**4. Discussion**

2 (16.67%) with antral hyperemia and 3 (25%) showed a normal mucosal aspect. In patients who were not previously treated, we observed macroscopic nodular antral gastritis in 15 cases (88.24%), antral hyperemia in 2 cases (11.76%) while a normal appearance of gastric mucosa was never detected (**Table 3**). There was not a statistically significant association between the severity of mucosal damage at endoscopy and the existence of a previous therapy against the

**Figure 2.** Endoscopical aspect of *Helicobacter pylori* gastritis in children (macroscopic nodular antral gastritis).

**Endoscopic features n (%)** Macroscopic nodular antral gastritis 22 (75.86%)

Nodular antral gastritis (only) 12 Nodular gastritis of corpus (with) 8 Erosive bulbitis (with) 1 Esophagitis (with) 1

Antral hyperemia without macroscopic nodularity 4 (13.79%) Normal 3 (10.34) Total 29 (100%)

In our study, bleeding was the presenting symptom in 4 children; three of them had pan

gastritis, and one had nodular gastritis and esophagitis.

**Table 2.** Endoscopic features associated to *Helicobacter pylori* infection.

40 Helicobacter Pylori - New Approaches of an Old Human Microorganism

infection (p = 0.06).

There is a clear association between *H. pylori* and gastritis, gastric ulcer, and duodenal ulcers. Studies have shown that this pathogen causes mucosa-associated lymphoid tissue (MALT) lymphoma in both children and adults. In fact, when the organism is eradicated, extra gastric metastases or sites of MALT lymphoma resolve [4].

The finding of *H. pylori-*associated gastritis without duodenal or gastric mucosal lesions puts the pediatric gastroenterologist in a dilemma on recommending eradication treatment. *H. pylori-*associated gastritis without PUD rarely gives rise of symptoms or progresses to severe complications of the disease during childhood [5]. The risk of *H. pylori*- associated cancer or MALT-lymphoma during childhood is extremely low in Europe and North America. Ohno reported two cases in Japanese children, a 14-year-old boy and another 6-year-old boy with MALT and *H. pylori* infection [5]. The lower risk of complications in children may be in part explained by a different immune response against the infection. In comparison with adults, gastric biopsies obtained from children infected with *H. pylori* show a lower degree of inflammation. In addition, a higher number of immunosuppressive regulatory T cells and a more prominent IL-10 mediated anti-inflammatory response have been detected in pediatric patients [1].

During childhood, *H. pylori* is associated with antral predominant gastritis and duodenal ulcers [6].

In our study, the most frequent lesion identified by endoscopy was macroscopic antral nodular gastritis, which was present in 22 patients (78.86%). This high frequency is in accordance with a retrospective study from Japan that also found out a marked prevalence of nodular antral gastritis associated with *H. pylori* infection (98.5%) [7]. A nodular antral gastritis frequency of 82.53% was also reported by a Turkish study conducted in adults and adolescents [8]. In a pediatric polish study, the sensitivity of antral nodularity associated with *H. pylori* was 91.6%, and the specificity was 91% [9]. A slightly lower value of specificity of antral nodularity, similar to our results (75.86%), was detected by several authors and ranged from 64 to 85.2%. Higher specificity was found by others [7–9].

The sex difference between the *H. pylori*-positive and *H. pylori*-negative group is also of great interest. We found female preponderance in the study group (65.51%), similarly with another

Endoscopical Aspects of *Helicobacter pylori* Gastritis in Children

http://dx.doi.org/10.5772/intechopen.81437

Studies have unanimously shown a male preponderance for peptic ulcer disease in children. It is still not known why primary peptic ulcers predominantly develop in infected male children. Epidemiological studies do not suggest any sex predilection in *H. pylori* infection [16]. Median age for patients with previous therapies was 14.5 ± 3.74 years, comparative with 13 ± 4.71 years for patients without previous therapies, results or else expected. We do not have data to express if it is failure of antimicrobial therapy or reinfection. 1/12 patient with previous therapies had family history of peptic ulcer disease. We do not investigate all the family member of each child, and therefore we do not know the real status of *H. pylori* infection. Familial history for gastrointestinal disease was collected for interview. Magistà et al. [18] identified two variables by logistic regression analysis as predictors of *H. pylori* reinfection: age of primary infection and having an infected sibling. Multivariable analysis revealed that only age at primary infection correlates with an increased risk of

