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Helicobacter pylori pdf

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Helicobacter pylori was considered by a previous IARC Working Group in ( IARC, ). Since that time Monographs/volB/BTablepdf). The first isolation of Helicobacter pylori in by Marshall and Warren () ushered in a new era in gastric microbiology. Although spiral organisms had been. bacter pylori and its role in gastritis and peptic ulcer disease.” The number of peer-reviewed publications on Helicobacter has rapidly increased, from less than .


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Helicobacter pylori (H. pylori) is a spiral-shaped bacterium that is found in the gastric mucous layer or adherent to the epithelial lining of the stomach. H. pylori. INTRODUCTION. Helicobacter pylori infection remains one of the most common chronic bacterial infections affecting humans. Since publication of the last. H. pylori is a bacterium (germ) that can infect the human stomach. Its significance for human disease was first recognised in The bacterium lives in the.

Br J Cancer. Intestinal parasites, especially helminthes, are more frequent in the warm tropical climates. The treatment of H. Please review our privacy policy. A critical review of the evidence. The type of gastritis observed is predominantly non-atrophic Figure 5 with very low proportion of metaplastic changes [ 46 ]. There is no unanimous judgment regarding the use of probiotic agents:

The diet tends to be high in salt [ 33 ] and low in animal proteins Camargo et al, unpublished data as well as in fruits and fresh vegetables [ 34 ].

Interventional measures such as H. Multifocal atrophic gastritis in a Colombian subject residing in a high gastric cancer risk area, infected with a cagA -positive vacA s1m1 H. Marked inflammatory infiltrate and loss of glandular structures are observed. Multifocal atrophic gastritis with intestinal metaplasia colonic type in a Colombian subject residing in a high gastric cancer risk area, infected with a cagA -positive vacA s1m1 H. Normal glands seen on the left side display neutral mucins magenta.

Metaplastic epithelium, on the right side, displays acidic mucins purple in the goblet cells and neutral mucins in the columnar cells. AB-PAS stain. This is presently the case of Japan and probably South Korea. In general, these societies have high prevalence of multifocal atrophic gastritis and intestinal metaplasia [ 37 ], as observed in other high risk populations. These two countries for many years displayed the highest cancer incidence and mortality rates in the world.

The reasons for such high rates are poorly understood, but may be related to the high virulence of the prevalent H. Some recent reports have suggested a relatively high frequency of gastric corpus atrophy, not seen frequently in low SES populations. It is not clear if this is a new development in such populations and if it may be related to recent ecological changes. In these societies, the high SES is relatively recent and has been accompanied by changes in their diet, especially lower salt intake [ 40 ].

A nationwide screening and early detection program for gastric cancer has been conducted in Japan for several decades. As a result, decreasing mortality rates in the presence of continued high incidence rates have been observed in Japan [ 16 , 40 ].

These societies are represented by most African countries and some coastal and low altitude regions of Latin America [ 42 - 45 ]. They usually have a high prevalence of H.

The type of gastritis observed is predominantly non-atrophic Figure 5 with very low proportion of metaplastic changes [ 46 ]. Studies suggest that they may have a higher proportion of low virulence strains when compared to populations at high gastric cancer risk, but it is doubtful that the differences in strains are large enough to fully explain their differences in cancer risk [ 30 , 31 ].

One main difference is the diet: These types of foods are rich in antioxidants. Another possible factor has to do with the type of immune reaction of the host to the H. Intestinal parasites, especially helminthes, are more frequent in the warm tropical climates. They tend to drive an anti-inflammatory Th2-type immune response against the H.

Eosinophilic infiltration of the gastric mucosa, linked to Th2-type response, may be prominent Piazuelo et al, unpublished data. In an animal model, supporting this hypothesis, concurrent helminth infection reduced considerably Helicobacter -associated gastric inflammatory cytokines and chemokines associated with a Th1 response and gastric atrophy [ 49 ]. A similar phenomenon has been reported in a population indicating that a concurrent helminth infection Schistosoma japonicum modifies the immune response to H.

Non-atrophic chronic gastritis in a subject residing in a low gastric cancer risk area, infected with a cagA -negative vacA s2m2 H. Mild to moderate mononuclear infiltrate and well preserved glandular structures are observed.

It has been reported that duodenal ulcer frequency began to rise in Europe and the United States in the 19 th century and is becoming less frequent in recent decades [ 51 , 52 ] displaying the temporal pattern of an epidemic.

