Acid indigestion

Jump to navigation Jump to search

WikiDoc Resources for Acid indigestion


Most recent articles on Acid indigestion

Most cited articles on Acid indigestion

Review articles on Acid indigestion

Articles on Acid indigestion in N Eng J Med, Lancet, BMJ


Powerpoint slides on Acid indigestion

Images of Acid indigestion

Photos of Acid indigestion

Podcasts & MP3s on Acid indigestion

Videos on Acid indigestion

Evidence Based Medicine

Cochrane Collaboration on Acid indigestion

Bandolier on Acid indigestion

TRIP on Acid indigestion

Clinical Trials

Ongoing Trials on Acid indigestion at Clinical

Trial results on Acid indigestion

Clinical Trials on Acid indigestion at Google

Guidelines / Policies / Govt

US National Guidelines Clearinghouse on Acid indigestion

NICE Guidance on Acid indigestion


FDA on Acid indigestion

CDC on Acid indigestion


Books on Acid indigestion


Acid indigestion in the news

Be alerted to news on Acid indigestion

News trends on Acid indigestion


Blogs on Acid indigestion


Definitions of Acid indigestion

Patient Resources / Community

Patient resources on Acid indigestion

Discussion groups on Acid indigestion

Patient Handouts on Acid indigestion

Directions to Hospitals Treating Acid indigestion

Risk calculators and risk factors for Acid indigestion

Healthcare Provider Resources

Symptoms of Acid indigestion

Causes & Risk Factors for Acid indigestion

Diagnostic studies for Acid indigestion

Treatment of Acid indigestion

Continuing Medical Education (CME)

CME Programs on Acid indigestion


Acid indigestion en Espanol

Acid indigestion en Francais


Acid indigestion in the Marketplace

Patents on Acid indigestion

Experimental / Informatics

List of terms related to Acid indigestion

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Acid indigestion, also called dyspepsia, is a type of indigestion involving an excess of hydrochloric acid in the stomach. Frequent occurrence of acid indigestion can lead to aggravation of the duodenum or to an aggravation of the lining of the stomach, both of which can lead to ulcers which can be life-threatening. However, it is important to note that some 85 to 95% of all stomach ulcers are caused by infection with the bacterium Helicobacter pylori, and not by excess acidity. Acid indigestion should be distinguished from heartburn, which typically involves aggravation of the esophagus.


Common Causes

Common contributors to acid indigestion are:

  • Eating foods with too much fat in them
  • Eating foods with too much spice in them
  • Excess consumption of:
  • Smoking
  • Overeating
  • Eating too late in the evening, or eating just before sleeping

Over the counter remedies (antacids) are available at almost all grocery stores and drugstores. However, a kind of dependence can develop on these medications, and other complications can arise from excess use of antacids.

Causes of Acid Indigestion in Alphabetical Order

Historical Perspective

  • Acid indigestion was first discovered in the 1980s by a group of clinicians and researchers who at the time described it as discomfort behind the sternum (retrosternal) or in the abdominal region (epigastric) related to the gastrointestinal system, occurring within a time-frame of greater than four weeks. Patients were sub-classified into various groups based on cause, mechanism of disease, and presenting symptoms. This was done to assist clinicians in selecting the most appropriate therapy. These include: Reflux-like, ulcer-like, dysmotility-like, and unspecified dyspepsia [1]. They disregarded the reflux-like subgroup with the opinion that they should be considered as having Gastro-esophageal Reflux Disease (GERD) until proven otherwise. Currently, this is widely accepted but still has an ongoing discussion. They concluded that acid indigestion should be described as pain only centered in the abdominal region (epigastric) without a specific duration [2] [3].
  • Irritable Bowel Syndrome (IBS) is also a diagnosis of exclusion [4].


  • Acid Indigestion may be classified according to Rome II Classification into 3 subtypes/groups [2] [3]:
  • Ulcer-like - Significant pain in the upper abdomen.
  • Dysmotility-like - Non-painful discomfort in the upper abdomen e.g. early satiety, bloating, or nausea.
  • Unspecified - Cannot be classified into either of the above groups.


