Rapid Recurrence of<i>Helicobacter pylori</i>Infection in Peruvian Patients after Successful Eradication

Ramírez-Ramos, Alberto; Gilman, Robert H.; León-Barúa, Raúl; Recavarren-Arce, Sixto; Watanabe, José; Salazar, Guillermo; Checkley, William; McDonald, Jeff; Valdez, Yanet; Cordero, Luis; Carrazco, Juan

doi:10.1086/516083

Cited by 71 publications

(29 citation statements)

References 9 publications

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“…In the developing world, the reinfection rates have ranged widely, from 1.1% at 2 years in China, to 73% at 8 months in studies from Peru. [16][17][18][19][20][21][22] Intermediate rates of reinfection are found in the Mediterranean region and Japan, ranging from 1.5% to 16.7%. 15,[28][29][30][31][32][33][34] It is sometimes difficult to distinguish between reinfection, defined as the complete eradication of an H. pylori infection followed by the introduction of a new H. pylori infection and recrudescence, defined as the apparent clearance of an H. pylori infection due to suppression but not eradication of the organism, followed by a positive test for H. pylori.…”

Section: Discussionmentioning

confidence: 99%

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Reinfection after successful eradication of Helicobacter pylori: a 2‐year prospective study in Alaska Natives

McMahon

Bruce

Hennessy

et al. 2006

Aliment Pharmacol Ther

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Section: Discussionmentioning

confidence: 99%

“…In developed countries, annual reinfection rates range from 0.36% in Australia to 5.7% in Italy [8][9][10][11][12][13][14][15] and in developing countries from 1.1% in China to 73% in Peru. [16][17][18][19][20][21][22] However, information regarding risk factors for reinfection is scanty.…”

Section: Introductionmentioning

confidence: 99%

Reinfection after successful eradication of Helicobacter pylori: a 2‐year prospective study in Alaska Natives

McMahon

Bruce

Hennessy

et al. 2006

Aliment Pharmacol Ther

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“…Furthermore, because there are widespread antimicrobial resistance, high recurrence rates of H. pylori, and a high incidence of gastric cancer in developing countries such as Peru, there is a stronger argument against the use of empiric antibacterial therapy as the primary means of preventing the longterm sequelae of H. pylori-induced gastritis (15).…”

Section: Discussionmentioning

confidence: 99%

Posttreatment Follow-Up of Helicobacter pylori Infection Using a Stool Antigen Immunoassay

Roth

Taylor

Gilman

et al. 2001

Clin Diagn Lab Immunol

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The Helicobacter pylori stool antigen enzyme immunoassay (HpSA) was evaluated during posttreatment follow-up of patients in a country with a very high prevalence of H. pylori infection. From among 273 dyspeptic individuals (18 to 55 years) initially recruited from a shantytown in Lima, Peru, 238 participants who met the inclusion criteria and were suspected to be H. pylori positive based on 14 C urea breath test (UBT) results underwent endoscopy. Participants with endoscopy-proven infections received standard eradication therapy and were monitored by UBT and HpSA at 1 month following treatment and at 3-month intervals for 9 months posttreatment. A second endoscopy was performed if UBT results showed evidence of treatment failure or H. pylori recurrence. Biopsy results were considered the "gold standard" in all analyses. Among patients who underwent endoscopy, HpSA had a pretreatment sensitivity of 93%. Two-hundred thirty patients completed the treatment regimen, of whom 201 (93%) were considered to have had successful treatment outcomes based on a negative follow-up UBT. Thirty-two patients with UBT-defined treatment failures or H. pylori recurrences at any point during the 9-month follow-up underwent a second endoscopy. In the posttreatment setting, HpSA had an overall sensitivity of 73% and a specificity of 67%. Agreement between UBT and HpSA diminished throughout the follow-up. Among 14 participants in whom HpSA remained positive at 1 month following treatment despite UBT evidence of treatment success, 12 (86%) became HpSA negative within 3 months posttreatment. Although this study confirmed the validity of the HpSA in the initial assessment of dyspeptic patients, the test demonstrated a reduced overall accuracy in the detection of treatment failures and H. pylori recurrences during 9 months of posttreatment follow-up. Furthermore, in some patients it may take up to 3 months after successful eradication for antigen shedding to diminish to levels within the negative HpSA range.Helicobacter pylori was first linked with gastritis in 1975 and was subsequently shown to be associated with peptic ulcer in 1985. Since then, the detection of the spiral bacterium in the gastric mucosa has become a principal aspect of the diagnostic investigation of patients with upper gastrointestinal symptoms suggestive of peptic ulcer disease (7). Chronic superficial gastritis due to infection with H. pylori is responsible for up to 95% of duodenal ulcers and 80% of gastric ulcers throughout the world (25). Perhaps the most convincing evidence for the pathogenic role of H. pylori is the dramatic effect of antibiotic therapy. Current treatment regimens combining at least two antibiotics and a proton pump inhibitor can eradicate H. pylori infections in greater than 90% of patients (21), and they significantly reduced ulcer recurrence in long-term follow-up studies (29). The organism has also been classified as a class I carcinogen due to its pathogenic role in intestinal-type gastric adenocarcinoma and has further been linked to diffus...

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“…Treatment failure is mainly due to antibiotic resistance and an increase of adverse effects, which in turn decrease eradication rates [26]. In developing countries, prevalence of H. pylori can reach 90%, and reinfection rates are very high [26,59]. Unfortunately, intensive antibiotic use is not possible both logistically and economically, and this seriously hampers any gastric cancer prevention strategy [6].…”

Section: Introductionmentioning

confidence: 99%

Peptide Extracts from Cultures of Certain Lactobacilli Inhibit Helicobacter pylori

Vuyst

Vincent

Makras

et al. 2009

Probiotics & Antimicro. Prot.

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Helicobacter pylori inhibition by probiotic lactobacilli has been observed in vitro and in vivo. Carefully selected probiotic Lactobacillus strains could therefore play an important role in the treatment of H. pylori infection and eradication. However, the underlying mechanism for this inhibition is not clear. The aim of this study was to examine if peptide extracts, containing bacteriocins or other antibacterial peptides, from six Lactobacillus cultures (Lactobacillus acidophilus La1, Lactobacillus amylovorus DCE 471, Lactobacillus casei YIT 9029, Lactobacillus gasseri K7, Lactobacillus johnsonii La1, and Lactobacillus rhamnosus GG) contribute to the inhibition of H. pylori. Peptide extracts from cultures of Lact. amylovorus DCE 471 and Lact. johnsonii La1 were most active, reducing the viability of H. pylori ATCC 43504 with more than 2 log units within 4 h of incubation (P < 0.001). The four other extracts were less or not active. When six clinical isolates of H. pylori were tested for their susceptibility towards five inhibitory peptide extracts, similar observations were made. Again, the peptide extracts from Lact. amylovorus DCE 471 and Lact. johnsonii La1 were the most inhibitory, while the three other extracts resulted in a much lower inhibition of H. pylori. Protease-treated extracts were inactive towards H. pylori, confirming the proteinaceous nature of the inhibitory substance.

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Rapid Recurrence ofHelicobacter pyloriInfection in Peruvian Patients after Successful Eradication

Cited by 71 publications

References 9 publications

Reinfection after successful eradication of Helicobacter pylori: a 2‐year prospective study in Alaska Natives

Reinfection after successful eradication of Helicobacter pylori: a 2‐year prospective study in Alaska Natives

Posttreatment Follow-Up of Helicobacter pylori Infection Using a Stool Antigen Immunoassay

Peptide Extracts from Cultures of Certain Lactobacilli Inhibit Helicobacter pylori

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