Postprandial Distress Syndrome (PDS)

What causes PDS?

The etiology of PDS is likely multifactorial, influenced by alterations in:

• Gastric accommodation– The process by which the proximal part of the stomach relaxes once food is ingested to prevent an increase in intragastric pressure.
• Gastric emptying– Delayed emptying is more common, but some do experience emptying faster than others.
• Vagal function– Vagal dysfunction may be caused by damage to the vagal nerve through inflammation, infection, and diabetic neuropathy. Functional impairment may also be caused by physical or psychological stress.
• Visceral hypersensitivity– There is an exaggerated sensory response to stimuli even in the setting of normal gastric compliance. While this can occur independently of any impaired signaling from the brain, somatization is higher in those with anxiety and depression.
• Mucosa– Abnormalities in the mucosa include increased permeability and inflammation with the presence of increased levels of eosinophils and mast cells.
• Microbiota composition of the duodenum.

Clinical Characteristics of PDS

• Postprandial fullness and or early satiation without the implication of any identifiable organic, systemic, or metabolic etiology.
• Symptoms must occur at least 3 days a week for the last 3 months and onset of symptoms 6 months prior.