  • The exact pathogenesis of acid indigestion is still currently under discussion. Various mechanisms has been previously described. There is the iatrogenic cause of acid indigestion, which could be due to pill esophagitis or non-steroidal anti-inflammatory drug intolerance. Symptoms of this can be derived from history of patient and review of systems[5].
  • The major pathophysiological mechanism include: Gastrointestinal motor abnormalities; altered visceral sensation; psychosocial factors. An interplay between all 3 better explains the mechanism behind this disease.
  • Gastrointestinal motor abnormalities underlying the pathogenesis of acid indigestion includes: Delayed emptying, unequal distribution of food within the stomach, hypo-motility of the antrum, irregular rhythm in the gastrointestinal system. These have been observed in patients with the pathology, together with nauseous feelings and probably subsequent vomiting, or gastric distension.
  • Patients with acid indigestion has been known to have increased feeling of physiological stimuli, which could only be minor, in both fasting, and post-prandial states. This implies a pathology in either the afferent or efferent to the gastrointestinal system. Mechanical distension of the gastrointestinal wall induces the already mentioned dyspeptic symptoms. Increased sensitivity of the mucosa wall, and impaired relaxation of the proximal stomach, also plays a role in the pathology.
  • Helicobacter pylori has an important role as well. It has been associated with the development of acid indigestion.
  • Genetics could also explain acid indigestion but there is little statistics supporting this hypothesis. Over time, it has been observed that people who are diagnosed with acid indigestion have a long family history of abdominal pain, which could likely be explained by a polymorphism in their gene. This has not exactly been completely proven.
  • Psychology has a role to play in Acid Indigestion. There is some evidence that some patients are usually anxious before the onset of indigestion. Studies have shown that those with high anxiety levels have an increased risk of developing acid indigestion. Changes in circadian rhythm has also been linked to acid indigestion, as well as various somatic complaints. Although all these are psychological, those with somatic complaints may have a structural explanation for their acid indigestion. Depression on the other hand, has not been linked in any way with acid indigestion.
  • A theory also poses that acid indigestion could develop after a bacterial, parasitic or viral gastroenteritis. Post-infectious eosinophilia, post-infection early satiety, post-infection gastric discomfort, has all been noted, and these are signs of acid indigestion, as well as other pathologies such as irritable bowel syndrome, which need to be ruled out, except it is co-existing with acid indigestion, before concluding on a diagnosis.

Differentiating Acid Indigestion from other Diseases

Epidemiology and Demographics

  • Acid indigestion is a common disease affecting people of different age range.[8] [9]
  • The epidemiology of the disease is difficult to assess because it does not have a unique pathogenesis, and it has symptoms similar to other diseases such as irritable bowel syndrome, e.t.c.


  • Acid indigestion is not associated with any particular age group, although all the studies conducted has been done on participants greater than 18 years of age.
  • A Canadian survey showed peak prevalence to be within 45 - 54 years in patients not yet diagnosed; in those already diagnosed, but Chinese subject, peak prevalence was noted to be within 41 - 50 years, and in Japanese, 50 - 59 years.
  • Subsets of acid indigestion has been observed to possibly affect some age groups. The ulcer-subtype is commonly observed in patients < 39 years of age. The reflux subset is seen among middle aged patients. Dysmotility subtype commonly observed in patients <59 years of age.
  • Some studies also postulates that the possibility of developing this disease decreases with age, for instance it is more common in patients >60 years of age, and less in patients < 70 years of age.


  • Acid Indigestion has been known to affect men and women equally.
  • Females are presumably more commonly affected with acid indigestion than men. A study done in Australia showed that more females presented with symptoms of acid indigestion.[10] [11]


  • Racial predilection for acid indigestion has not been discussed. Several studies point towards African-Americans and the Chinese to be at greater risk for undiagnosed acid indigestion. Overall, there is no statistic proof to back the predilection of this disease in any particular ethnic group.[11]

