Functional dyspepsia often gets mistaken for gastro-oesophageal reflux disease (GORD), say the authors of a new paper published in Australian Prescriber.

The researchers, from the John Hunter Hospital and the University of Newcastle, say the defining symptoms of functional dyspepsia – early satiety and epigastric pain – are easily overlooked as they overlap with those of GORD and irritable bowel syndrome.

“Recent evidence suggests GORD is often the diagnostic label applied to patients even if they have typical symptoms of functional dyspepsia with little or no heartburn,” the researchers write.

“Correctly diagnosing functional dyspepsia is important to guide appropriate therapy and reduce unnecessary procedures or treatments,” they add.

The condition, which affects 10% of the population and is more prevalent among women, has two subtypes, the largest of which is characterised by early satiety, or postprandial fullness. Around 30% have the second subtype, and experience ulcer-like pain or burning, known as epigastric pain syndrome.

A history of early satiety or postprandial fullness is enough for a clinical diagnosis and to start treatment, although a range of red flag symptoms, including new onset in older age, weight loss, vomiting, bleeding, anaemia, family history of upper GI cancer or progressive dysphagia should prompt referral and an endoscopy.

The many treatment options available include:

• Reassurance and explanation to relieve stress;
• A change of diet, usually to smaller, regular low-fat meals;
• Acid suppression with PPIs or an H2 receptor antagonist;
• Prokinetics such as cisapride or ondansetron;
• Fundic relaxors, if unresponsive to prokinetics;
• Tricyclic antidepressants for epigastric pain;
• Rifaximin;
• Psyhcological therapy.

Functional dyspepsia has long been regarded as an idiopathic disorder, but recent research is changing this view. Cases in which the condition occurs after infectious gastroenteritis suggests that acute inflammation may play a role.

It has been proposed that either an infection, microbiome alteration or a food allergen induces increased duodenal permeability and eosinophilia, which activates a mucosal immune response. Local reflex responses to inflammation then alters gastroduodenal function.

“If correct, this model represents a paradigm shift with profound treatment implications,” the researchers write.

You can access the full paper here.