Postprandial distress syndrome: stratification and management

ABSTRACT

Introduction: Functional dyspepsia (FD), defined by the Rome consensus as the presence of functional symptoms originating from the gastroduodenum, is one of the most common functional gastrointestinal disorders. FD is subdivided into postprandial distress syndrome (PDS), with meal-related symptoms such as postprandial fullness and early satiation, and epigastric pain syndrome (EPS), with meal-unrelated symptoms such as epigastric pain or burning. We used a literature search for a narrative review on the current state of knowledge regarding PDS.

Areas covered: Epidemiological studies support PDS as a separate entity and the biggest FD subgroup. The pathophysiology of PDS is heterogeneous, and disorders of gastric sensorimotor function as well as low grade duodenal inflammation have been implicated. Although prokinetic agents may provide the most pathophysiology-oriented treatment option, there is a paucity of suitable agents, and proton pump inhibitors are the traditional first-line therapy. Other options include agents that enhance gastric accommodation, such as acotiamide and 5-HT_1A agonists, neuromodulators such as mirtazapine, and traditional medicine approaches.

Expert commentary: PDS is highly prevalent, with probably heterogeneous underlying pathophysiology. Motility modifying agents and neuromodulators are the cornerstone of PDS therapy, but there is a need for high quality studies of new therapeutic approaches.

KEYWORDS:

• Functional dyspepsia
• postprandial distress syndrome
• gastric accommodation
• gastric emptying
• gastric hypersensitivity
• eosinophils
• prokinetic
• mirtazapine
• rikkunshito

Declaration of interest

J. Tack has served as an advisor for: AlfaSigma, Allergan, Christian Hansen, Danone, Grünenthal, Ironwood, Kyowa Kirin, Menarini, Mylan, Neutec, Novartis, Noventure, Nutricia, Shionogi, Shire, Takeda, Theravance, Tramedico, Tsumura, Zealand, Zeria. J. Tack has also received research support funding from: Shire, Tsumura, Zeria. J. Tack has also served as a paid speaker for: Abbott, Allergan, Ironwood, Kyowa Kirin, Menarini, Mylan, Novartis, Shire, Takeda, Zeria. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper is supported by funding from Leuven University, Methusalem grant (to J. Tack).