Risk Factors


Diagnostic Criteria

  • The diagnosis of acid indigestion is made when we have successfully ruled out all other possibilities. An esophagogastroduodenoscopy (EGD) is done to rule out pathologies within the esophagus, stomach, small intestine or any malignancy. The most common complaint these patients present with it is early satiety. Some diagnostic methods has been embarked on to assist in diagnosis [14]. They include:
  • Nutrient Meal Test: This is an affordable and non-invasive method for assessing symptoms associated with acid indigestion. The major symptoms under consideration include: epigastric pain, abdominal fullness, retrosternal burning, nausea. They test gastric motility and altered visceral sensation. This test, although helpful, has not been clinically proven and is still currently undergoing further research. A solid meal was also used with the same symptoms assessed. It was shown that the symptoms were heightened in patients with complaint of acid indigestion as compared with their healthy counterparts; and even in those who did not present with meal-associated symptoms.
  • Differentiating Acid Indigestion from gastroparesis: Delayed gastric emptying is associated with these pathologies, so care has to be taken in patients who present with these as the principal symptom. Upper gastrointestinal endoscopy as well as other imaging studies should be done to differentiate these and arrive at an appropriate diagnosis.
  • Differentiating Acid Indigestion from Gastroesophageal Reflux Disease (GERD): Patients could present with symptoms suspecting any of these pathology. Classic symptoms such as heartburn tends to be more associated with GERD, and so has not been included in the widely accepted symptoms associated with Acid Indigestion, although they could still present with heartburn.A barium swallow, endoscopy, or manometry could be used in diagnosing GERD.
  • Brain Imaging: The pathogenesis of Acid Indigestion talks about its relationship with abnormal motor and sensory function in the gastrointestinal system which could also be linked to an abnormality in the brain, as this is the source of the sensory nerves. Imaging studies such as Positron Emission Tomography (PET), and Functional Magnetic Resonance Imaging (FMRI) can be used to assess any abnormality in the brain or sensory perception in the gastrointestinal system. Further research is been done to find its association with meals.


  • Symptoms of Acid Indigestion may include the following [15]:
  • Epigastric pain
  • Nausea and vomiting
  • Upper abdominal fullness (bloating)
  • Distress and anxiety
  • Other non-common and non-specific symptoms include: acidic taste in mouth, rumbling stomach, belching and gas, burning feeling in the upper abdomen or stomach (heartburn)

Physical Examination [6]

  • Patients with acid indigestion usually appear normal, except epigastric tenderness which varies amongst patients. Due to the fact that this disease might present just as a number of other different diseases would, other physical examinations should be done to assist in diagnosis.
  • Assessing the patient's hemodynamic status is expected, not just as routine check, but to rule out blood loss, because signs of hypotension and/or tachycardia may be indicative of this. Stool culture and analysis should be done to know contents of stool and check any abnormalities. Examination of the oral cavity should be done, looking for signs of dental erosion, and any abnormality, which might be explain GERD. An examination of the mucosal bed, in the oral cavity, as well as the eyes, should be done to rule out jaundice as associated with most biliary tract disease. An abdominal examination, looking out for positive Murphy sign, should be done for biliary tract disease; also trying to elicit any tenderness. Indicators of thyroid pathology - hypothyroidism/hyperthyroidism, should be looked out for. Stigmatas of malignancy such as weight loss, palpable mass, enlarged lymph nodes should be further explored, and an immediate endoscopy should be done.

Laboratory Findings

  • There are no specific laboratory findings associated with Acid indigestion, although a detailed history should be obtained. Based on this, various tests should be done for any irregularity.
  • A Complete Blood Count (CBC) should be done to rule out anemia. Serum electrolyte level should be monitored in patients with nausea and vomiting. Liver function test, including but not limited to bilirubin, alkaline phosphatase and imaging should be done if any biliary tract pathology; amylase, lipase if any pancreas pathology is suspected. Urea breath test or serum antibody titers or antigen enzyme immunoassay could help towards a H. pylori infestation. If any malignancy is suspected, based on history, a biopsy is the definitive test of choice. [disease name].
  • Endoscopy is an important technique as it assists in achieving a final diagnosis [6].


Medical Therapy [14] [6] [11] [7]

  • Treatment for Acid Indigestion is based upon relieving symptoms of the patient and generally improving the health of the patient as well as his/her psychology.
  • The first recommendation is to carefully review diet to ascertain if there could be any causative agent from diet. Diets low in fat could also be beneficial to these patients.
  • The mainstay of therapy for Acid Indigestion includes: Endoscopy, empiric anti-secretory drug therapy, H. pylori testing and treatment. Treatment of H. pylori is the only definitive cure in patients with H. pylori as the causative agent.
  • Pharmacologically we could use: Acid suppression - proton pump inhibitors (first line treatment), H2 receptor antagonist; Centrally acting drugs (Anti-depressants) - tricyclic low dose, mirtazapine, buspirone; montelukast
  • There is no standard method of treatment, as it all depends on the symptoms the patient presents with. After assessment, a decision could be made as to which treatment method to be used depending on the socio-economic status as well as needs of the patients. Factors such as cost, culture, ethics, and preference of patient as well as physician, disease prevalence should be considered.
  • Patients whose acid indigestion is based on psychology could be treated with placebo, with recorded progress.


