Should we eradicate Helicobacter pylori in patients with recurrent gastro-oesophageal reflux disease?

The 1998 Guidelines of the American College of Gastroenterology recommend that diagnostic testing for Helicobacter pylori infection should only be performed if treatment is intended, and that testing for H. pylori is not indicated in patients on long-term treatment with a proton pump inhibitor (PPI) for gastro-oesophageal reflux disease (GORD). Moreover, a recent evidence-based workshop evaluating major clinical strategies for the management of GORD reported, with an 'A' category (maximum of evidence), that eradication of H. pylori does not heal or prevent relapse of GORD. In detail, it seems that H. pylori infection per se has no effect on the pathogenic mechanisms determining either reflux or its complications. The relationship between H. pylori and oesophagitis is mediated by the effect of H. pylori on gastric acid secretion; in particular, by the proximal extension of gastritis and related impairment of gastric secretory function. In general, if the corpus is infected, the amount of acid available for reflux is less and the probability of excessive oesophageal acid exposure leading to oesophagitis reduced. However, the clinical relevance of corpus H. pylori infection as a biological antisecretory agent (and of H. pylori eradication) seems small or absent, at least in the long run. Conversely, the previous claim of an increased risk of atrophic gastritis in H. pylori-infected patients treated long term with PPI drugs appears not to be confirmed by subsequent studies. In conclusion, H. pylori infection may, in some circumstances, be moderately favourable and, in other circumstances, it may be neutral, with respect to the management of GORD.     

Do we eradicate Helicobacter pylori in hospitalized patients with peptic ulcer disease?

BACKGROUND:

Helicobacter pylori infection is the most common chronic infection in humans. It is a major contributor to the cause of duodenal and gastric ulcers worldwide. Its eradication has been shown to reduce rates of H pylori-related ulcers as well as other complications such as gastric cancer.

OBJECTIVE:

To determine the rate of appropriate treatment in patients following a diagnosis of H pylori infection on biopsy during esophagoduodenoscopy for upper gastrointestinal bleeding over a four-year period at a tertiary centre in Vancouver, British Columbia. Also evaluated was the rate of eradication confirmation using the urea breath test.

METHODS:

A retrospective review of 1501 inpatients who underwent esophagoduodenoscopy for upper gastrointestinal bleeding (January 2006 to December 2010) was undertaken. Patients who were biopsy stain positive for H pylori were selected for drug review either via a provincial database (PharmaNet) or via records from patients’ family practitioners. Data were also obtained via two provincial laboratories that perform the urea breath test to determine the rates of confirmation of eradication.

RESULTS:

Ninety-eight patients had biopsy-proven H pylori. The mean (± SD) age was 56.13±17.9 years and 65 were male. Data were not available for 22 patients; the treatment rate was 52.6% (40 of 76). Of those treated, 12 patients underwent a post-treatment urea breath test for eradication confirmation.

CONCLUSION:

There was substantial discrepancy between the number of diagnosed H pylori infections and the rate of treatment as well as confirmation of eradication. Numerous approaches could be taken to improve treatment and eradication confirmation.     

What consideration should be given to Helicobacter pylori in treating nonsteroidal anti-inflammatory drug ulcers?

Although Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) both cause peptic ulcers, they do so by different mechanisms so any interaction is not necessarily harmful. H. pylori has been shown to enhance gastric mucosal prostaglandin synthesis, while NSAIDs suppress it Pragmatically, there is no compelling evidence in favour of H. pylori eradication in all patients who take NSAIDs. As a broad generalisation, in therapeutic studies of NSAID users, those who have no ulcer at trial entry are more prone to ulcer development if they are H. pylori-positive. By contrast, in those who have ulcers at baseline, H. pylori-positive individuals are less likely to develop ulcers, particularly if taking acid-suppressive therapy. Trials of H. pylori eradication therapy tend to replicate this dichotomy. In one study of patients starting NSAIDs for the first time, with no ulcer history and no baseline ulcer, use of bismuth-based eradication therapy was associated with a lower incidence of gastric ulcer at 2 months. Conversely, in a study of patients with endoscopically proven ulcers and/or troublesome dyspepsia, proton pump inhibitor based eradication treatment had no effect on outcome (of acid suppression) over 6 months. H. pylori eradication has been associated with significantly slower healing of gastric ulcers compared with patients who did not undergo eradication. However, the effect of H. pylori eradication on healing of NSAID-associated duodenal ulcers does not appear to be so dramatic, and limited evidence suggests that it may be possible to prevent H. pylori-associated duodenal ulcer by eradicating the infection. An evidence-based approach to treatment would suggest that NSAID users should undergo H. pylori eradication therapy if they have a duodenal ulcer, whether or not they continue NSAIDs. Because COX-2 inhibitors appear not to be ulcerogenic, management of H. pylori in patients taking these drugs can be based upon the same risk assessment as in patients not taking anti-arthritis drugs. H. pylori eradication should not be used universally or in high-risk gastric ulcer patients who require management with acid suppression.     

