusion of H.pylori does not overlap the prevalence of H.pylori- related illnesses. Filippo Cremonini, Silvio Danese Maurizio Gabrielli Antonio Gasbarrini Internal Medicine and Medical Pathology, Catholic University of Sacred Heart, Policlinico Gemelli, Largo Gemelli, 1, 00168 ROMA 1 Dominici P, Bellentani S, Di Biase AR, Saccoccio G, Le Rose A, Masutti F et al. Familialm clustering of Helicobacter pylori infection: population based study. BMJ 1999;319:537-41 2 Stroffolini T, Rosmini F, Ferrigno L, Fortini M, D'Amelio R, Matricardi PM. Prevalence of Helicobacter pylori infection in a cohort of Italian military students. Epidemiol Infect 1998;120:151-55 3 Covacci A, Censini S, Bugnoli M, et al. Molecular characterization of the 120 kDa immunodominant antigen of Helicobacter pylori associated with cytotoxicity and duodenal ulcer. Proc Natl Acad Sci USA 1993;90:5791- 5795 4 Axon AT. Are all helicobacters equal? mechanisms of gastroduodenal pathology and their clinical implications. Gut 1999;45 Suppl 1:I1-4 |
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Derek Gillen
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Dear Sir Thomson`s recent commentary on Helicobacter pylori was presumably intended to inform and update the general medical community (1). In relation to H.pylori eradication in non-ulcer dyspepsia (NUD), he states that, " a recent prospective study strongly suggests that there is no basis for this (2)". However, for many years this topic has been, and remains, keenly debated. It is therefore unfortunate that he omits to mention the UK MRC Dyspepsia Trial from Glasgow (3) and a study from Ireland (4). Both of these studies show a positive benefit for one-off eradication therapy in NUD of about 10% over placebo. This level of benefit is similar to that of any other chronic therapy, such as proton pump inhibitors, previously studied in NUD. Both of these studies were published prior to the study which he quotes (2). Furthermore, the other previously published trial which he omits (5), although showing no benefit which reaches statistical significance at a power of 80% to show a 20% benefit over placebo, does show a positive trend of a similar level to the other two trials (3, 4). The omission of these 3 trials, all published in advance of the one quoted, suggests either a lack of balance, a lack of acquaintance with the literature or overly stringent editorial restrictions. At best, this commentary is therefore worthless with regard to informing and updating on the current evidence in the management of NUD. At worst, it is misleading. Yours faithfully Derek Gillen Lecturer in Medicine and Gastroenterology Kenneth E L McColl Professor of Medicine and Gastroenterology 1 Thomson M.Helicobacter pylori- the story so far. BMJ 1999; 319: 541. 2 Talley N, Janssens J, Lauritsen K Racz I, Bolling-Sternevald E. Eradication of Helicobacter pylori in functional dyspepsia: randomized double blind placebo controlled trial with 12 months` follow-up BMJ 1999; 318:833-6. 3 McColl KEL, Murray L, El-Omar E, Dickson A, El-Nujumi A, Wirz A et al. Symptomatic benefit from eradicating Helicobacter pylori infection in patients with nonulcer dyspepsia. NEJM 1998; 339: 1869-1874. 4 Gilvarry J, Buckley MJM, Beattie S, Hamilton H, O`Morain CA. Eradication of Helicobacter pylori affects symptoms in nonulcer dyspepsia. Scand J Gastroenterol 1997; 32: 535-540. 5 Blum AL, Talley NJ, O`Morain C, Veldhuysen Van Zanten S, Labenz J, Stolte M et al. Lack of effect of treating Helicobacter pylori infection in patients with NUD. NEJM 1998; 339: 1875-81. |
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