In addition to the central nervous system, the gastrointestinal tract plays a significant role in appetite regulation and medical conditions of the individual organs of this multi-organ system are of fundamental importance for nutritional behaviours and the nutritional condition of persons. An inflammatory condition of the gastric mucosa accompanied by a Helicobacter pylori (H. pylori) infection may also affect the appetite of sick children. The H. pylori influence on the secretion of ghrelin, called the “hunger hormone”, is one of the possible mechanisms here. It is synthesised by Gr cells located mostly in the gastric mucosa of the body of the stomach (1). It is a 28-amino-acid peptide encoded by the preproghrelin gene. Ghrelin is a strong stimulator of growth hormone secretion, it stimulates the appetite, resulting in an increase in the body weight (2). It influences pre-adipocyte differentiation, accumulation of fat in the fatty tissue as well as the energy balance of the human body (3), both in the short-term and long-term regulation (4). It also plays an important role in the regulation of stomach motility and hydrochloric acid secretion (5).

H. pylori infections occur all over the world and they affect over 50% of the adult population (5). In the population of children, the frequency of infections increases with the age (6). In view of little possibility of spontaneous eradication, this infection lasts for many years – from childhood to adulthood. Taking into consideration the frequent occurrence of the lack of appetite in children and its changeability in children infected with H. pylori, one can assume that altered ghrelin secretion can be one of the reasons for this. The results of serum/plasma ghrelin concentrations in persons infected with H. pylori are divergent.

The aim of this study is to assess serum ghrelin concentrations in children infected with H. pylori.

84 children aged 6-18, living in urban area (Bytom), took part in the study. The children were patients at the Chair and Department of Paediatrics in Bytom of the Medical University of Silesia in Katowice. In connection with reported chronic or recurrent abdominal pains located in the epigastric or middle abdominal regions, these children had diagnostic tests performed. There were no patients after H. pylori eradication in the group. Diagnostic tests included: blood tests (ESR, the concentrations of aminotransferases, urea and creatinine), urine and stool tests (tests for parasites, assessment of the presence of human haemoglobin in faeces) and an ultrasound examination of the abdomen.

On the basis of a fiberoscopic examination (Olympus GIF-XP 20) combined with a urease test (National Food and Nutrition Institute, Warsaw) and an histopathology assessment of gastric mucosa specimens collected from the prepyloric region, an H. pylori infection was diagnosed in 33 persons (23 girls and 10 boys – Group I), and it was ruled out in 51 children (23 girls and 28 boys – Group II). The gastric mucosa preparations were dyed with haematoxylin and eosin. A positive result of the urease test and/or confirmation of the presence of this bacteria obtained in the histopathologic examination were the basis for the diagnosis. Together with blood samples collected after night fast for tests connected with the reason of hospitalisation, 2 ml of blood was collected to determine the ghrelin concentration. After centrifuging, serum samples were frozen and stored until measurements at -30°C. The ghrelin concentration was determined by means of a radioimmunological method (Human Radioimmunoassay kit, total ghrelin; Millipore). The results are presented in pg/ml.

On the basis of the histopathologic assessment of gastric mucosa specimens, an H. pylori infection was ruled in or out and the normal picture of the gastric mucosa was found in 2 Group I patients and 20 Group II patients, gastritis chronica non activa minoris gradus in 25 Group I patients and 27 Group II patients, gastritis chronica activa minoris gradus in 8 persons from Group I and 2 persons from Group II.

An approval for the research was obtained from the Bioethics Committee of the Medical University of Silesia in Katowice (KNW/0022/KB1/208/11/12).

The Mann-Whitney U-test was used to compare ghrelin concentrations in Groups I and II and single classification analysis of variance (confirmed by Tukey’s test) was performed to examine the relationship between ghrelin concentrations and the type of histopathological lesions of the gastric mucosa in Group I, Group II and in both groups combined. Double classification analysis of variance was used to check the simultaneous influence of the patients’ gender and the presence of H. pylori infection on the levels of ghrelin concentrations in the serum and a simultaneous influence of the intensity of histopathological lesion and the presence of H. pylori on the serum ghrelin concentrations.

