**1. Introduction**

*Helicobacter pylori* (*H. pylori*) was first observed over 100 years ago yet its association with clinical diseases was not fully understanding until 1982 when Marshall and Warren identified and subsequently cultured the gastric bacterium. At their first attempt to culture the bacteria was not successful. Colonies finally grew when they accidentally left some culture plates over the Easter holiday. Dr. Barry Marshall subsequently inoculated himself with culture broth containing more than 1 billion organism to prove that this bacterium would cause peptic ulcers supporting Koch's postulate. He developed acute gastritis 1 week after the inoculation. *H. pylori* is a microaerophilic, spiral shaped, gram negative bacterium measuring about 3.5 microns in length and 0.5 microns in width. In vitro, this bacterium is a gradually growing organism that can be cultured on blood agar incubated at 37ºC in a microaerophilic condition (5% oxygen) for 4-7 days. The colony of this bacteria is tiny, uniformly sized and translucence (fig 2A).

*H. pylori* is a Gram-negative, spiral shaped, bacterium about 3.5 microns long and 0.5 microns wide. (fig 2B). This bacterium uses its 2-7 unipolar flagella to escape the harsh luminal acidity by burrowing into the mucus layer that covers the gastric mucosa and so reside in close proximity to the more neutral pH of the epithelial cell surface of the gastric mucosa. It can convert from a highly motile, helical (spiral) shape to a more dormant coccoidal form, perhaps a survival benefit depending upon its local environment. Being microaerophilic, *H. pylori* requires oxygen. *H. pylori* is biochemically characterized as positive for catalase, oxidase, and urease. The urease enzyme, which has been located on the surface of the bacteria, is important and likely to be vital for bacterial survival and colonization in the highly acidity milieu of the stomach. Urease breaks down the luminal urea normally produced by the gastric mucosa, yielding carbon dioxide and ammonia.

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Functional dyspepsia (FD) is one of the most common causes of dyspeptic symptoms. FD is recognized as heterogeneous group of symptoms located in the center of upper abdo‐ men. The prevalence of dyspepsia is variable in different populations and environmental factors. In 2006 the Rome III provides the diagnostic criteria, which are included one or

Functional Dyspepsia and *Helicobacter pylori* Infection

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

57

The FD patient must not have any evidence of structural disease to explain the dyspeptic symptoms. Symptom onset should occur at least 6 months prior to diagnosis while the criteria must be fulfilled for the last 3 months. FD also can be divided into two major syndromes: the postprandial distress syndrome and the epigastric pain syndrome. The postprandial distress syndrome type of FD constitutes bothersome postprandial fullness and early satiation, occurring after meal and at least several times per week. Upper abdominal bloating or postprandial nausea or excessive belching might be present. In contrast, the epigastric pain syndrome type of FD mostly suffers with intermittent epigastric pain or burning at least once a week. The pain should not refer to other abdominal or chest regions, and should not be

*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

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

*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

more of the following [5, 6]

**2.** Early satiation **3.** Epigastric pain

infection. [6]

**4.** Epigastric burning

**1.** Bothersome postprandial fullness

relieved by defecation of passage of flatus. [5]

among adult people is between 50-80%.

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

**Figure 1.** or 14C-urea is hydrolyzed by the *H pylori* urease enzyme and can be detected by CO2 in breath samples

**Figure 2.** A) *H. pylori* colonies; (B). *H. pylori* detected by gram stain

Ammonia then accepts a proton (H+ ), lessening the nearby acidity and forming protective surroundings that allow its survival. Furthermore, urease activity is clinically relevance in the form of several tests to diagnose infection such as rapid urease test and urea breath test. [1-4] The ammonia produced however is toxic to the epithelium, and aided by other products like proteases, vacuolating cytotoxin A (associated with cytotoxin-associated gene A ), and certain phospholipases damages the mucosa. *H. pylori* infection also increases gastric acid secretion (suppressing somatostatin to allow increased gastrin), down regulates mucosal defense mechanisms and elicits an inflammatory response.

*H. pylori* infects the gastric mucosa in 20-80 % of humans throughout the world, making it a very common bacterial infection. In developing countries, the infection tends to be acquired via the fecal-oral or oral-oral route during childhood and subsequently persists through adulthood. In developed countries, childhood infection is no longer common (rare under 10 years of age) though prevalence does increase during adulthood (>50% if over 50 years); the latter cohort likely acquired H. pylori during childhood. This bacteria is the major pathologic agent in the development of gastritis, gastric ulcer, duodenal ulcer, MALT lymphoma and gastric cancer. The International Agency for Research into Cancer has classified *H. pylori* as a class 1 carcinogen which is in the same class as cigarette smoke. [1-3]

Functional dyspepsia (FD) is one of the most common causes of dyspeptic symptoms. FD is recognized as heterogeneous group of symptoms located in the center of upper abdo‐ men. The prevalence of dyspepsia is variable in different populations and environmental factors. In 2006 the Rome III provides the diagnostic criteria, which are included one or more of the following [5, 6]


**Figure 1.** or 14C-urea is hydrolyzed by the *H pylori* urease enzyme and can be detected by CO2 in breath samples

surroundings that allow its survival. Furthermore, urease activity is clinically relevance in the form of several tests to diagnose infection such as rapid urease test and urea breath test. [1-4] The ammonia produced however is toxic to the epithelium, and aided by other products like proteases, vacuolating cytotoxin A (associated with cytotoxin-associated gene A ), and certain phospholipases damages the mucosa. *H. pylori* infection also increases gastric acid secretion (suppressing somatostatin to allow increased gastrin), down regulates mucosal defense

*H. pylori* infects the gastric mucosa in 20-80 % of humans throughout the world, making it a very common bacterial infection. In developing countries, the infection tends to be acquired via the fecal-oral or oral-oral route during childhood and subsequently persists through adulthood. In developed countries, childhood infection is no longer common (rare under 10 years of age) though prevalence does increase during adulthood (>50% if over 50 years); the latter cohort likely acquired H. pylori during childhood. This bacteria is the major pathologic agent in the development of gastritis, gastric ulcer, duodenal ulcer, MALT lymphoma and gastric cancer. The International Agency for Research into Cancer has classified *H. pylori* as a

**Figure 2.** A) *H. pylori* colonies; (B). *H. pylori* detected by gram stain

mechanisms and elicits an inflammatory response.

class 1 carcinogen which is in the same class as cigarette smoke. [1-3]

Ammonia then accepts a proton (H+

56 Dyspepsia - Advances in Understanding and Management

(A) (B)

), lessening the nearby acidity and forming protective

**4.** Epigastric burning

The FD patient must not have any evidence of structural disease to explain the dyspeptic symptoms. Symptom onset should occur at least 6 months prior to diagnosis while the criteria must be fulfilled for the last 3 months. FD also can be divided into two major syndromes: the postprandial distress syndrome and the epigastric pain syndrome. The postprandial distress syndrome type of FD constitutes bothersome postprandial fullness and early satiation, occurring after meal and at least several times per week. Upper abdominal bloating or postprandial nausea or excessive belching might be present. In contrast, the epigastric pain syndrome type of FD mostly suffers with intermittent epigastric pain or burning at least once a week. The pain should not refer to other abdominal or chest regions, and should not be relieved by defecation of passage of flatus. [5]
