| Motility disorders |
● Impaired volume accommodation of the fundus
● Disproportionate volume distribution in the stomach (too much in the antrum, too little in the fundus)
● Low volume uptake in drinking test
● Antral hypomotility and ↓ antral migratory motor complexes (phase III of interdigestive motoricity)
● Uncoordinated antroduodenal motility
● Increased postprandial duodenal motility
● Insufficient inhibitory components of the peristaltic reflex in the small intestine |
| Sensorimotor disorders |
● Reduced excitability of enteric nerves in the duodenum
● Gliosis in the duodenal submucous plexus
● ↓Parasympathetic tonus
● ↑ Acid sensitivity in the duodenum
● ↑ Fat sensitivity in the duodenum associated with ↑ CCK sensitivity
● ↑ Starved and postprandial CCK concentration but ↓ PYY concentration
● ↓ CgA+ enteroendocrine cells in the duodenum |
| Visceral hypersensitivity |
● ↑ Sensitivity after stomach expansion (on an empty stomach and after a meal)
● ↑ Sensitivity after duodenal, jejunal, and rectal expansion |
| Postinfectious plasticity of the duodenum |
● ↑ CD8+ cytotoxic T cells CD 68+ and CCR2+ macrophages
● ↓ CD4+ T-helper cells in the duodenum |
| Immune activation |
● ↑ GDNF, eosinophilic granulocytes and macrophages in duodenal mucosal biopsy samples
● ↑ Degranulation of the eosinophilic granulocytes in the duodenum
● TH2-mediated response in the duodenum
● ↑ GDNF and NGF expression in the H. pylori -positive gastric mucosa |
| Dysfunctional intestinal barrier |
● ↑ Permeability in the proximal small intestine |
| Genetic predisposition |
● ↑ GNβ3-TT genotype (increased signal transduction between receptor and target protein)
● ↓CCK-A receptor CC genotype |
| Biopsychosocial factors |
● ↑ Anxiety, depression, somatization, neuroticism
● ↑ Experience of abuse, stressful life events
● ↓ Functional connectivity of brain regions |
| Altered microbiota |
●↑ Prevotella
● Helicobacter pylori
|