Low absolute values of skewness and kurtosis (< 4) made it possible to use parametric tests.

The hypothesis of the existence of the influence of the patient’s gender and H. pylori infection on the serum ghrelin concentrations was verified by double classification analysis of variance. It was found that the influence of the gender is not significant in this respect and the influence of H. pylori was on the borderline of significance (p = 0.054). The interaction between the two variables was not significant (p = 0.72). No statistical relationship was between ghrelin concentrations and the intensity of histopathological lesions of the gastric mucosa in Group I and Group II and in both groups considered together.

H. pylori plays the key role in the aetiopathogenesis of gastritis, peptic ulcer disease in the stomach and duodenum as well as in stomach tumours (cancer, MALT lymphoma) (5). It was proven that in persons infected with this bacteria, the secretion of hydrogen ions and leptin is changed under the influence of a meal (7). Gao et al. found that ghrelin concentrations in persons infected with H. pylori (8) were lower, and Furuta et al. (9) described the eradication of these bacteria and an improvement of appetite. Thjodleifsson et al., on the other hand, suggest on the basis of multicentre research, that such infections may be a risk factor in the development of overweight (10). Konturek et al. think that H. pylori seems to be a factor affecting the appetite of infected adults (7). Thus, it could be expected that an inflammatory condition of the gastric mucosa caused by H. pylori infection will be a factor modifying ghrelin secretion in children.

In the described group of paediatric patients living in urban area, we did not find a significant relationship between ghrelin concentrations in the serum and H. pylori infection. This fact could confirm the results of our previously published research, in which we did not find a relationship between H. pylori infection and the appetite of the children who participated in the study, which was reported by parents as either very good or bad (11). Similarly, no difference between ghrelin concentrations in the serum of prepubertal children with a diagnosed or ruled-out H. pylori infection was found by Pacifico et al. (4). As in the group of patients presented in this study, the afore-mentioned authors did not find any features of gastric mucosa atrophy in the group infected with H. pylori or in the uninfected group. The differentiation in the plasma ghrelin concentration in H. pylori – infected children is confirmed by studies devoted to the influence of bacteria eradication on this concentration. Deng et al. (12) found an increase in ghrelin concentrations in the blood plasma and in the gastric mucosa after an effective eradication of H. pylori in children with functional dyspepsia diagnosed according to the Rome III criteria. Similar results were obtained by Konturek et al. (13) after treating H. pylori – infected children from shepherd families living in the Tatra Mountains. The results obtained by Pacifico et al. (4) were different – after the eradication of the bacteria, the ghrelin concentration in the children’s plasma decreased. In the serum of the children participating in our study, ghrelin concentrations were insignificantly lower in children uninfected with H. pylori. Isomoto et al. (14) suggest that the influence of H. pylori infection on ghrelin concentrations may depend on bacterial virulence – bacteria producing cagA and vacA have a greater influence on the reduction of ghrelin concentrations. Deng et al. (12), on the other hand, indicate differences between H. pylori strains occurring in developed and developing countries, which may be connected with socio-economic conditions. They may also be connected with differences in the results of research obtained in various countries, according to the authors quoted above. Such a suggestion shows that it is justified to verify what H. pylori strains occur in the environment under analysis. By relating the results of ghrelin determination to the clinical symptoms, such as appetite, one should take into account the fact that, apart from ghrelin, leptin and obestatin are also hormones synthesised in the gastric mucosa, which have an influence on the appetite regulation (2). Płonka et al. (15) compared the results of their own research conducted on children with research results on adults and suggested that H. pylori infection could have a different influence on leptin secretion by gastric mucosal cells at different ages. Therefore, this issue requires further research. Taking into account the influence of H. pylori infection on the appetite, it would be especially important to verify the ghrelin and obestatin levels at the same time. These peptides, which have opposite effects in the complex process of appetite regulation (obestatin has anorectic effects), are derived from a shared precursor – preproghrelin (2). These complex relationships, which can be modified by H. pylori infection, require further research.

Our results suggests that H. pylori infection with mild grade of gastric mucosa inflammation does not affect serum ghrelin level in children.