ESPE Abstracts

Introduction: The growth process in children depends on GH/IGF-1. Ghrelin is stimulator of GH synthesis. Ghrelin also stimulates the orexigenic center peptides responsible for appetite. It is synthesized in the stomach, thus its secretion may be alter by gastrointestinal tract deseases. Recently, high titers of antibodies against some neuropeptides (including anti-ghrelin) have been found in indyviduals with certain microflora components, e.g. Helicobacter pylori (HP) in the molecular mimicry phenomenon mechanism. The aim of the study was to analyze the relationship between the amount of ghrelin-positive cells in the stomach and serum concentration of ghrelin and anti-ghrelin antibodies in idiopathic short stature (ISS) children, taking into account the impact of HP infection.

Material and methods: The study group consisted of 77 children with ISS. In each child the endocrine diagnostics were performed, including two GH secretion stimulation tests as well as serum IGF-1, ghrelin and anti-ghrelin antibodies. Then, gastrological diagnostics were performed, including serum anti-HP antibodies, upper gastrointestinal tract endoscopy with urease test, the assessment of HP presence, the inflammatory process severity and the number of ghrelin-positive cells in the collected biopsies.

Results: A significant range of ghrelin-positive cells activity percentage in gastric mucosa has been demonstrated. Their distribution was left-skew, ranged from 1 to 92%, the average was 32.05%. Thus, the study group was divided into patients with lower activity of ghrelin-positive cells (1%-33%) - Group1 (n=47) and with higher activity of ghrelin-positive cells (34%-92%) - Group2 (n= 30). Significantly lower serum ghrelin concentration was found in Group1 than Group2: 1257.51±604.13 pg/ml vs 1940.59±1524.35 pg/ml, and significantly higher level of anti-ghrelin antibodies in Group1 than in Group2: 0.127±0.036 vs 0.101±0.021, p<0.01. Searching for the reasons for the reduced activity of ghrelin cells in the stomach, the possible impact of the HP presence was analyzed. Of the 21 cases of HP infection, 16 were found in Group1 (34.0%), while only 5 in Group2 (16.7%). It has been shown that in children with HP and a lower number of ghrelin-positive cells, the severity of short stature was greater, but there was no effect on the nutritional status.

Conclusion: In short stature children, gastritis associated with HP infection reduces the number of ghrelin-positive cells as well as the synthesis of ghrelin and increases production of anti-ghrelin antibodies. It seems that this may have an impact on the growth deficiency observed in ISS children.