Introduction
Dyspepsia_Disease BackgroundDyspepsia refers to the pain or discomfort centered in the upper abdomen. The discomfort refers to a subjective sensation that the patient does not interpret as pain, which may be characterized by or associated with upper abdominal fullness, early satiety, epigastric burning, bloating, belching, or nausea and vomiting. Centered refers to the pain or discomfort in or around the midline. Dyspepsia is commonly referred to as indigestion and it is considered a symptom complex rather than a specific diagnosis.
Uninvestigated dyspepsia refers to dyspeptic symptoms in individuals who have not yet undergone diagnostic investigations and in whom no specific diagnosis explaining these symptoms has been established.
Epidemiology
Functional Dyspepsia or Non-Ulcer Dyspepsia
The global prevalence of functional dyspepsia is 5-11%, with the prevalence
of uninvestigated dyspepsia and functional dyspepsia at 5-30% in Asian countries.
The lowest prevalence rate was found in Japan and high prevalence rates were
found in Egypt, Brazil, Russia and the USA. This is more common in women than men, in
smokers and nonsteroidal anti-inflammatory drugs (NSAIDs) users. Based on several studies, the prevalence of
functional dyspepsia declines with increasing age and is highest among younger
adults. This commonly overlaps with
other disorders of gut-brain interaction (DGBIs) (eg IBS and functional
heartburn) and with gastroesophageal reflux disease
(GERD).
Etiology
Peptic ulcer disease and GERD are
the predominant identifiable etiologies of dyspeptic symptoms. Although less
prevalent, upper gastrointestinal (GI) malignancies
and celiac disease represent important organic causes. Dyspepsia-like symptoms
may arise from various GI disorders,
including infectious, inflammatory, and infiltrative diseases affecting the upper GI tract.
Dyspepsia is a frequent adverse effect of numerous medications and
these effects may arise from gastric mucosal injury, altered GI motility or sensation, increased
gastroesophageal reflux, or idiosyncratic reactions. NSAIDs
have been most extensively studied due to their potential to cause GI ulceration. Chronic use of aspirin and other
NSAIDs may lead to dyspeptic symptoms.
Pathophysiology
Functional Dyspepsia or Non-Ulcer Dyspepsia
The pathophysiology is multifactorial, and local factors (eg prevalence
of GI malignancy and Asian dietary habits) must be considered. The microscopic
physiologic mechanisms of functional dyspepsia include barrier function
impairment from altered sensitivity to duodenal acid or lipids that impair
mucosal integrity, low-grade gastroduodenal inflammation, gut microbiome
alteration and H pylori infection. Low-grade
inflammation could lead to a neuroimmune dysregulation affecting GI motility,
sensitivity and brain-gut perceptions leading to symptoms. The macroscopic
physiological mechanisms include GERD, stomach morphology, impaired gastric
accommodation, delayed or rapid gastric emptying, gastric dysrhythmias, antral
hypomotility, and visceral hypersensitivity alterations in the nervous system.
Other factors that may have a role in the development of functional dyspepsia
include anxiety, depression, sleep disturbance, stress, history of abuse,
family history and genetic factors, demographic factors (female sex, BMI,
socioeconomic status), lifestyle (eg smoking and alcohol consumption) and
dietary practices (fat-rich meals, restrictive eating).