Trace minerals and vitamins are essential for life. They act as essential cofactors of enzymes and as organizers of the molecular structures of the cell. Deficiencies of micronutrients influence immune homeostasis and thus affect infection-related morbidity and mortality . H. pylori can change the secretion and acidification functions of the stomach, because it penetrates especially into the stomach. This situation can affect digestion and absorption of some components of the nutrients and micronutrients .
The present study showed that the mean age of our children was significantly higher in H. pylori-positive group (11.56 years) than in H. pylori-negative group (8.43 years) (Table 2 and Fig. 1). This finding is similar to that reported by Malaty et al.  and Jafar et al.  who found that there were increasing prevalence rates of H. pylori infection with increasing age in all age groups.
Regarding the accuracy of rapid urease test in the diagnosis of H. pylori infection, the present study found that rapid urease test had a sensitivity of 88.9% and a specificity of 92.9% (Table 3). This finding is nearly similar to that reported by previous studies who found that the sensitivity of various rapid urease tests as primary diagnostic tests is high and has been reported to vary between approximately 80% and 100% and specificity between 97% and 99% [24, 25]. The rapid urease test is a test for the presence of the urease enzyme. The actual results will depend on the gastric disease and the likelihood of atrophic changes or exogenous factors that reduce the bacterial load (such as the use of antibiotics, bismuth-containing compounds, or proton pump inhibitors) and thus produce false-negative results . The two most common reasons for false-negative results are the recent use of proton pump inhibitors and the presence of intestinal metaplasia. H2-receptor antagonists do not reduce the bacterial density and can be used up to the day of the test . Also, false-negative results can occur if the distribution within the stomach is patchy or if organism loads are low and the presence of atrophic gastritis with or without intestinal dysplasia . False-positives are rare and when present may be due to the presence of other urease-containing organisms such as Proteus mirabilis, Citrobacter freundii, Klebsiella pneumonia, Enterobacter cloacae, and Staphylococcus aureus .
Concerning the gross endoscopic picture of studied cases, the present study found that antral affection and nodularity were significantly higher among H. pylori-positive cases than H. pylori-negative cases (11 versus 2 with P = 0.012) (Fig. 3). In agreement with this finding, Bahú et al.  concluded that endoscopic findings of antral nodularity in children suggest the presence of H. pylori infection and follicular gastritis and may identify cases of severe gastritis and marked bacterial colonization. Also, Tomasević et al.  reported that H. pylori infection is known to be the most common cause of chronic gastritis having some endoscopic and pathologic characteristics as determined by the Sydney System for Gastritis Classification. They found that there is an association of H. pylori infection and of lymphoid follicles with the nodular gastric mucosa. Similarly, Romero-Flores et al.  found that there was a strong correlation between nodular gastritis and H. pylori, but only after rigorous evaluation.
H. pylori infection is significantly associated with lymphoid follicle formation on histopathological examination. Lymphoid follicles and aggregates have been detected in 32.9–85% of chronic gastritis patients on histological examination of biopsy specimens, and appear more common in the antral mucosa than in the corpus mucosa . The severity of gastritis is also correlated with the presence of lymphoid follicles and aggregates. A close relationship exists between lymphoid follicles and H. pylori-associated gastritis. The endoscopic features of such lymphoid follicles have been reported as nodular gastritis. Nodular gastritis (antral nodularity) is a unique type of chronic gastritis caused by H. pylori infection . Chen et al.  concluded that the prevalence and density of lymphoid follicles and aggregates in gastric antral mucosal biopsies correlated closely with H. pylori infection. Similarly, Hayashi et al.  concluded that the endoscopic finding of nodules could be observed at any site of the gastric mucosa in H. pylori-associated gastritis, and represented histological lymphoid follicles. Moreover, these follicles are thought to represent the pathophysiologic substrate for mucosa-associated lymphoid tissue-lymphomas .
Regarding the serum zinc levels, the present study found that the mean levels were significantly lower in H. pylori-positive cases than in the control group and lower than H. pylori-negative cases but not statistically significant (Table 5). Brown et al.  stated that a protein that strongly binds to zinc has been identified on the membrane and in the cytosol of H. pylori. Because zinc is absorbed mainly in the small intestine, by binding dietary zinc in the stomach, H. pylori may possibly contribute to serum zinc deficiency. Wu et al.  reported that the serum zinc level was lower in H. pylori-infected patients compared with H. pylori-negative cases. However, the difference was not statistically significant.
