Functional dyspepsia is a gastrointestinal disorder manifesting in stomach pain and motility-related complaints. In order to distinguish this condition from peptic ulcer disease, it is sometimes also referred to as non-ulcer dyspepsia.
While upper abdominal pain is one of the more frequent symptoms of FD, diagnostic criteria as established by the Rome foundation only require one of the symptoms sensation of fullness, satiation despite having consumed only small amounts of food, abdominal pain or burning. As per definition, epigastric pain and burning sensations are characteristic for FD, but some patients describe lower abdominal pain, too . It cannot be ruled out, though, that lower abdominal pain results from concurrent irritable bowel syndrome rather than from FD itself. The vast majority of FD patients presents with more than one of the aforementioned symptoms. Additionally, nausea, eructation and vomiting may be experienced.
Clinically, PDS and EPS are distinguished. Patients suffering from PDS report an exacerbation of symptoms shortly after ingestion of food. It is not uncommon to hear that determined foods are more likely to trigger indigestion than others. Some patients claim intake of hot food to be more frequently associated with FD symptoms. In contrast, EPS patients suffer from similar symptoms that do, however, not manifest in any temporal connection to meals. Patients may experience periods of PDS and EPS.
KEY RESULTS: Upper abdominal bloating scores were higher in post-Nissen dyspepsia patients (P=.016) and symptoms of postprandial distress syndrome (PDS) were more present in post-Nissen dyspepsia patients compared to the other two groups (P=.07). [ncbi.nlm.nih.gov]
Single/divorced or widowed marital status, nausea, bloating, and a feeling of incomplete emptying after bowel movements were independent risk factors for IBS-FD overlap among IBS patients. [ncbi.nlm.nih.gov]
Further down in the stomach, a surface reaction results in upper-middle abdominal pain and nausea; sometimes nausea and even vomiting are triggered. [nutramed.com]
I experience nausea every day, sometimes gets to the point where I feel as though I am going to vomit. this is often made worse after eating as well as the abdominal pain (on a bad day, going to the toilet straight after eating). [healthunlocked.com]
We are here for you as we are suffering the pain, nausea etc also. For years I felt so alone in this illness before I found this site. I have learned how to eat from the GP diet. I'm now enteral fed formula 24/7. [inspire.com]
Eating six small, low-fat meals per day may reduce early feelings of fullness, bloating after a meal, or nausea. Avoidance of caffeine, alcohol or smoking may also help. [aboutgimotility.org]
The cardinal symptoms include postprandial fullness (early satiety), nausea, vomiting and bloating. [ncbi.nlm.nih.gov]
Some patients induce vomiting to avoid discomforts after eating. Recurrent irritation in the upper GIT is food-caused until proven otherwise. [nutramed.com]
When to call your healthcare provider Call your healthcare provider right away if you have any of these: Symptoms that don’t get better, or get worse New symptoms Vomiting that doesn’t stop Vomiting blood Bloody stool or black tarry stool Unexplained [saintlukeskc.org]
- Abdominal Pain
Abstract As defined by Rome III, there are 4 abdominal pain-related functional gastrointestinal disorders in children: irritable bowel syndrome, functional dyspepsia (FD), abdominal migraine, and functional abdominal pain. [ncbi.nlm.nih.gov]
One of the most commonly used medications for Irritable Bowel Syndrome, Functional Abdominal Pain, and FD is amitriptyline, an antidepressant. [jefflazarusmd.com]
Symptoms vary; among the common complaints are epigastric/abdominal pain, discomfort, bloating or even reflux symptoms like heartburn and regurgitation. [star2.com]
Episodes often persist for 1-2 h after the meal, and the regurgitant consists of partially digested food that is recognizable in its taste. Regurgitation is typically effortless or preceded by a sensation of belching. [ncbi.nlm.nih.gov]
Published: 18 August 2014 Gastroesophageal reflux disease (GERD) and functional dyspepsia (FD) are common problems in the pediatric population, with up to 7% of school-age children and up to 8% of adolescents suffering from epigastric pain, heartburn, and regurgitation [mdpi.com]
Patients with any documented history of endoscopic esophagitis, or predominant heartburn or acid regurgitation, and a history of abdominal surgery (except appendectomy, cholecystectomy or hysterectomy, tubal ligations, bladder slings, and vasectomies) [niddkrepository.org]
While diagnosis of FD is based on clinical criteria, anamnesis, physical examination and additional diagnostic measures are indicated to identify a possibly underlying disease. Here, patients may benefit from a multidisciplinary approach. The following tests may be valuable:
- Laboratory analysis of blood samples. In FD patients, serotonin levels may be decreased . Alterations regarding immunoglobulin levels may indicate celiac disease. Blood biochemistry may also point at infection or inflammation if these trigger indigestion.