Patients with duodenal ulcer typically have an antral diffuse non-atrophic, active chronic gastritis. The strains of H. The decline in duodenal ulcer incidence is related to the decline in the prevalence of H. The reasons behind the rise in duodenal ulcer in the 19 th century in Europe and the United States are obscure. It coincided with the beginning of the decline in H. It has been proposed that that the initial increase in duodenal ulcer reflects a change in the equilibrium that existed for centuries between H.

The alteration in that equilibrium could have affected the pattern of colonization of H. This altered equilibrium could have resulted in excessive acid secretion, a forerunner of duodenal ulcer. It has also been reported that the first infection with H. The dynamics of the relationship between host and infectious agent may differ according to the age at first infection.

It has been hypothesized that a very early infection may colonize the gastric mucosa at a time when the acid secretion apparatus has not been fully matured to permit duodenal ulcer development. Such subjects may present early development of atrophy with increased risk of gastric ulcer and carcinoma [ 54 ]. Among them, the prevalence of H. The diagnosis of the infection may be an incidental finding during routine health screening procedures. The proportion of low virulence strains of H.

Colonization with such strains leads to mild non-atrophic gastritis, with well-preserved gastric architecture [ 3 ].

Some of such populations have a history of high risk for gastric cancer decades before. Probably the type and severity of chronic gastritis were different then. Since clinically tangible sequelae of the infection are absent, it could be argued that anti- H. The decrease in prevalence of H. These conditions are associated with hyperacidity, which has been reported after curing the H. Accordingly, a protective effect of H.

Chronic gastritis is the unavoidable manifestation of H. It varies considerably in type and severity among populations and individuals. Its phenotype and consequences are determined by a complex interaction of etiologic factors derived from the bacterium and its human host as they have co-evolved throughout the centuries. In populations at high cancer risk, the full spectrum of the precancerous cascade is observed: Corpus atrophy has been associated with higher gastric cancer risk and usually represents an extension to the corpus of a multifocal atrophic gastritis.

Corpus atrophy without antral atrophy is characteristic of autoimmune gastritis, as seen in the pernicious anemia syndrome, less frequently observed at the present time. Gastric peptic ulcer is part of the multifocal atrophic gastritis complex. By contrast, duodenal peptic ulcer is not associated with atrophy, does not increase cancer risk, and seems to follow an epidemic pattern in populations in transition from high- to low- gastric cancer risk.

Populations with low gastric cancer risk and low SES may have high prevalence and early infection of H. Affluent Western populations present low H. Among them, gastroesophageal reflux-related diseases are increasing in incidence, coinciding with further decrease in H. Another possible negative influence of the absence of H. It postulates that improvements in sanitation and widespread use of antibiotics have resulted in the disappearance of infections of the respiratory and digestive systems, especially in children, required to shape and maintain the homeostasis of the human immune system [ 58 , 59 ].

The increasing incidence of asthma, eczema and auto-immune diseases in developed countries seem to reflect a bias in the development of the immune system towards Th2-type responses. Studies suggest that H. The spectrum of H. The chronic gastritis phenotype presents marked inter-population differences depending on the socioeconomic status and the gastric cancer risk.

To increase our knowledge in H. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

The authors declare that there is no conflict of interest. National Center for Biotechnology Information , U. Dig Liver Dis. Author manuscript; available in PMC Jul Blanca Piazuelo , MD 1.

Blanca Piazuelo. Author information Copyright and License information Disclaimer. Copyright notice. The publisher's final edited version of this article is available at Dig Liver Dis.

See other articles in PMC that cite the published article. Abstract This report describes the modalities of chronic gastritis induced by Helicobacter pylori infection in different populations.

Helicobacter Pylori Infection

Introduction Helicobacter pylori H. Open in a separate window.

Pylori pdf helicobacter

Figure 1. The Bacterium and its Pathogenicity H.

Pylori pdf helicobacter

Figure 2. Epidemiology and Natural History A steady decrease in the prevalence of H. Figure 3. Figure 4. The African enigma These societies are represented by most African countries and some coastal and low altitude regions of Latin America [ 42 - 45 ]. Figure 5. Epilogue Chronic gastritis is the unavoidable manifestation of H.

Practice points H. Research agenda To increase our knowledge in H. Identification of genetic markers of host susceptibility to gastric cancer. Footnotes Publisher's Disclaimer: Molecular characterization of the kDa immunodominant antigen of Helicobacter pylori associated with cytotoxicity and duodenal ulcer.