The present study also reported that the serum zinc concentration had a significant negative correlation with the severity of inflammatory infiltrate, mucosal atrophy, and H. pylori density with insignificant negative correlation with the severity of inflammatory activity (Table 6). This is in agreement with Sempertegui et al.  who reported that the more severe the H. pylori infection, the lower concentration of zinc in gastric mucosa.
Regarding the serum selenium levels, it was slightly higher in H. pylori-positive patients than in H. pylori-negative patients and controls with no significant differences between H. pylori-positive cases and either the negative cases or the control group (Table 5). Wu et al.  have shown that serum selenium level had no significant difference between H. pylori-positive and H. pylori-negative groups. However, the serum selenium levels decrease after H. pylori eradication therapy.
In this study, there was a significant positive correlation between serum selenium level and the H. pylori density (Table 6). Üstündag et al.  reported that plasma selenium levels were similar between H. pylori-positive gastritis and healthy controls, but in the gastric tissue selenium levels were significantly higher in H. pylori-positive gastritis. There was a statistically significant decrease in mucosal selenium levels in patients after successful H. pylori eradication therapy. The increased selenium levels may be explained on the basis of elevated reactive oxygen species in association with H. pylori infection.
In the present study, the mean serum vitamin C levels were significantly lower in H. pylori-positive cases than in the negative cases and the control group (Table 5). In line with our results, Waring et al.  reported that vitamin C plasma concentration was 20% lower in H. pylori-infected subjects than in negative controls, even after correction for confounding factors, such as dietary habits.
Also, regarding the serum vitamin C levels, there was a significant negative correlation with the severity of inflammatory infiltrate, lymphoid follicles, mucosal atrophy, and H. pylori density (Table 6). In line with these results, Park et al.  found that vitamin C levels in whole blood, plasma, and gastric juice were closely related to the severity of H. pylori infection and the histological changes in the stomach. These authors reported that vitamin C can have a role in the initiation and progression of H. pylori infection. They also reported that vitamin C levels in whole blood, plasma, and gastric juice exhibited a significant negative correlation with the histologic density of H. pylori, the degree of active and chronic gastritis, and the severity of H. pylori infection (based on urease positivity and histologic density of H. pylori). There are several explanations for the reduction of ascorbic acid in the gastric juice of H. pylori-infected subjects. First of all, ascorbic acid may be consumed acting as a scavenger against reactive oxygen species, produced by gastric inflammation.
Regarding the serum vitamin B12 levels, the present study found that the mean levels were significantly lower in H. pylori-positive cases than in the negative cases and the control group (Table 5). In addition, it was found that serum vitamin B12 levels showed a significant negative correlation with the severity of inflammatory infiltrate, mucosal atrophy, and H. pylori density (Table 6). Similar to these results, Akcam et al.  found a statistically significant relation between H. pylori infection and serum vitamin B12 levels that were independent of gastric atrophy and suggested that H. pylori infection had a negative effect on serum vitamin B12 levels in children. Similarly, Ravi et al.  reported a significant relationship between the B12 levels and the H. pylori status, where 58% of the H. pylori-positive patients had vitamin B12 values below 100 pg/mL in contrast to 38% of H. pylori-negative cases. Hence, the H. pylori-positive patients group had a significantly lower vitamin B12 value compared to the H. pylori-negative patients group.
Annibale et al.  demonstrated that almost two-thirds of pernicious anemia patients had evidence of H. pylori but only those with an active H. pylori infection had distinct functional and histological features. These findings support the hypothesis that H. pylori infection could play a triggering role in a subgroup of patient with pernicious anemia and suggest the possibility that H. pylori is involved in the early stages of pernicious anemia that lead to severe corpus atrophy. The later progress of gastritis seems to be dependent on factors other than H. pylori, most likely “autoimmune” mechanisms.
Serin et al.  demonstrated that the histopathological scores for H. pylori density, inflammation, and neutrophil activity were all inversely correlated with serum vitamin B12 level and the linear regression analysis revealed that only H. pylori density was significantly correlated with serum B12 level. After treatment, the serum vitamin B12 levels were significantly increased, and the inflammation and neutrophil activity scores in the antrum and corpus were significantly decreased, regardless of eradication status. With patients categorized according to eradication status, the elevation in serum vitamin B12 level was more pronounced in the group in which the organism had been completely eradicated than in those with persistent infection.
Several limitations of the present study should be discussed. First, the relatively small number of patients. Furthermore, we measured only plasma levels of the trace elements and vitamins with lack of measurement of gastric mucosal trace elements. Third, the lack of measurement of the plasma levels of the trace elements and vitamins after eradication therapy.