Helicobacter pylori infection in patients with autoimmune thrombocytopenic purpura

AIM:To compare the prevalence of Helicobacter pylori(Hpylon)infection in autoimmune thrombocytopenic purpura(AITP)patients with that of nonthrombocytopenic controls,and to evaluate the efficacy of the treatment in H pylori( )and H pylor(-)AITP patients.METHODS:The prevalence of gastric H pylori infection in38 adult AITP patients(29 female and 9 male;median age27 years;range 18-39 years)who consecutively admittedto our clinic was investagated.RESULTS:H pylori infection was found in 26 of 38 AITPpatients(68.5%).H pylori infection was found in 15 of 23control subjects(65.2%).The difference in H pylori infectionbetween the 2 groups was not significant.Thrombocytecount of H pylori-positive AITP patients was significantlylower than that of H pylori-negative AITP patients(P<0.05).Thrombocyte recovery of H pylori-positive group was lessthan that of H pylori-negative group(P<0.05).CONCLUSION:H pylori infection should be considerecd inthe treatment of AITP patients with H pylori infection.     

Are COX-2 inhibitors preferable to non-selective non-steroidal anti-inflammatory drugs in patients with risk of cardiovascular events taking low-dose aspirin?

Cyclo-oxygenase-2 selective inhibitors and non-selective non-steroidal anti-inflammatory drugs (NSAIDs) are associated with increased risk of acute cardiovascular events. Only aspirin offers primary and secondary cardiovascular prophylaxis, but trials have not answered directly whether low-dose aspirin is cardioprotective with COX-2 inhibitors. A large inception cohort study showed that concomitant use of aspirin reduced risk of cardiovascular events when given with rofecoxib, celecoxib, sulindac, meloxicam, and indometacin but not when given with ibuprofen. In large trials assessing gastrointestinal safety, there were fewer gastrointestinal events in patients using both COX-2 inhibitors and aspirin than in those using non-selective NSAIDs and aspirin; significantly fewer uncomplicated upper gastrointestinal events took place in the MEDAL trial. Analysis of VIGOR and two capsule endoscopy studies showed significantly less distal gastrointestinal blood loss with COX-2 inhibitors than with non-selective NSAIDs. Endoscopy trials showed that low-dose aspirin does not diminish the gastrointestinal benefits of COX-2 inibitors over non-selective NSAIDs. In an elderly epidemiological cohort receiving aspirin, both celecoxib and rofecoxib reduced risk of admission for gastrointestinal events. Comparison of the cardiovascular and gastrointestinal risks is difficult: likelihood and severity of cardiovascular events differ between individuals, agents, and exposure. Mortality associated with gastrointestinal events is less frequent than with cardiovascular events, but asymptomatic ulcers can result in severe complications. Data support the conclusion that COX-2 inhibitors are preferable to non-selective NSAIDs in patients with chronic pain and cardiovascular risk needing low-dose aspirin, but relative risks and benefits should be assessed individually for each patient.     

Seroprevalence of Helicobacter pylori infection in inflammatory bowel disease: is Helicobacter pylori infection a protective factor?

BACKGROUND: The mechanisms for the observed low prevalence of Helicobacter pylori infection in inflammatory bowel disease (IBD) are unknown, but might be important for the pathogenesis of IBD. We have studied the seroprevalence of H. pylori in different categories of IBD and evaluated the role of medical therapy, smoking and social status. We also analysed the effect of seropositivity on the age of onset of IBD in order to find possible evidence for the protective effect of the infection. METHODS: We studied 296 (mean age 43 years, range 18-79; women 144) unselected patients with IBD, including 185 with ulcerative colitis (UC). 94 with Crohn disease (CD), and 17 with indeterminate colitis (IC). Seventy healthy age- and sex-matched subjects served as controls. Serum samples were studied for H. pylori antibodies. Detailed clinical history was obtained from patient records and by face-to-face interview. RESULTS: The prevalence of H. pylori infection was lower in IBD patients (24%) than in controls (37%; P = 0.029), and in CD lower (13%) than in UC (30%; P = 0.002). Seropositivity was not related to sulphasalazine treatment or smoking. Age of onset of IBD was higher in seropositive (mean 40 years) than in seronegative patients (30 years: P < 0.001). The age of onset of IBD showed unimodal distribution in H. pylori seronegative patients, with a peak between 30 and 40 years, although there was some evidence of bimodality in CD. In contrast, H. pylori seropositive patients had clear bimodal pattern with peaks at 20-40 and 50-60 years of age. CONCLUSIONS: Our results confirm the low prevalence of H. pylori infection in IBD, and in particular in CD. The significantly higher age of onset and bimodal pattern of age-specific incidence in seropositive IBD patients suggest that H. pylori infection significantly modifies the development of IBD and may have a protective effect.     

Does HIV infection alter the incidence or pathology of Helicobacter pylori infection?

Gastrointestinal (GI) discomfort is a common complaint among patients infected with HIV. GI symptoms can be caused by a myriad of factors including but not limited to coinfections, antiretroviral therapy, medications for opportunistic infections, and nutritional status. Some researchers have hypothesized that Helicobacter pylori infection may be more common among HIV-infected patients as a result of immune suppression. An increased incidence of H. pylori infection would contribute to the prevalence of GI complaints in this population. Several epidemiologic studies have examined the relationship between H. pylori infection and HIV. While studies have generally reported conflicting results that may be related to the use of varied study designs, some identifiable patterns can be discerned. It does appear that the incidence of H. pylori infection is lower among patients with AIDS compared to matched HIV-infected and -uninfected controls. This review discusses the various epidemiologic trials that have been conducted in this area and describes the potential physiologic mechanisms to explain these findings. The clinical applicability of these studies as well as limitations are also discussed. A greater number of well-designed and controlled trials are needed before any definitive conclusions regarding these diseases can be made, until such time clinicians should be aware of the potential issues regarding H. pylori screening and management in the context of HIV. Research in this area might also provide information relating to HIV-associated GI changes and the role of these changes in HIV pathogenesis.