Functional dyspepsia (FD) -defined as discomfort or pain in the upper abdomen, often related to food intake, but with no apparent organic cause- is one of the most prevalent functional gastrointestinal disorders.

However, the therapeutic benefits and future perspectives of the currently available strategies for modifying gut microbiota in functional bowel disorders is still under research.

A primer, led by Prof. Paul Enck from the Department of Internal Medicine VI: Psychosomatic Medicine and Psychotherapy, at the University Hospital Tübingen (Germany), provides an update of FD in adults, addressing epidemiology, pathophysiological mechanisms, diagnosis, screening and prevention as well as management.

According to the Rome IV classification (2016), functional dyspepsia is diagnosed if a patient reports 1 or more of the following -postprandial fullness, early satiation, epigastric pain, and epigastric burning- for the past 3 months with onset at least 6 months before diagnosis and without evidence of structural disease that can account for the symptoms. It comprises three subtypes with presumed different pathophysiology and aetiology: postprandial distress syndrome (PDS), epigastric pain syndrome (EPS) or both. Gas-related symptoms, repetitive eructation, and abdominal bloating and distension are frequently reported by patients with FD. In particular, alarm symptoms should be detected on time when collecting the patient’s medical history; for instance, substantial weight loss.

The population prevalence of FD is quite variable across the globe. Discrepancies in FD global epidemiology exist, mainly due to the fact that it is a disease entity that overlaps with irritable bowel syndrome (IBS; ‘overlap syndrome’ is the term suggested for designating functional dyspepsia and IBS), other functional gastrointestinal disorders and some somatic diseases and functional non-intestinal diseases.

FD is a multifactorial disorder with different pathophysiological mechanisms hypothesized at both macroscopic and microscopic levels. Its symptoms can be caused by disturbed gastroduodenal motility and sensitivity, impaired permeability of the epithelial barrier, duodenal eosinophilia and subtle mucosal inflammation in the duodenum; there is contradictory evidence on the role of small-intestinal bacterial overgrowth. It should be noted that Helicobacter pylori-related dyspepsia is considered a separate entity.

Besides this, a genetic predisposition could be also involved, though it is less evident than in other functional gastrointestinal disorders. On the other hand, psychiatric comorbidity and psychopathological state and trait characteristics could also play a role, although these are less pronounced than in other gastrointestinal functional disorders such as IBS. Psychiatric comorbidities that are much more prevalent in functional dyspepsia than in IBS are eating disorders (for example, bulimia or anorexia nervosa). The authors suggest that inconsistencies about the role of brain-gut and gut-brain pathways in pathogenesis reflect differences in the inclusion criteria of patients with FD and controls, sample sizes, together with differences in disease subtypes, geographical and ethnic variations and environmental factors.

Management of FD includes dietetic advice and H. pylori eradication treatment in patients with FD who are infected. Regarding dietary management, it is still unknown how dietary factors are effective in alleviating dyspeptic symptoms. Dietary patterns observed in patients with FD and unknown potential underlying mechanisms of food intolerances contribute to the difficulty of making personalized dietetic recommendations in these cases.

With the exception of H. pylori eradication, the preferred pharmacological therapy (including prokinetic drugs, fundus-relaxing drugs and acid-suppressive drugs) is primarily based on the subtype of functional dyspepsia, whereas centrally active neuromodulators and herbal drugs play a minor role. It should be noted that although pharmacological therapy is considered in a large proportion of patients, drugs with established efficacy are lacking for patients with FD as a group. Regarding psychotherapy, it may be effective only in a small subset of patients. Future therapies might include novel compounds that attempt to treat the underlying gastric and duodenal inflammation.

 

Reference:

Enck P, Azpiroz F, Boeckxstaens G, et al. Functional dyspepsia. Nat Rev Dis Primers. 2017; 3:17081. doi: 10.1038/nrdp.2017.81.