A low rate of reinfection following effective therapy against Helicobacter pylori in a developing nation (China)

Mitchell, Hazel M.; Hu, Pinjin; Yi, Chunhai; Chen, Min Hu; Li, Yu Yuan; Hazell, Stuart L.

doi:10.1016/s0016-5085(98)70475-5

Cited by 82 publications

(73 citation statements)

References 25 publications

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“…Contrasting reinfection rates have been shown in different studies. Data from developed countries are in accord with a recent study from China, 3 showing that after the eradication of DU, the average annual reinfection rate was 1.08%, while recurrence occurred in 6/184 (3.2%). In two of three patients reinfected, the fingerprint analysis demonstrated nonidentical strains before and after treatment, a clear indication of a newly acquired infection.…”

Section: Discussionsupporting

confidence: 86%

“…1 In the event of a recurrence, DU can be due to reinfection or recrudescence by H. pylori, therapy with nonsteroidal anti-inflammatory drugs (NSAIDs), or rare and less clear pathogenetic mechanisms. Differences in H. pylori reinfection rates have been reported in several studies, [2][3][4] and a comparison of strains obtained prior to and after therapy by fingerprint analysis was rarely possible. Therefore, it remains speculative whether true reinfection occurred, or whether it was simply a recrudescence of the previous bacterial infection.…”

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confidence: 99%

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Lack of Reinfection after Helicobacter Pylori Eradication in Duodenal Ulcer Disease: A Prospective Study from Turin, Italy

Pellicano

Arena

et al. 1999

Ann Saudi Med

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Turin, Italy. 1999; 19(4): 376-377 Helicobacter pylori (H. pylori) infection plays an important role in the cause of duodenal ulcer (DU). Successful cure of the infection modifies the natural history of the disease, leading to a dramatic reduction of recurrence. 1 In the event of a recurrence, DU can be due to reinfection or recrudescence by H. pylori, therapy with nonsteroidal anti-inflammatory drugs (NSAIDs), or rare and less clear pathogenetic mechanisms. Differences in H. pylori reinfection rates have been reported in several studies, 2-4 and a comparison of strains obtained prior to and after therapy by fingerprint analysis was rarely possible. Therefore, it remains speculative whether true reinfection occurred, or whether it was simply a recrudescence of the previous bacterial infection. 5 The objective of our study was to assess the incidence of reinfection and new ulceration events after demonstrated Helicobacter pylori eradication, in a cohort of patients with recurrent duodenal ulcers. Materials and MethodsWe followed up the natural history of duodenal ulcer disease in 115 patients (83 males, mean age 54.8 years). All of them had a previous diagnosis of recurrent duodenal ulcer documented by endoscopy, and associated H. pylori infection as shown by histology and serology.The starting point of the study was considered the confirmed eradication of the bacterium and DU absence at three months after the end of antibiotic treatment. Each patient underwent the monitoring scheme at 6, 12 and 24 months after the starting point.The presence of Helicobacter pylori infection was judged: 1) by histology (Giemsa staining) on biopsies obtained during endoscopy from the antrum and the fundus; and 2) by measuring specific IgG antibodies against H. pylori by a commercial enzyme-linked immunosorbent assay (ELISA).The infection was considered eradicated when: 1) histology did not demonstrate the bacterium either in the antrum or in the fundus; and 2) the level of circulating anti-Helicobacter pylori antibodies decreased in titer by at least 50% of the initial value. The patients whose levels of specific antibodies did not decrease were offered, independent of the histologic result, a 13 C urea breath test ( 13 C-UBT), using the European Standard Protocol. 6The 13 C-UBT was administered to every patient in case of an ulcer recurrence. We defined reinfection, the positivity for H. pylori infection, as a significant increase of specific IgG antibodies, confirmed by evidence on histology and/or positivity on 13 C-UBT at 12 or 24 months after a demonstrated eradication at six months. Patients were excluded from the study if they were on ulcerogenic drugs, or were taking long-term maintenance antisecretory therapy with proton pump inhibitors or H 2 -receptor blocker drugs. ResultsSeven of the initial 115 patients were lost to follow-up. None of the 108 patients followed up during the average period of 24 months (range 20-27) had a reinfection. Five patients (4.6%) had a duodenal ulcer recurrence, and their mean age was 57...

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Section: Discussionsupporting

confidence: 86%

mentioning

confidence: 99%

Lack of Reinfection after Helicobacter Pylori Eradication in Duodenal Ulcer Disease: A Prospective Study from Turin, Italy

Pellicano

Arena

et al. 1999

Ann Saudi Med

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“…For example, in Bangladesh, Ͼ50% of 2-to 9-year-old children from rural families are infected (1)(2)(3). Once acquired in childhood, this bacterium is able to establish a life-long relationship with its host (4).…”

Section: N the United States And Canada As Well As In Northern Andmentioning

confidence: 99%

The complete genome sequence of a chronic atrophic gastritis Helicobacter pylori strain: Evolution during disease progression

Oh¹,

Kling-Bäckhed

Giannakis

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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200

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Helicobacter pylori produces acute superficial gastritis in nearly all of its human hosts. However, a subset of individuals develops chronic atrophic gastritis (ChAG), a condition characterized in part by diminished numbers of acid-producing parietal cells and increased risk for development of gastric adenocarcinoma. Previously, we used a gnotobiotic transgenic mouse model with an engineered ablation of parietal cells to show that loss of parietal cells provides an opportunity for a H. pylori isolate from a patient with ChAG (HPAG1) to bind to, enter, and persist within gastric stem cells. This finding raises the question of how ChAG influences H. pylori genome evolution, physiology, and tumorigenesis. Here we describe the 1,596,366-bp HPAG1 genome. Custom HPAG1 Affymetrix GeneChips, representing 99.6% of its predicted ORFs, were used for whole-genome genotyping of additional H. pylori ChAG isolates obtained from Swedish patients enrolled in a casecontrol study of gastric cancer, as well as ChAG-and cancerassociated isolates from an individual who progressed from ChAG to gastric adenocarcinoma. The results reveal a shared gene signature among ChAG strains, as well as genes that may have been lost or gained during progression to adenocarcinoma. Wholegenome transcriptional profiling of HPAG1's response to acid during in vitro growth indicates that genes encoding components of metal uptake and utilization pathways, outer membrane proteins, and virulence factors are among those associated with H. pylori's adaptation to ChAG. acid regulation ͉ comparative microbial genomics ͉ ecogenomics ͉ functional genomics ͉ gastric cancer

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“…Helicobacter pylori colonization of the gastric mucosa is established during childhood and persists for decades without clearance by the immune system (1,2). Infection is associated with inflammation that, in most cases, is asymptomatic but develops into severe gastric pathology in a subset of infected individuals (3,4).…”

mentioning

confidence: 99%

An enzymatic ruler modulates Lewis antigen glycosylation of Helicobacter pylori LPS during persistent infection

Nilsson

Skoglund

Moran

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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A low rate of reinfection following effective therapy against Helicobacter pylori in a developing nation (China)

Cited by 82 publications

References 25 publications

Lack of Reinfection after Helicobacter Pylori Eradication in Duodenal Ulcer Disease: A Prospective Study from Turin, Italy

Lack of Reinfection after Helicobacter Pylori Eradication in Duodenal Ulcer Disease: A Prospective Study from Turin, Italy

The complete genome sequence of a chronic atrophic gastritis Helicobacter pylori strain: Evolution during disease progression

An enzymatic ruler modulates Lewis antigen glycosylation of Helicobacter pylori LPS during persistent infection

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