Lack of association between Helicobacter pylori infection and extracardiac atherosclerosis in dyspeptic elderly subjects

Pilotto, Alberto; Rumor, F; Franceschi, Marilisa; Leandro, Gioacchino; Novello, R.; Soffiati, Giuliano; Scagnelli, Mariuccia; Mario, F. Di; Valerio, G.

doi:10.1093/ageing/28.4.367

Cited by 19 publications

(11 citation statements)

References 22 publications

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“…This outcome reinforces the emerging evidence that gastric Helicobacter infection most likely does not exacerbate or accelerate atherosclerotic lesion development (6,33,36).…”

Section: Discussionsupporting

confidence: 83%

GastricHelicobacterInfection Induces a Th2 Phenotype but Does Not Elevate Serum Cholesterol in Mice Lacking Inducible Nitric Oxide Synthase

et al. 2005

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Persistent Helicobacter felis infection in (C57BL/6 ؋ 129SvEv)F 1 mice induces chronic gastritis. Expression of inducible nitric oxide synthase (iNOS) is upregulated in response to Helicobacter infection. In this study, 20 10-week-old iNOS ؊/؊ mice and 20 wild-type [(C57BL/6 ؋ 129SvEv)F 1 ] mice were infected with H. felis by oral gavage and were assessed histologically and serologically at 32 weeks postinfection. Equal numbers of uninfected controls were sham inoculated. The mice were scored for severity of gastric inflammation, hyperplasia, glandular atrophy, and mucous metaplasia in the corpus and for the level of helicobacter colonization. The immunoglobulin G1 (IgG1), IgG2a, and IgG2c antibody responses to H. felis were determined. As a secondary measure, serum cholesterol levels were assessed. iNOS ؊/؊ mice have a propensity for increased serum cholesterol, and although controversial, several human epidemiologic studies have demonstrated an association between Helicobacter infection and several risk factors for cardiovascular disease, including elevated serum cholesterol. Nevertheless, no differences in serum cholesterol levels were observed between the H. felis-infected and -uninfected iNOS ؊/؊ mice in this study. The uninfected animals had minimal to no gastric pathology. The gastric pathology scores for the infected animals were reduced significantly in the iNOS-deficient mice relative to those for the wild-type mice (all P < 0.01). Helicobacter-infected iNOS ؊/؊ mice had chronic lymphoid infiltration and negligible to mild glandular atrophy and mucous metaplasia in the fundic mucosa, while H. felis-infected wild-type mice had severe atrophic and metaplastic mucosal changes. The atrophic gastritis in the infected wild-type mice, particularly the female mice, was also accompanied by greater granulocytic infiltration, antral hyperplasia, and diminished antral colonization, unlike that in the infected iNOS ؊/؊ mice. iNOS

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“…This outcome reinforces the emerging evidence that gastric Helicobacter infection most likely does not exacerbate or accelerate atherosclerotic lesion development (6,33,36).…”

Section: Discussionsupporting

confidence: 83%

GastricHelicobacterInfection Induces a Th2 Phenotype but Does Not Elevate Serum Cholesterol in Mice Lacking Inducible Nitric Oxide Synthase

et al. 2005

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“…The few studies previously performed in elderly populations failed to find any association between H. pylori infection and coronary heart disease [26] or extracardiac atherosclerosis [27]. However, a study from Japan reported that mean serum levels of high‐density lipoprotein cholesterol (HDLC) were significantly lower in H. pylori ‐positive than in H. pylori ‐negative subjects.…”