In patients with anterior therapies, the endoscopic features were less serious than in those without any previous treatment. All three patients with normal endoscopic mucosa were anteriorly treated. These results suggest that children might become "tolerant" to the bacterium or that the growing child is more resistant to *H. pylori*-induced lesions. The evidence that *H. pylori* infection in children coexist with normal gastric mucosa was reported in a percent comparable with our results (11%) [19]. This is the reason for which we strongly recommend to take biopsies at least for histological exam in children and adolescents, even if a normal

The ability of *H. pylori* to manipulate the immune response (activation or inactivation of Toll-like receptors dependent response) may be responsible for bacterial survival and a mild

The main endoscopic feature found in our study was macroscopic nodular antral gastritis, in 75.86%. In 10.34% of cases the endoscopic aspect of mucosa was normal. All patients with normal endoscopic mucosa were previously treated. These results suggest that children might become "tolerant" to the bacterium or that the growing child is more resistant to *H.* 

The authors thank Dr. Augustina Enculescu for her histological support.

report in our geographic area (78.49%) [17].

appearance of mucosa is observed during endoscopy.

course of infection in children [20].

**5. Conclusions**

*pylori*-induced lesions.

**Acknowledgements**

reinfection [18].

Although the mechanisms underlying nodular gastritis in children is not clear yet, it is thought that lymphoid follicles with germinal center form nodules on gastric mucosa or that inflammatory reaction generated by *H. pylori* infection results in an exaggerated appearance of a normal gastric mucosa [10].

In a 14-year-old boy we observed erosions at endoscopy. The frequency of these lesions in our study (3.45%) is similar to the one measured by another study conducted in Italy (3.40%) [11].

A prospective study, carried out during 1-month simultaneously in 19 centers among 14 European countries, showed a frequency of 8.1% of ulcers and/or erosions in children, occurring mainly in the second decade of life, but *H. pylori* infection and toxic gastric medications were less frequently implicated than expected in their development. On a total of 56 children with ulcers or erosions, *H. pylori* was present in 15 patients (27%), 8 used NSAIDs, 5 were treated with steroids, 5 with immune-suppressive drugs, 6 with antibiotics, 1 with antacids, 6 with H<sup>2</sup> blockers and 8 with proton pump inhibitors (more than one risk factor was detected in 32 of 56 children) [12].

For years, reports have noted an association between peptic ulcer disease and families with a strong history of upper gastrointestinal tract disease, in particular between gastric and duodenal ulcers. Family history of gastric cancer is an important component in the diagnosis and management of *H. pylori* infection in children. Children with a mother or a father with gastric cancer are considered to be at very high risk owing to shared genetic characteristics, environmental factors, and virulence features of the infecting strain of *H. pylori* [4].

In countries with an elevated risk for gastric cancer, however, eradicating *H. pylori* in childhood could be more effective in preventing gastric atrophy, and ultimately, cancer development [13]. It still remains to be determined whether *H. pylori*-infected children with gastric atrophy are at increased risk for gastric cancer [14].

Recently, a decreasing proportion of *H. pylori*-positive peptic ulcers in adults has been observed, along with a decrease in the prevalence of infection, while, on the other hand, an increasing number of patients that use non-steroidal anti-inflammatory drugs (NSAIDs) has been noted [7, 15]. Regarding children, there are a few available data in the literature that investigate the trend of *H. pylori* prevalence in peptic ulcer [16].

In our study, four patients had a family history of *H. pylori* infection, none of gastric cancer, two of peptic ulcer, and two of *H. pylori* chronic gastritis. In this situation, the period of the onset of symptoms and to presentation to the doctor was less than 3 months, so that the average duration of symptoms are 3.75 ± 3.69 months in comparison with 8.66 ± 5.42 months for those without family history for gastric or duodenal ulcers. Influence of family history for upper gastrointestinal tract diseases to the period of the onset of symptoms and diagnosis, can be explained by the consciousness of the disease and the risks than derive from it.

The sex difference between the *H. pylori*-positive and *H. pylori*-negative group is also of great interest. We found female preponderance in the study group (65.51%), similarly with another report in our geographic area (78.49%) [17].

Studies have unanimously shown a male preponderance for peptic ulcer disease in children. It is still not known why primary peptic ulcers predominantly develop in infected male children. Epidemiological studies do not suggest any sex predilection in *H. pylori* infection [16].

Median age for patients with previous therapies was 14.5 ± 3.74 years, comparative with 13 ± 4.71 years for patients without previous therapies, results or else expected. We do not have data to express if it is failure of antimicrobial therapy or reinfection. 1/12 patient with previous therapies had family history of peptic ulcer disease. We do not investigate all the family member of each child, and therefore we do not know the real status of *H. pylori* infection. Familial history for gastrointestinal disease was collected for interview. Magistà et al. [18] identified two variables by logistic regression analysis as predictors of *H. pylori* reinfection: age of primary infection and having an infected sibling. Multivariable analysis revealed that only age at primary infection correlates with an increased risk of reinfection [18].

