Functional dyspepsia: modern pathogenetic aspects and therapeutic approaches

Functional dyspepsia, affecting up to 20% of individuals worldwide, remains both a cause of decreased activity of patients’ daily life and an obvious economic burden due to healthcare costs. Despite extensive research, the etiology of dyspepsia is unknown in most patients. Intestinal motility dysfunction has long been considered the major culprit, but recent studies suggest that immune pathophysiological and molecular effects in the duodenum are far more likely predisposing factors. Eosinophilia and an increase in mast cells in both the duodenum and gastric mucosa are identified in most patients with this disease. More and more data on the significant role of impaired paracellular permeability of the intestinal mucosa are now available. It is associated with subclinical inflammation in the submucosal layer in patients with functional dyspepsia. This explains the poor effectiveness of the treatments taken. The evidence from practice suggests that symptoms persist or return after eradication therapy in most patients. Proton pump inhibitors and antidepressants do not ease postprandial distress syndrome. Montelukast and cromolyn therapy has been proposed, but this approach is not yet widely popular. Therefore, there is an obvious need in finding other therapeutic approaches. One of them is the increased use of prokinetics, the most recent of which is acotiamide. Its mechanism of action is similar to that of prior generation prokinetics (inhibition of acetylcholinesterase activity), but is distinguished by the absence of impact on dopaminergy, due to which the drug has far fewer side effects. In addition, its effect on the production of ghrelin, which physiological role is being actively studied, is discussed.