**2. Epidemiology of** *H. pylori* **infection and FD**

*H. pylori* is a global bacterial infection. Its prevalence varies greatly from 10-80% between countries, being quite elevated in developing countries in Asia, Africa, and South America but rather low in North America and Western Europe. In developed countries, approximately 20% of the population under the age of 40 years and 50% of those over the age of 60 years carry the infection. [6]

The prevalence of *H. pylori* infection also varies depending on age, socioeconomic status, sanitation and ethnic group [4, 7-9]. Typically, the infection is acquired in childhood before the age of 10 and the rate of acquisition is related inversely to household hygiene and the general levels of sanitation; wherever sanitation and standards of living have improved, the incidence of transmission has declined. The low prevalence in middle and upper socioeco‐ nomic populations in Western Europe and North America reflect better sanitation and quality of living. In the United States, the prevalence rate is approximately 50% in African Americans, 60% in Mexican Americans, and 26% in whites. [4] In developing countries, the prevalence among adult people is between 50-80%.

*H. pylori* infection may be evident in 20-60% of patients with functional dyspepsia, but the clinical relevance in most instances is confounded by the background frequency of this bacteria in the general population. A large scale nationwide community-based endoscopic survey of 2,488 adult subjects identified an overall *H. pylori* infection at 40.2% that was no different in dyspeptic subjects compared to asymptomatic persons. Differences amongst geographic regions likely related to differences in socioeconomic status and community hygiene during childhood period. [8] The frequency of functional dyspepsia is common in Asia, varying between 8-23% in most reported studies. [10] In fact, given the common frequency of *H. pylori* infection and challenges in obtaining endoscopy to eliminate organic causes of dyspepsia, it is difficult to discern the extent this microorganism is the basis for dyspepsia in Asia. [10, 11]

explained by variation in *cagA* between the Asian- and Western-types. *CagA* genotype can be divided into *cagA 1a* and *2a* [17] and *cagA 1a* strain of *H. pylori* demonstrated more virulence and associated with more gastric inflammation due to activation of proinflammatory cytokines such as increased production of IL-1β and IL-8 in the gastric mucosa. [21] Previous metaanalysis study reported that *cagA*-positive strain increases the likelihood of successful eradication. [22] The mechanism for the effect of *cagA* on eradication outcome might be explained by the presence of *cagA* induces secretion of inflammatory cytokine in gastric epithelial cells and increased gastric inflammatory response. [22] Consequently, the increase blood flow may help in the diffusion of antibiotics. [23] Another possibility might be explained by the density of *H. pylori* in gastric mucosa which has been reported to be higher in *cagA*positive strains than *cagA*-negative strains, thus *cagA*-positive strains might be proliferative faster than *cagA*-negative strains. [24, 25] As antibiotics are more active on rapidly growing

Functional Dyspepsia and *Helicobacter pylori* Infection

http://dx.doi.org/10.5772/56652

59

bacteria, *cagA*-positive strains would be more susceptible to antibiotic activity [23].

larly in regions with high prevalence.

**4.** *H. pylori* **diagnostic tests in FD**

**a.** Noninvasive tests for *H. pylori*

**1.** Serological tests

PPI and antibiotics) that may influence test results.

The effect of *H. pylori* eradication on dyspeptic symptoms in FD patients has revealed incon‐ clusive results in several studies, both in developed countries and in Asia. [26, 27, 28, 29] Dyspeptic patients who are infected with *H. pylori* often have functional dyspepsia rather than peptic ulcer disease, yet the outcome of eradicating *H. pylori* infection may be suboptimal in FD compared with that for established duodenal ulcer disease. [30] Nevertheless, at a popu‐ lation level, a Cochrane systemic review indicated that there was a 10% relative risk reduction of persistent symptoms in the *H. pylori*-eradication group compared to placebo; the number needed to treat to cure one case of dyspepsia was 14. [31] A recent meta-analysis of the Chinese literature showed that dyspepsia symptoms in FD improved after *H. pylori* eradication with an odds ratio of 3.61, suggesting that this infection might have a greater role in Asian than in Western countries. [32] Thus, *H. pylori* eradication overall does improve dyspepsia, particu‐

Tests to diagnosis *H pylori* infection are divided into those that are invasive requiring endos‐ copy versus those that are noninvasive, not requiring endoscopy. The choice of test depends on issues such as cost (variable in each country), availability, clinical situation, prevalence of infection, pretest probability of infection, and presence of confounding factors (eg, the use of

The noninvasive tests available in clinical practice include serologic tests, urea breath tests,

IgM and IgA antibody tests have not proven to be useful clinically, whereas anti–*H pylori* IgG has a better result. anti–*H pylori* IgG usually can be detected by 3-4 weeks after infection. The

and stool antigen tests. The choice of test is important in terms of validity

There are many FD patients in Asian as well as Western countries. The reported prevalence of *H. pylori* infection in patients with FD varies from 39% to 87%. [14] Several epidemiological studies have shown that *H. pylori* infection occurs more frequently in FD than in matched control populations. A meta-analysis published in 1999 reported a summary odds ratio for *H. pylori* infection in FD of 1.6 (95% CI, 1.4 to 1.8). [15]