Helicobacter pylori genotypes, host factors, and gastric mucosal histopathology in peptic ulcer disease. Hum Pathol. Nomura A. Infection with Helicobacter pylori strains possessing cagA is associated with an increased risk of developing adenocarcinoma of the stomach. Cancer Res. Helicobacter pylori CagA protein variation associated with gastric cancer in Asia. J Gastroenterol. Biological activity of the Helicobacter pylori virulence factor CagA is determined by variation in the tyrosine phosphorylation sites.

Relationship between the diversity of the cagA gene of Helicobacter pylori and gastric cancer in Okinawa, Japan.

The vacuolating cytotoxin of Helicobacter pylori. Mol Microbiol. Mosaicism in vacuolating cytotoxin alleles of Helicobacter pylori. Association of specific vacA types with cytotoxin production and peptic ulceration. J Biol Chem. Expanding allelic diversity of Helicobacter pylori vacA. J Clin Microbiol. Clinical and pathological importance of heterogeneity in vacA, the vacuolating cytotoxin gene of Helicobacter pylori.

Helicobacter pylori genotypes are associated with clinical outcome in Portuguese patients and show a high prevalence of infections with multiple strains. Scand J Gastroenterol. Helicobacter pylori genotypes may determine gastric histopathology. Am J Pathol. Epidemiology of gastric cancer. Helicobacter pylori infection and the development of gastric cancer.

NATURAL HISTORY OF HELICOBACTER PYLORI INFECTION

N Engl J Med. Diagnosis without treatment, i. Moreover, any treatment that is carried out to eradicate the pathogen should be followed-up by testing to determine the success of treatment; this can be done with a breath test or stool antigen test, in cases where follow-up endoscopy is not already indicated for other reasons.

This requirement is derived from the fact that 3. An especially important recommendation for clinical practice is that patients with a history of ulcer disease should undergo testing for, and eradication of, H. The indications are summarized in the Box. A meta-analysis has shown that H. The evidence regarding low-dose ASA is not entirely clear, but it is recommended that the pathogen should be eradicated in the subgroup of patients with a history of an ulcer 3 , 5.

Thus, in general, there seems to be a preventive effect of H. It must nonetheless be stressed that, strictly speaking, this situation necessitates the performance of two non-invasive tests that are not reimbursable in Germany when performed for this purpose. If pharmacotherapy is to be reinstated later on, this must be done with caution. The protective effect of successful H.

The risk of gastric carcinoma in Germany is relatively low incidence In parts of the world where the prevalence of gastric carcinoma is high, e. Therefore, according to the German guideline, H. Such persons include the first-degree relatives of patients with gastric carcinoma, persons with a type of gastritis that puts them at elevated risk pangastritis or gastritis mainly affecting the corpus , persons who have undergone the endoscopic or surgical resection of gastric adenomas or early-stage carcinomas, persons with multifocal atrophy, and persons taking PPI over the long term.

The last-mentioned risk factor is the least well-documented. A systematic review of the literature that took 16 studies into account, including a total of patients using PPI, did not reveal any elevated risk of gastric tumors On the other hand, H.

A recent study has shown that the risk of gastric carcinoma is elevated in persons who have been taking PPI for a long time even if H. The timing of treatment has a major effect of the efficacy of H. There is a protective effect mainly when no pre-neoplastic changes such as atrophy or intestinal metaplasia have yet arisen 24 — This has led to the postulation of a point of no return in the pathogenesis of gastric carcinoma, beyond which malignant changes are inevitable 27 figure 2.

We now know that H. A recent meta-analysis of 24 studies including a total of 48 individuals with cases of gastric carcinoma revealed that the risk of gastric carcinoma was cut in half after successful H.

Pylori pdf helicobacter

The same meta-analysis showed that the preventive effect of H. It must be borne in mind that H. This was the conclusion of a cohort study of patients with intestinal metaplasia and severe atrophy, in whom the risk of developing gastric carcinoma was still elevated even after successful pathogen eradication Antibiotic treatment for the eradication of H.

An accepted indication and the detection of the pathogen are prerequisites to eradication treatment 5. What is the concrete procedure for H.

A network meta-analysis on the first-line treatment of H. This criterion is met, however, if the duration of treatment is extended to 10—14 days of if quadruple therapy is provided. The German guideline envisions 7 to 14 days of standard triple therapy and 10 days of quadruple therapy including bismuth or triple therapy including fluoroquinolone 5. We find that giving triple therapy for only seven days is no longer acceptable. Any recommendation for treatment must take this state of affairs into account.

