Managing dyspepsia

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Applied Evidence

Managing dyspepsia

J Fam Pract. 2015 June;64(6):350-357

Although most cases of dyspepsia lack a structural cause, patients often suffer intermittently for years. In this article and treatment algorithm, the author presents an optimal patient management approach.

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References

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PRACTICE RECOMMENDATIONS

› Review the medications taken by patients who suffer from dyspepsia, as many drugs—bisphosphonates, antibiotics, steroids, and nonsteroidal anti-inflammatory drugs, among others—are associated with this condition. B
› Order an esophagogastroduodenoscopy for patients ages 55 years or older with new-onset dyspepsia and those who have red flags for more serious conditions, eg, a history of upper gastrointestinal (GI) cancer, unintended weight loss, GI bleeding, dysphagia, or a palpable mass. C
› Prescribe acid suppression therapy as first-line treatment for patients who have dyspepsia but are at low risk or have tested negative for Helicobacter pylori infection. A

Strength of recommendation (SOR)

A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series

Each year, an estimated 25% to 30% of the US population suffers from dyspepsia.¹ Most self-treat with home remedies and over-the-counter products, but others seek medical care. Dyspepsia accounts for an estimated 2% to 5% of primary care visits annually,² mostly by patients who are found to have no organic, or structural, cause for their symptoms.^1,3

Compared with the general public, patients with functional dyspepsia have higher levels of anxiety, chronic tension, hostility, and hypochondriasis, and a tendency to be more pessimistic.

Such patients are said to have functional dyspepsia (FD), a category that applies to about two-thirds of those with dyspepsia.¹ A small number of cases are categorized as organic dyspepsia, indicating the presence of a clear structural or anatomic cause, such as an ulcer or mass. The remainder are said to have undifferentiated dyspepsia, which simply means that their signs and symptoms do not rise to the level for which further investigation is warranted and thus it is not known whether it is functional or organic.

There are many possible causes of FD, ranging from medications^3,4 to abnormal gastroduodenal motility^5,6 to Helicobacter pylori infection,⁷ and a comprehensive differential diagnosis. The first step in an investigation is to rule out red flags suggestive of gastrointestinal (GI) cancer or other serious disorders.

Patients with FD, like the vast majority of those you’ll treat in a primary care setting, suffer significant morbidity. Most have chronic symptoms, with intermittent flare-ups interspersed with periods of remission.⁸ In the text and dyspepsia treatment ALGORITHM^5,7-12 that follow, you’ll find an evidence-based patient management approach.

Symptoms and causes: What to look for

The primary symptoms of dyspepsia include bothersome postprandial fullness, early satiety, and epigastric pain and burning. To meet the Rome criteria for dyspepsia, these symptoms must have been present for the last 3 months and have had an onset ≥6 months prior to diagnosis.² Recurrent belching and nausea are also common, but are not included in the Rome diagnostic criteria.

Symptom severity is a poor predictor of the seriousness of the condition, however, and more intense symptoms are no more likely than milder cases to have an organic cause.^13,14 Indeed, anxiety is a common comorbidity in patients with FD and a risk factor for the diagnosis. Compared with the general public, patients with FD have been found to have higher levels of anxiety, chronic tension, hostility, and hypochondriasis, and a tendency to be more pessimistic.¹⁵

Possible causes of FD

While the etiology of organic dyspepsia is clear, the cause of FD is often far more difficult to determine.

Medication use should always be considered, as many types of drugs—including bisphosphonates, antibiotics, narcotics, steroids, iron, metformin, and nonsteroidal anti-inflammatory drugs (NSAIDs)—are associated with dyspepsia.^3,4

Gastroduodenal motility and accommodation, which has been found in numerous studies of patients with FD, is a proposed etiology.^5,6

Visceral hypersensitivity also appears to play a role. In one study of patients with severe dyspepsia, 87% of those with FD had a reduced or altered GI pain threshold, compared with 20% of those with organic dyspepsia.¹⁶

H pylori, commonly linked to peptic ulcer disease (PUD), is also associated with both organic dyspepsia and FD.^17,18 The gram-negative rod-shaped bacterium is present in approximately half of the population worldwide, but is more common in developing nations.⁷H pylori immunoglobulin G (IgG) is more prevalent in patients with dyspepsia, particularly in those younger than 30 years of age. The exact mechanism by which H pylori causes non-ulcerative dyspepsia is not clear, but inflammation, dysmotility, visceral hypersensitivity, and alteration of acid secretion have all been proposed.¹⁷

Dysfunctional intestinal epithelium is increasingly being considered in the pathophysiology of dyspepsia, among other conditions. Researchers theorize that certain foods, toxins, infections, and/or other stressors lead to changes in the structure and function of tight junctions, resulting in increased intestinal permeability.¹⁹ This in turn is thought to allow the outflow of antigens through the leaky epithelium and to stimulate an immune response—a process that may play a role in the increased GI inflammation or hypersensitivity associated with dyspepsia. The “leaky gut” theory may eventually lead to new ways to treat dyspepsia, but thus far, highquality evidence of the efficacy of treatments aimed at this mechanism is lacking.