Antral inflammatory cells, gastric emptying, and electrogastrography in pediatric functional dyspepsia.

The aims of the current study were to determine the activation states of antral eosinophils and mast cells and to evaluate the interactions of antral inflammatory cells with gastric emptying and electrogastrography (EGG) in 30 pediatric patients with functional dyspepsia. Eosinophil degranulation was moderate in 42% and extensive in 54% of patients. Mast cell degranulation was > 50% in 81% of patients. Elevated mast cell density was associated with slower one hour gastric emptying and increased preprandial dysrhythmia. Mast cell density correlated with the preprandial percentage tachygastria. CD3+ cell density correlated with the preprandial percentage tachygastria also, but only in patients with increased eosinophil density. In conclusion, antral eosinophils and mast cells are significantly activated in pediatric functional dyspepsia. Mast cell density is associated with delayed gastric emptying and preprandial dysrhythmia, suggesting that there may be an interaction between antral inflammation and gastric electromechanical dysfunction in the pathophysiology of pediatric functional dyspepsia.

Electrogastrography in pediatric functional dyspepsia: relationship to gastric emptying and symptom severity.

OBJECTIVES: The aims of this study were to determine the electrogastrographic patterns in children with functional dyspepsia and to investigate the correlations among electrogastrogram (EGG), gastric emptying (GE), and pain severity. METHODS: We studied 30 children (19 F; mean age 11.4 years) with functional dyspepsia. Electrogastrography was performed for 30 minutes fasting and for 1 hour during a GE test after ingestion of an isotope-labeled solid meal. The percent emptying was measured every 10 minutes for 1 hour after the meal. The dominant frequency of the EGG, the change in the postprandial peak power (deltaP), and percent dysrhythmia during each recording session were calculated. Specific symptoms were graded from 0 (none) to 4 (severe) by the patient. RESULTS: Of 30 patients, 14 (47%) had slow GE, and 15 (50%) had abnormal EGG (dysrhythmia > or = 30% or deltaP < 0). GE was slow in 73% of patients with an abnormal EGG but was slow in only 20% of patients with normal EGG (P = 0.009). GE was negatively correlated with fasting bradygastria (r = -0.383, P = 0.04). Abdominal pain was the most severe dyspeptic symptom, both during fasting and after the meal. Patients with an abnormal EGG had an increased mean pain severity score (3.5 +/- 0.2 vs. 2.5 +/- 0.2, P = 0.002). CONCLUSIONS: Sixty percent of functional dyspepsia subjects had either slow GE or abnormal EGG. Patients with abnormal EGG were more likely to have slow GE. EGG abnormalities were associated with more severe postprandial pain and should be considered a possible mechanism for dyspeptic symptoms.