- Endoscopic examination of stomach and duodenum. This is the method of choice to rule out peptic ulcers as the source of abdominal complaints. In patients claiming lower abdominal pain or those suspicious for irritable bowel disease due to other symptoms, colonoscopy is indicated. Anatomical anomalies may be identified by means of endoscopy, too. Biopsies should be obtained during any of the two endoscopic exams. Histopathological analysis of these tissue samples may reveal pathologic alterations of the gastrointestinal wall.
- Since considerable parts of small and large intestines are not accessible with endoscopic instruments, diagnostic imaging such as plain radiography, magnetic resonance imaging or computed tomography scans may be required to visualize these organs. Application of contrast agents may be helpful.
- Urea breath test. Ingestion of radiolabeled urea results in exhalation of labeled carbon dioxide if hydrolysis of urea is catalyzed by urease. H. pylori typically expresses that enzyme. Intake of antacids, acid-reducing drugs or antibiotics may alter test results.
- Hydrogen breath test. This test is performed to rule out small intestinal bacterial overgrowth. Alterations are not expected in FD.
- Stool tests. Stool should be examined for the presence of intestinal parasites and blood. These tests are negative in samples obtained from FD patients.
Causative treatment is not available. Any therapy aims at relieving symptoms and improving life quality and psychological condition of the patient.
Dietary adjustments may be helpful and FD patients are generally recommended to prefer many small meals over few bigger ones. If patients identified determined foods that exacerbate their condition, such comestibles should be avoided. Food rich in fat may delay gastric emptying and worsen the symptoms. Thus, it should be consumed in very small amounts.
With regards to drug therapy, prokinetics and acid-reducing drugs, i.e., proton pump inhibitors (omeprazole, lansoprazole, pantoprazole and others) and histamine receptor antagonists (e.g., cimetidine, ranitidine) are most frequently administered. Antacids have not proven effective.
Antibiotic therapy in order to eradicate H. pylori is only recommended if an infection with this pathogen has been verified. Otherwise, side effects likely outweigh the benefits of this therapeutic approach.
Patients may highly benefit from psychological support and psychotropic medication, particularly if suffering from disorders like anxiety or depression .
A variety of etiologic factors has been related with FD.
Acute FD may result from administration of determined drugs. Non-steroidal anti-inflammatory drugs are widely used for a plethora of pathologic conditions and may induce non-ulcer dyspepsia as well as peptic ulcer disease.
Infection with Helicobacter pylori (H. pylori) is more frequently associated with peptic ulcer disease. However, this pathogen may contribute to FD and presence of H. pylori is not uncommon in FD patients. Several studies have been conducted regarding the effect of H. pylori treatment on improvement of FD symptoms, but results are inconsistent . While some patients may benefit from such therapy, others may not experience any improvement of indigestion and may suffer from side effects.
Eosinophilic gastroenteritis may play a role in FD etiology and although their causal relation is not clear, the former may contribute to delayed gastric emptying and thus trigger FD symptoms . The causes of eosinophilic gastroenteritis are not well understood either, but presumably, hypersensitivity reactions, infiltration of gastrointestinal tissues and subsequent inflammation account for its symptoms.
For a long time, FD has been considered a psychosomatic disease. Although this hypothesis holds no longer true, mental stress, anxiety and depression may exacerbate symptoms. Some individuals may be predisposed FD and only develop symptoms during periods of increased psychological strains. In severe cases, this relation may lead to a vicious cycle where persistent indigestion reduces life quality and augments the risk for psychological disorders and vice versa.
Although some patients report that consumption of determined foods exacerbates their condition, there is no scientific prove for such a relation.