Section: Indications For Treatment Of the Elderlymentioning

confidence: 99%

Helicobacter pylori infection in geriatrics

Pilotto

Salles

2002

Helicobacter

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The prevalence of Helicobacter pylori infection increases with age worldwide. However, the percentage of H. pylori-positive elderly patients who are tested and treated for their infection remains very low. We now have data that demonstrate the benefit of curing H. pylori infection in elderly patients with H. pylori-associated peptic ulcer disease and severe chronic gastritis. Furthermore, the cure of H. pylori may prevent progression of intestinal metaplasia and gastric atrophy. Studies are needed to clarify the role of eradication for elderly patients who have nonulcer dyspepsia, gastroesophageal reflux disease and who use nonsteroidal anti-inflammatory drugs. H. pylori infection may be easily diagnosed by histological evaluation, rapid urease test or culture performed on gastric biopsies taken during endoscopy. However, the biopsy site must be carefully selected in elderly patients. For noninvasive monitoring of H. pylori infection after treatment, the 13C-urea breath test has significantly higher accuracy than serology in the elderly. The role of the H. pylori stool antigen test in old age still needs to be clarified. One-week PPI-based triple therapy regimens including clarithromycin, amoxycillin and/or nitroimidazoles are highly effective and well tolerated in elderly patients. Low doses of both PPIs and clarithromycin (in combination with standard doses of amoxycillin or nitroimidazoles) are sufficient. Antibiotic resistance and low compliance are the main factors related to treatment failure at any age.

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“…A scientific debate has arisen about the possible association of H. pylori infection with extradigestive diseases, principally cardiovascular diseases, but also liver and biliary tract diseases, skin diseases, iron deficiency and pernicious anaemia 37 . The few studies performed in elderly populations failed to find any association between H. pylori infection and coronary heart disease 38 , 39 or extracardiac atherosclerosis 40 . To date, the presence of extradigestive diseases in subjects is not an indication for the testing or treatment of H. pylori .…”

Section: Indications For Treatment In the Elderlymentioning

confidence: 99%

“…37 The few studies performed in elderly populations failed to find any association between H. pylori infection and coronary heart disease 38,39 or extracardiac atherosclerosis. 40 To date, the presence of extradigestive diseases in subjects is not an indication for the testing or treatment of H. pylori.…”

Section: Extradigestive Diseasesmentioning

confidence: 99%

An approach toHelicobacter pyloriinfection in the elderly

Pilotto

Malfertheiner

2002

Aliment Pharmacol Ther

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The prevalence of Helicobacter pylori infection increases with age world‐wide, reaching levels of 40–60% in asymptomatic elderly subjects and over 70% in elderly patients with gastroduodenal diseases. However, the percentage of H. pylori‐positive elderly patients who are treated for their infection remains very low. Data are now available that demonstrate the benefit of curing H. pylori infection in elderly patients with H. pylori‐associated peptic ulcer disease and severe chronic gastritis. Furthermore, the cure of H. pylori may prevent the progression of intestinal metaplasia and gastric atrophy. New studies are needed to clarify the role of eradication in elderly patients with non‐ulcer dyspepsia and gastro‐oesophageal reflux disease and in those who use non‐steroidal anti‐inflammatory drugs. H. pylori infection may be easily diagnosed by histological evaluation, rapid urease test or culture performed on gastric biopsies taken during endoscopy. However, the biopsy site must be carefully selected in elderly patients. For non‐invasive monitoring of H. pylori infection after treatment, the 13C‐urea breath test has significantly higher accuracy than serology in the elderly; further studies are needed to clarify the role of the H. pylori stool antigen test in old age. One‐week proton pump inhibitor‐based triple therapy regimens, including clarithromycin, amoxicillin and/or nitroimidazoles, are highly effective and well tolerated in elderly patients. Low doses of both proton pump inhibitors and clarithromycin (in combination with standard doses of amoxicillin or nitroimidazoles) are sufficient. Low compliance and antibiotic resistance are the main factors related to treatment failure in old age.

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Lack of association between Helicobacter pylori infection and extracardiac atherosclerosis in dyspeptic elderly subjects

Cited by 19 publications

References 22 publications

GastricHelicobacterInfection Induces a Th2 Phenotype but Does Not Elevate Serum Cholesterol in Mice Lacking Inducible Nitric Oxide Synthase

GastricHelicobacterInfection Induces a Th2 Phenotype but Does Not Elevate Serum Cholesterol in Mice Lacking Inducible Nitric Oxide Synthase

Helicobacter pylori infection in geriatrics

An approach toHelicobacter pyloriinfection in the elderly

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