online ISSN 2415-3176
print ISSN 1609-6371
logoExperimental and Clinical Physiology and Biochemistry
J. 2015, 70(2): 61–69
https://doi.org/10.25040/ecpb2015.02.061

Clinical physiology and biochemistry


Role of helicobacter pylori infection for the development of gastroduodenal pathology in children

LYCHKOVSKA O.
Abstract

Helicobacter infection is an undeniable and important risk factor for the formation of gastroduodenal pathology (GDP). However, data on the role of Helicobacter pylori (Hp) in the formation of GDP in children are not definitive – from the recognizing of the leading role of Hp in the changes of the mucosa up to Hp(–) forms prevailing in most cases of upper gastrointestinal tract diseases.

The current study aimed at investigation of the role of Hp infection in the formation of GDP in children.

The study involved 83 children aged from 6 to 11 years old with GDP, including 21 children with functional dyspepsia (FD), 43 of them were diseased with gastroduodenitis, 19 - with destructive forms of GDP. Evaluation and treatment of the children were conducted according to the existing protocols. Hp infection diagnostic was carried out due to histological study and test of stools for Hp antigen.

Hp was revealed in 35 children, that composes 42,2 %. Results of the tests for the morphology and for Hp antigen in stool coincided in all patients. In cases of FD the share of Hp(+) patients was 33,3 %, of gastritis/gastroduodenitis – 41,9 %, of destructive forms of GDP – 52,6 %. Thus, the highest level of infection was found among children with destructive GDP, whereas in FD infection rate does not exceed the average age related rate in population. No significant differences in the clinical manifestation of GDP in case of the presence or absence of Hp infection in children were revealed. Comparing the severity of morphological changes of gastric mucosa in Hp(+) and (–) children significantly higher incidence of severe inflammatory changes accompanying Hp(+) status was found. However, the data of morphological studies confirm the statement that chronic active gastritis is not always shaped by the invasion of Hp. The formation of GDP depends significantly on the condition of the macroorganism, including genetic factors that may influence the inflammatory response of the gastric mucosa or development of susceptibility to Hp infection.

To study the effect of genetic factors the distribution of alleles HLA DQA1 gene depending on Hp status of children with GDP was analyzed. Statistically significant differences were found for the frequency of occurrence of alleles HLA DQA1*0102 and *0301. For all that allele *0301 was revealed significantly more frequent in Hp(+) patients which makes it possible to identify it as a risk factor for Hp infection. Allele HLA DQA1*0102 was revealed significantly more often among Hp(-) children. Family history of GDP, especially maternal, was detected in Hp(+) patients.

Hp is one of the important but not the only factor in the formation of the GDP in children. We have not found any clinical signs that would enable us to suspect or cancel Hp nature of GDP in children. The presence of Hp infection is accompanied by severe inflammatory changes of gastric mucosa. Family history of GDP, especially maternal, was detected in Hp(+) patients. Certain genetic factors associated with resistance to Hp infection (*0102 allele) and to the formation of GDP in children (*0201 allele) were revealed, while predispositive factor (allele *0301) affects both susceptibility to Hp infection and severe duration of GDP with the development of destructive forms. The results of current study can be the basis for optimization and individualization of therapeutic and preventive measures in children with GDP. Particularly for the formation of „risk groups” concerning Hp infection and development of chronic gastroduodenal diseases the following factors should be considered: maternal history of GDP, HLA DQA1*0301, on the other hand DQA1*0102 can be defined as protective factor.

Keywords: gastroduodenal pathology in children, Helicobacter pylori

Full text: PDF (Ukr)

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