FD is a very common but presumably underdiagnosed condition. Epidemiological studies are complicated by lack of pathognomonic symptoms, symptom overlap with irritable bowel syndrome or functional constipation and patients who present more than one of these diseases. Considering these limitations, it has been estimated that about 10% of the world's population suffer from this gastrointestinal disorder . Elsewhere, even higher numbers have been reported .
While racial predilection has not been described, females seem to be affected by FD more often than males. Those patients presenting with psychological disorders are at higher risks of developing FD. This also applies to those individuals previously diagnosed with irritable bowel syndrome but, as has been stated above, this disease may largely mimic FD .
Pathophysiological mechanisms triggering FD symptoms are very heterogeneous and probably little specific. In fact, many patients diagnosed with either FD, irritable bowel syndrome or functional constipation present with more than one of these disorders. Due to frequent reports of burning sensations, gastroesophageal reflux disease may also be mentioned at this point and in a retrospective study analyzing disease progress in almost 1,500 individuals, about 40% of all patients were diagnosed with several of the aforementioned gastrointestinal disorders within a period of ten years .
Some of the above described etiological factors may affect gastric emptying and indeed, the majority of FD patients shows reduced gastric motility. Delayed gastric emptying may explain the most characteristic symptoms of FD, i.e., prolonged retention times in the stomach may cause early satiety and a feeling of fullness, stomach pain and burning sensations. But while the theory of motility disturbances accounting for FD is widely accepted, a direct relation between dysmotility and severity of FD symptoms could not always be proven  . Also, H. pylori infections don't seem to diminish gastric emptying times . Thus, additional factors seem to play a role in FD pathogenesis.
Enhanced secretion of gastric acid has also been proposed to account for FD. The fact that many FD patients claim perigastric burning sensations argues for this theory. However, the precise conditions yielding either FD or peptic ulcer disease are not fully understood and this applies to excess gastric acid as well as H. pylori infection.
Functional dyspepsia (FD) is a general and descriptive term referring to a variety of abdominal complaints, e.g., pain in the upper abdominal region, nausea, vomiting, sensation of fullness and bloating after consumption of small meals or determined foods. While FD does not result from gastric function impairment due to peptic ulcers, any metabolic, muscular, neurologic or other systemic disorder affecting the stomach function may cause FD. Unfortunately, symptoms do not allow for an identification of the underlying disease and a thorough workup is required to achieve this aim. Pathogenetic mechanisms are largely unclear.
The Rome foundation, a nonprofit organization aiming at improving diagnosis and treatment of gastrointestinal disorders, has recently proposed the presence of postprandial fullness, early satiation, epigastric pain and/or epigastric burning as diagnostic for FD if these findings cannot be explained by other pathological conditions . Additionally, FD patients may either present with postprandial distress syndrome (PDS), i.e., the above mentioned symptoms generally manifest after eating, or with epigastric pain syndrome (EPS). Patients suffering from the latter report symptoms without a temporal connection to their last meal. Symptoms may resemble those experienced by patients suffering from irritable bowel syndrome or functional constipation .
If a primary disease can be detected, treatment aims at remedying this pathological condition. Otherwise, only supportive therapy can be provided. Retrospective analyses suggest PDS patients to benefit from prokinetics, while acid-reducing drugs seem to be indicated in those individuals affected by EPS. To date, no drugs have been approved for treatment of FD, but the highly promising, prokinetic compound acotiamide is currently tested in phase III clinical trials  .
Delayed gastric emptying, excess secretion of gastric acid and infection with Helicobacter pylori have all been related to FD. According to current knowledge, FD is a multifactorial disease since neither of the aforementioned factors is able to induce the disease on its own. Also, not all patients suffering from prolonged retention times in the stomach, hyperacidity or bacterial infections does indeed develop the disease.
Increased psychological burdens, e.g., mental stress, anxiety and depression, may exacerbate the disease. Because FD may significantly reduce the patient's quality of life, the disorder itself constitutes psychological stress, so both conditions may become mutually dependent. However, FD is not a mere psychosomatic disorder.