The first thing to be considered is the probability of primary resistance to clarithromycin and other antibiotics 3 — 5 , which can only be estimated qualitatively or, at best, semiquantitatively. A treatment algorithm for patients with a low rate of primary clarithromycin resistance is shown in Figure 3 , while one for patients with a high rate is shown in Figure 4. These two figures contain all of the relevant treatment recommendations found in the guidelines 3 — 5.

Southern or eastern European ethnic origin and prior treatment with macrolides are risk factors for clarithromycin resistance. The latter, however, can hardly be ascertained by history-taking, but frequent antibiotic use in the past can be taken pragmatically as an indirect index of macrolide use.

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Treatment algorithm for H. PAC, proton-pump inhibitor, amoxicillin, and clarithromycin; PMC, proton-pump inhibitor, metronidazole, and clarithromycin. Important measures to promote the success of treatment include detailed patient education about how to take the medications, including motivation of the patient to adhere to the prescribed course of treatment.

There is no unanimous judgment regarding the use of probiotic agents: A meta-analysis of 19 randomized and controlled trials that could not be considered in the creation of the guideline led to the finding that individual types of probiotic agent can prevent side effects of treatment and thereby improve the success of H. Individual types of probiotic agent can prevent side effects of treatment and thereby improve the success of H.

Participation in the CME certification program is possible only over the Internet: This unit can be accessed until 16 September Submissions by letter, e-mail or fax cannot be considered. The EFN must be stated during registration on www. What treatment regimen is recommended when there is a low rate of primary clarithromycin resistance? What combination of drugs should be given after the failure of bismuth quadruple therapy? How can Helicobacter pylori be reliably detected by noninvasive means?

The consumption of what two kinds of drugs elevates the risk of a gastric or duodenal ulcer or of an ulcer bleed in a patient infected with H.

According to the Toronto consensus report, what should be the duration of treatment to eradicate Helicobacter pylori infection? What is the main reason for the failure of standard triple therapy to eradicate Helicobacter pylori? What diagnostic method serves as the basis for the precise classification of gastritis recommended for patients who receive an initial diagnosis of gastritis at age 50 or above?

What does the current German guideline have to say about the role of probiotic agents in the treatment of Helicobacter pylori? Conflict of interest statement. Fischbach has received payment from Aptalis for authorship of a publication. He has also received payment from Aptalis and Allergan for the preparation of continuing medical education events, as well as financial support from Aptalis for a research project that he initiated.

Malfertheiner has served as a paid advisor for biohit and Allergan. He has received payment from Allergan, Biocodex, and Bayer for the preparation of scientific meetings. National Center for Biotechnology Information , U.

Journal List Dtsch Arztebl Int v. Dtsch Arztebl Int. Published online Jun Wolfgang Fischbach , Prof. Author information Article notes Copyright and License information Disclaimer. Received Oct 11; Accepted May 2. Copyright notice. This article has been cited by other articles in PMC.

Abstract Background Infection with Helicobacter pylori H. Methods This review is based on pertinent publications retrieved by a selective search in PubMed and the Cochrane Database, with particular attention to three international consensus reports and the updated German S2k guideline. Results H. Conclusion The new, clinically relevant developments that are presented and commented upon in this review now enable evidence-based management of H. Learning objectives After reading this article, the reader should know: Indications for Helicobacter pylori eradication.

Helicobacter pylori is an infectious disease It was first explicitly formulated in the Kyoto Global Consensus Report that H. Mass screening for H. Helicobacter-pylori-associated dyspepsia and functional dyspepsia The recommendation contained in the German S3 guideline of 8 to the effect that patients with functional dyspepsia and H.

Open in a separate window. Figure 1. Diagnostic evaluation Eradication in patients with functional dyspepsia. Diagnostic evaluation. Checking on the success of treatment. Indications for eradication Indications for eradication. BOX Indications for Helicobacter pylori eradication 5.

Incidence of gastric carcinoma. Figure 2. The pathogenesis of gastric carcinoma after [27]. Hp, Helicobacter pylori. The treatment of H. Figure 3. Figure 4. Probiotic agents. CME credit for this unit can be obtained via cme.

Only one answer is possible per question. Please choose the most appropriate answer. Footnotes Conflict of interest statement Prof. References 1. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Kyoto global consensus report on Helicobacter pylori gastritis. The Toronto Consensus for the treatment of Helicobacter pylori infection in adults.