In patients with anterior therapies, the endoscopic features were less serious than in those without any previous treatment. All three patients with normal endoscopic mucosa were anteriorly treated. These results suggest that children might become "tolerant" to the bacterium or that the growing child is more resistant to *H. pylori*-induced lesions. The evidence that *H. pylori* infection in children coexist with normal gastric mucosa was reported in a percent comparable with our results (11%) [19]. This is the reason for which we strongly recommend to take biopsies at least for histological exam in children and adolescents, even if a normal appearance of mucosa is observed during endoscopy.

The ability of *H. pylori* to manipulate the immune response (activation or inactivation of Toll-like receptors dependent response) may be responsible for bacterial survival and a mild course of infection in children [20].

#### **5. Conclusions**

[8]. In a pediatric polish study, the sensitivity of antral nodularity associated with *H. pylori* was 91.6%, and the specificity was 91% [9]. A slightly lower value of specificity of antral nodularity, similar to our results (75.86%), was detected by several authors and ranged from 64 to

Although the mechanisms underlying nodular gastritis in children is not clear yet, it is thought that lymphoid follicles with germinal center form nodules on gastric mucosa or that inflammatory reaction generated by *H. pylori* infection results in an exaggerated appearance

In a 14-year-old boy we observed erosions at endoscopy. The frequency of these lesions in our study (3.45%) is similar to the one measured by another study conducted in Italy (3.40%) [11].

A prospective study, carried out during 1-month simultaneously in 19 centers among 14 European countries, showed a frequency of 8.1% of ulcers and/or erosions in children, occurring mainly in the second decade of life, but *H. pylori* infection and toxic gastric medications were less frequently implicated than expected in their development. On a total of 56 children with ulcers or erosions, *H. pylori* was present in 15 patients (27%), 8 used NSAIDs, 5 were treated with steroids, 5 with immune-suppressive drugs, 6 with antibiotics, 1 with antacids, 6

For years, reports have noted an association between peptic ulcer disease and families with a strong history of upper gastrointestinal tract disease, in particular between gastric and duodenal ulcers. Family history of gastric cancer is an important component in the diagnosis and management of *H. pylori* infection in children. Children with a mother or a father with gastric cancer are considered to be at very high risk owing to shared genetic characteristics,

In countries with an elevated risk for gastric cancer, however, eradicating *H. pylori* in childhood could be more effective in preventing gastric atrophy, and ultimately, cancer development [13]. It still remains to be determined whether *H. pylori*-infected children with gastric

Recently, a decreasing proportion of *H. pylori*-positive peptic ulcers in adults has been observed, along with a decrease in the prevalence of infection, while, on the other hand, an increasing number of patients that use non-steroidal anti-inflammatory drugs (NSAIDs) has been noted [7, 15]. Regarding children, there are a few available data in the literature that

In our study, four patients had a family history of *H. pylori* infection, none of gastric cancer, two of peptic ulcer, and two of *H. pylori* chronic gastritis. In this situation, the period of the onset of symptoms and to presentation to the doctor was less than 3 months, so that the average duration of symptoms are 3.75 ± 3.69 months in comparison with 8.66 ± 5.42 months for those without family history for gastric or duodenal ulcers. Influence of family history for upper gastrointestinal tract diseases to the period of the onset of symptoms and diagnosis,

can be explained by the consciousness of the disease and the risks than derive from it.

environmental factors, and virulence features of the infecting strain of *H. pylori* [4].

blockers and 8 with proton pump inhibitors (more than one risk factor was detected

85.2%. Higher specificity was found by others [7–9].

42 Helicobacter Pylori - New Approaches of an Old Human Microorganism

atrophy are at increased risk for gastric cancer [14].

investigate the trend of *H. pylori* prevalence in peptic ulcer [16].

of a normal gastric mucosa [10].

with H<sup>2</sup>

in 32 of 56 children) [12].

The main endoscopic feature found in our study was macroscopic nodular antral gastritis, in 75.86%. In 10.34% of cases the endoscopic aspect of mucosa was normal. All patients with normal endoscopic mucosa were previously treated. These results suggest that children might become "tolerant" to the bacterium or that the growing child is more resistant to *H. pylori*-induced lesions.

#### **Acknowledgements**

The authors thank Dr. Augustina Enculescu for her histological support.