Patients suffering from FD may not be able to consume a regular meal, since sensations of satiation, fullness and bloating manifest after having eaten small amounts of food. Also, pain or burning in the upper abdomen are typical for FD. Patients may present one or more of the aforementioned symptoms; they may be experienced either during or after having a meal (corresponding to postprandial distress syndrome, one form of FD) or without any apparent temporal connection to ingestion of food (epigastric pain syndrome).
While diagnosis of FD is essentially based on clinical criteria, a thorough workup is necessary to identify a possibly underlying disease. In this context, blood and stool samples will be analyzed and breath tests may be carried out to check for an infection with H. pylori and to detect alterations of the physiological intestinal flora.
Additionally, stomach and duodenum may be visualized by means of endoscopy. This technique does not only allow for the unequivocal diagnosis of peptic ulcer disease but also permits obtaining tissue samples for histopathological analysis. While peptic ulcers are a common trigger of stomach pain and symptoms similar to those manifested in FD, peptic ulcer disease constitutes a different entity and is not characteristic for FD.
In many cases, no underlying disorder can be detected.
Causative treatment is not available. However, delayed gastric emptying, excess gastric acid and H. pylori infection may be treated with prokinetics, acid-reducing drugs like proton pump inhibitors and histamine receptor antagonists, and antibiotics, respectively. Eradication of H. pylori is only indicated if an infection with this pathogen has been verified before. Nevertheless, it cannot be guaranteed that symptoms improve after such treatment.
Due to the apparent relation between psychological disorders and FD symptoms, patients may benefit considerably from psychological support and possibly medication to treat anxiety, depression or other mental diseases.
- Stanghellini V, Talley NJ, Chan F, et al. Rome IV - Gastroduodenal Disorders. Gastroenterology. 2016.
- Palsson OS, Whitehead WE, van Tilburg MA, et al. Rome IV Diagnostic Questionnaires and Tables for Investigators and Clinicians. Gastroenterology. 2016.
- Talley NJ. Functional dyspepsia: new insights into pathogenesis and therapy. Korean J Intern Med. 2016; 31(3):444-456.
- Ueda M, Iwasaki E, Suzuki H. Profile of acotiamide in the treatment of functional dyspepsia. Clin Exp Gastroenterol. 2016; 9:83-88.
- Du LJ, Chen BR, Kim JJ, Kim S, Shen JH, Dai N. Helicobacter pylori eradication therapy for functional dyspepsia: Systematic review and meta-analysis. World J Gastroenterol. 2016; 22(12):3486-3495.
- Mahadeva S, Goh KL. Epidemiology of functional dyspepsia: a global perspective. World J Gastroenterol. 2006; 12(17):2661-2666.
- Talley NJ. Functional dyspepsia: new insights into pathogenesis and therapy. Korean J Intern Med. 2016; 31(3):444-456.
- Ford AC, Forman D, Bailey AG, Axon AT, Moayyedi P. Fluctuation of gastrointestinal symptoms in the community: a 10-year longitudinal follow-up study. Aliment Pharmacol Ther. 2008; 28(8):1013-1020.
- Sha W, Pasricha PJ, Chen JD. Correlations among electrogastrogram, gastric dysmotility, and duodenal dysmotility in patients with functional dyspepsia. J Clin Gastroenterol. 2009; 43(8):716-722.
- Kindt S, Dubois D, Van Oudenhove L, et al. Relationship between symptom pattern, assessed by the PAGI-SYM questionnaire, and gastric sensorimotor dysfunction in functional dyspepsia. Neurogastroenterol Motil. 2009; 21(11):1183-e1105.
- Leontiadis GI, Minopoulos GI, Maltezos E, et al. Effects of Helicobacter pylori infection on gastric emptying rate in patients with non-ulcer dyspepsia. World J Gastroenterol. 2004; 10(12):1750-1754.
- Cheung CK, Lee YY, Chan Y, et al. Decreased Basal and postprandial plasma serotonin levels in patients with functional dyspepsia. Clin Gastroenterol Hepatol. 2013; 11(9):1125-1129.
- Lacy BE, Talley NJ, Locke GR, 3rd, et al. Review article: current treatment options and management of functional dyspepsia. Aliment Pharmacol Ther. 2012; 36(1):3-15.