Refers to dyspepsia that occurs in the absence of a clinically identifiable structural lesion.
A syndrome of unexplained epigastric pain or burning, postprandial fullness, and meal restricting early satiety, and often bloating and nausea in varying combinations
Refers to a constellation of symptoms referable to the gastrointestinal area of the upper G.I. tract.
Upper gastrointestinal tract symptoms accounts for 5% of all primary care visits.
Dyspepsia symptoms affect up to 40% of the adult population.
Likely a collection of different diseases with multiple causes.
A subset of the syndrome may arise from local microinflammation, driven by an anberrant immune response by type 2 helper (Th2) cells.
Systemic immune activation with small intestinal homing T cells and cytokines correlate with symptoms and delayed gastric emptying.
Studies have shown 26% of patients with functional dyspepsia have two and more markers of systemic autoimmune disorder, especially those with joint hyper mobility and coexisting autonomic dysfunction.
Antigenic triggers may include foodborne pathogens, environmental allergens, ordysbiosis, and duodenal permeability.
Post infectious alterations in the plasticity of the nervous system and visceral afferents, bile salt dysregulation, or dietary constituents are additional non-inflammatory causes.
A moderate increase in eosinophils and mast cells have been noted in the duodenum, and less often in the stomach of patients with functional dyspepsia.
Mast cells are more enormous, in patients with IBS overlap, suggesting a common pathophysiology.
Eosinophilic activation and degranulation correlates with symptoms, as do submucosal neuronal responses and gliosis in the duodenum.
Apparent macrophage activation with loss of in interstitial cels of Cajal has been observed in the motor plexus of the stomach
Impairment of gastric accommodation is seen in 40% of patients, hypersensitivity to gastric distention in 40%, and mild delays in gastric emptying in 30%: 30% of patients have none of these problems, however.
Worldwide FD’s syndrome is present in 7.2% of adults (10.1% in the US), affects women 1.6 times as often as men, and is more common in persons younger than 40 years of age.
Acute gastrointestinal infections can precipitate functional dyspepsia in at least 10% of cases.
Heavy smoking is a strong risk factor for FD.
Hereditability is weak about 5%.
Approximately 1/3 of people with FD have anxiety or depression or both, a number similar to the persons with organic dyspepsia, or other chronic disorders.
The incidence of FD is estimated to be 3 to 4% per year.
Patients have moderate to severe impairment in their quality of life, and 2/3 of patients after persistence, symptoms, overtime with high rates of healthcare use and high socioeconomic costs.
Patients have an increased risk in hospitalization, suicide and death from any cause.
Approximately 1/3 to 1/2 of affected patients meet the criteria for both functional dyspepsia and irritable bowel syndrome.
More than 30% of patients with FD have symptoms suggestive of GERD and more than 40% of patients with GERD have FD symptoms.
It is more common in women.
A relapsing and remitting process.
Rome III criteria for diagnosis consists of sensation of pain or burning in the epigastric area, early satiety, fullness during or after meal, or a combination of these symptoms.
symptoms alone, or insufficient to distinguish functional dyspnea from other G.I. disorders.
Disturbances in gastrointestinal function are believed to be causal in the development of symptoms.
Disturbances in gastrointestinal motility and sensory function play key roles in symptoms.
Lack of association between symptoms and meals should also should raise questions about the diagnosis.
Pathophysiologic factors include changes in gastric motility, visceral hypersensitivity, genetic susceptibility, psychosocial factors and H pylori infection.
Symptoms must be chronic and occur at least weekly over a period of at least six months in the absence of an organic explanation.
Divided into two syndromes: the epigastric pain syndrome and the postprandial distress syndrome.
Epigastric pain syndrome consists of intermittent abdominal pain or burning in the epigastric area that occurs at least once per week.
The postprandial distress syndrome is characterized by occurrence at least several times a week of bothersome postprandial fullness occurring after normal sized meals or by early satiety preventing the person from finishing a regular meal.
Global prevalence is between five and 11%.
Approximately 80% of patients with epigastric pain have a normal endoscopic examination.
Approximately 80% of persons with D report this symptoms are aggravated by the ingestion of a meal.
Gastrointestinal endoscopy can identify most causes of dyspepsia and shows that less than 10% of patients have a peptic ulcer, less than 1% have a gastroesophageal cancer and more than 70% have functional dyspepsia.
Upper gastrointestinal endoscopy has a low rate of identification of organic disease and is not desirable nor realistic to perform this type of testing in all patients with dyspepsia.
Upper G.I. endoscopy is a reasonable first line strategy if there is considerable concern about the presidency of H. Pylori.
Celiac disease is not significantly increased among persons reporting dyspepsia
Medications are usually not implicated in causing dyspepsia.
Functional dyspepsia and gastroparesis have symptoms which frequently overlap and are hard to distinguish.
FD can be confused with G.I. manifestations outside the gastroduodenal region including other functional disorders.
Mechanisms include antral hypomotility, impaired stomach accommodation, disordered gastric electrical activity, and visceral hypersensitivity.
Associated with anxiety, depression and neuroses.
Symptoms are not able to reliably distinguish between organic disease and functional forms of dyspepsia.
Negatively affects attendance and productivity.
Costs associated in 2009 in excess of $18 billion.
Treatment is unsatisfactory with present agents such as histamine H2 receptor antagonists, proton pump inhibitors, antacids or the eradication of H. pylori organisms.
Cisapride demonstrated superiority to placebo in these patients but is no longer available in the U.S.
Itopride improves pain and fullness symptoms exerting prokinetic effects by way of antidopaminergic and antiacetylcholinesterase actions.
Acid suppression with PPI therapy has moderate efficacy, and this may be secondary to the treatment of atypical gastroesophageal reflux disease.
H pylori eradication provide significant benefits in patients with functional dyspepsia (HEROES Trial).
Tricyclic antidepressants are considered first line treatment neuromodulators and act on pain principally by inhibiting monoamine uptake in the spinal cord:they are also potent antagonist of the histamine H1 and two lesser extent, H2 receptors:The number needed to treat is six to reduce symptoms in one patient.
Recognition and treatment of anxiety and depression is important in all cases of functional dyspepsia.
Study support the use of cognitive behavior, therapy, mindfulness based stress reduction, and hypnotherapy with benefits lasting up to 12 months.
Other treatments include combination of Basilis coagulans and B. Subtilis, the antibiotic agent rifaxmin uuu787 have been reported to provide relief.