Functional Dyspepsia: Upper Abdominal Pain and Fullness Without an Ulcer — Symptoms, Rome IV Criteria and Treatment

The Rome IV classification, published in Gastroenterology in 2016, defines functional dyspepsia as the presence of one or more of four symptoms — postprandial fullness, early satiation, epigastric pain or epigastric burning — that remain unexplained after a routine clinical evaluation. In practice the criteria require symptoms to be bothersome and present over the last three months, with onset at least six months before diagnosis.

Rome IV distinguishes two subtypes that may overlap. Postprandial distress syndrome (PDS) is a meal-related pattern: fullness after an ordinary portion and early satiety that makes it hard to finish a meal. Epigastric pain syndrome (EPS) is pain or burning in the epigastrium that does not occur exclusively after meals — it can appear on an empty stomach and sometimes even improves after eating.

The distinction has practical value because the response to treatment can differ. In the large randomised amitriptyline trial discussed below, for example, the benefit was clearly greater in people with an “ulcer-like” picture, close to EPS, than in those with a “dysmotility-like” picture, close to PDS. Keep in mind, though, that the division is not sharp and many people have a mixed picture.

Functional dyspepsia is a heterogeneous disorder — no single mechanism explains every case. Several overlapping processes are usually named. The first is impaired relaxation of the gastric fundus after a meal (impaired accommodation): the stomach does not “expand” properly, so food produces fullness and tension after a small portion. The second is visceral hypersensitivity, a lowered threshold for pain from the stomach and duodenum — stimuli that other people do not notice are experienced as pain or discomfort. The third is altered gastric emptying, which is delayed in some people. Finally, low-grade inflammatory infiltrates in the duodenum and disturbed communication along the gut-brain axis have been described.

It should be stressed that this is largely an explanatory model rather than a set of measurable changes that can be used to diagnose an individual patient. Routine gastric emptying testing is not recommended as a standard in every dyspeptic patient: the 2017 ACG/CAG guideline explicitly advises against routine upper GI motility testing while allowing it in selected cases. The link between what is seen on a test and what the patient feels is limited.

A similar caution applies to the role of stress. Stress, anxiety and sleep problems frequently coexist with dyspepsia and can amplify symptom perception — we discuss the connection between chronic stress and the digestive system in more detail in our knowledge base. This does not mean that functional dyspepsia is a “mental illness”. In one meta-analysis the benefit of psychotropic drugs disappeared once people with coexisting mood disorders were excluded from the analysis — more on this below.

In the population meta-analysis mentioned above, dyspepsia was more common in women (odds ratio 1.24), smokers (1.25), users of non-steroidal anti-inflammatory drugs (1.59) and people infected with Helicobacter pylori (1.18). The associations were modest rather than dramatic, but they show what is worth checking first: smoking, regular use of ibuprofen, diclofenac or naproxen, and H. pylori infection.

A functional diagnosis is a diagnosis of exclusion, so it matters what exclusion has really been carried out. The joint guideline of the American College of Gastroenterology and the Canadian Association of Gastroenterology (ACG and CAG) from 2017 proposes an approach based on age and alarm features.

For the patient this means a practical sequence: first a review of medicines (especially non-steroidal anti-inflammatory drugs), then an H. pylori test — most often a urea breath test or a stool antigen test — and gastroscopy where age or alarm features call for it. We describe the endoscopic examination of the upper gastrointestinal tract in a separate knowledge base entry. If H. pylori infection is found, treatment details are covered in our article on Helicobacter pylori symptoms and treatment.

It is worth adding that the guideline does not treat alarm features as an automatic indication for gastroscopy in younger people, because their predictive value for cancer is low. That does not mean they can be ignored: they are assessed in the context of the whole clinical picture, and some of them — weight loss, difficulty swallowing or anaemia — almost always warrant at least a conversation with a doctor about further investigation.

Yes, but the effect is modest — and that matters for anyone hoping that one course of antibiotics will make the symptoms disappear altogether. The most complete meta-analysis of randomised trials to date compared eradication therapy with control treatment (acid suppression, prokinetics or placebo) in H. pylori-positive people with functional dyspepsia.

What does this mean in practice? An NNT of 9 means that about nine infected people need to be treated for one to experience improvement in dyspeptic symptoms beyond what control treatment would have achieved. That is not many, and many people will not feel any difference — but treatment has another justification: H. pylori infection is itself a risk factor for ulcer and gastric cancer, so removing it makes sense whether or not dyspepsia improves. This is why “test and treat” is the first step in the guidelines.

They do, but only in some people and clearly less than in reflux. A 2017 Cochrane review (25 trials, 8,453 participants) showed that a few weeks of PPI treatment is more effective than placebo at relieving overall symptoms of functional dyspepsia.

The practical conclusion: PPIs are a reasonable short therapeutic trial, not treatment “for ever”. With an average benefit corresponding to an NNTB of 11, most patients will see little or no effect. A sensible approach is to reassess after a few weeks — if symptoms do not settle, there is no reason to prolong therapy. Long-term PPI use is linked with possible adverse effects, including lower magnesium and vitamin B12, which we cover in a separate article and in the knowledge base entry on proton pump inhibitors.

And prokinetics? A 2018 Cochrane review suggested that they reduce global symptoms (RR 0.81; NNTB = 7), but the evidence was rated as very low quality, with high heterogeneity between trials (I² = 91%), and some of the drugs analysed — such as cisapride — are no longer widely available for safety reasons. Prokinetics therefore have a place in the guidelines, but as a second- or third-line drug and with cautious interpretation.

For many people, the suggestion of an antidepressant for pain in the upper abdomen sounds like a hint that “it is all in your head”. In this setting, however, these drugs are used as neuromodulators — they change how pain signals from the gut are processed, independently of mood. The best-documented group is the tricyclic antidepressants (TCAs).

Broader analyses confirm this pattern. A 2017 meta-analysis (13 trials, 1,241 patients) showed a benefit of psychotropic drugs over placebo (RR of symptoms not improving 0.78; NNT = 6), but only for antipsychotics and TCAs, and the benefit disappeared once people with coexisting mood disorders were excluded; adverse events were more common (NNH = 21). A 2021 network meta-analysis (71 trials, 19,243 participants) ranked TCAs second for efficacy (RR 0.71) and first in low-risk-of-bias trials, noting however that most TCA trials enrolled patients refractory to other drugs. SSRIs such as escitalopram showed no benefit in the Talley trial.

Diet in functional dyspepsia attracts the most beliefs and the least solid research. There are no large randomised trials pointing to one “dyspepsia diet”. What doctors usually suggest rests mainly on clinical observation and expert opinion, not on meta-analyses.

If the complaints are dominated by bloating and gas rather than epigastric pain, it is worth reading our article on bloating after eating. Where frequent belching dominates, we discuss belching disorders and their behavioural treatment separately.

The same family of beliefs includes the myth that “if the tests are normal there is nothing to treat”. Functional dyspepsia is a full diagnosis, and the available methods — from H. pylori eradication to neuromodulators — have proven, if moderate, effectiveness. A normal gastroscopy does not mean the symptoms are any less real.

Functional dyspepsia is a diagnosis worth taking seriously, but without catastrophising. A structured pathway — medication review, H. pylori test, gastroscopy where age or alarm features require it, a short PPI trial and, further down the line, a neuromodulator — is evidence-based, even though no single element is a “miracle” drug. Honest information about the size of the effect (NNT from 6 to 14) helps avoid disappointment and unnecessary use of drugs that do not help.