  • Surgery is seldomly indicated in the mainstay of therapy for acid indigestion.

Prevention [11]

  • In order to prevent acid indigestion, patients must first of all abstain from foods that trigger this. Patient has to be aware of which food precipitates these findings.
  • Patients should eat slowly whilst avoiding food, fruits and vegetables with high acidic content. Reduce beverages containing caffeine.
  • Reduce alcohol consumption. Quit smoking.
  • Good sleep hygiene.


  1. {{cite journal |vauthors=Agréus L |title=Natural history of dyspepsia |journal=Gut |volume=50 Suppl 4 |issue= |pages=iv2–9 |date=May 2002 |pmid=11953337 |pmc
    • In [year], [gene] mutations were first identified in the pathogenesis of [disease name].
    • Subsequently, in 1991, the Rome II Classification reviewed the subgroups for dyspepsia <ref name="urlCiNii 論文 -  Functional dyspepsia : a classification with guidelines for diagnosis and management">"CiNii 論文 -  Functional dyspepsia : a classification with guidelines for diagnosis and management".
  2. 2.0 2.1 "CiNii 論文 -  Functional dyspepsia : a classification with guidelines for diagnosis and management".
  3. 3.0 3.1 "Functional gastroduodenal disorders | Gut".
  4. Elvert P, Gabel M, Poppe S, Papstein HJ, Grosse F (June 1991). "[Growth studies of bulls of black-and-white dairy cattle during low feed levels. 4. Derivation of energy requirements]". Arch Tierernahr (in German). 41 (5): 541–50. PMID 1953337.
  5. "Pathophysiology of functional dyspepsia | Gut".
  6. 6.0 6.1 6.2 6.3 "Evaluation and Management of Dyspepsia - American Family Physician".
  7. 7.0 7.1 "".
  8. Lefkowitz RJ, Smith RJ, Bryant RG, Freedman P, Smith EC, Höltje JV, Mirelman D, Sharon N, Schwarz U, Ehrhart IC, Parker PE, Weidner WJ, Dabney JM, Scott JB, Haddy FJ, Schmoldt A, Benthe HF, Haberland G, Hachet JL, Laxenaire MC, Piens C, Byron TJ, Talley NJ (September 1975). "Identification of adenylate cyclase-coupled beta-adrenergic receptors with radiolabeled beta-adrenergic antagonists". Biochem. Pharmacol. 24 (18): 1651–8. doi:10.1152/ajplegacy.1975.229.3.754. PMC 5417776. PMID 11.
  9. Mahadeva S, Goh KL (May 2006). "Epidemiology of functional dyspepsia: a global perspective". World J. Gastroenterol. 12 (17): 2661–6. PMC 4130971. PMID 16718749.
  10. Ford AC, Marwaha A, Sood R, Moayyedi P (July 2015). "Global prevalence of, and risk factors for, uninvestigated dyspepsia: a meta-analysis". Gut. 64 (7): 1049–57. doi:10.1136/gutjnl-2014-307843. PMID 25147201.
  11. 11.0 11.1 11.2 11.3 "Functional Dyspepsia: Symptoms, Diagnosis and Treatment - Symptoma®".
  12. Shaib Y, El-Serag HB (November 2004). "The prevalence and risk factors of functional dyspepsia in a multiethnic population in the United States". Am. J. Gastroenterol. 99 (11): 2210–6. doi:10.1111/j.1572-0241.2004.40052.x. PMID 15555004.
  13. Shah SS, Bhatia SJ, Mistry FP (2001). "Epidemiology of dyspepsia in the general population in Mumbai". Indian J Gastroenterol. 20 (3): 103–6. PMID 11400800.
  14. 14.0 14.1 Talley NJ (May 2017). "Functional Dyspepsia: Advances in Diagnosis and Therapy". Gut Liver. 11 (3): 349–357. doi:10.5009/gnl16055. PMC 5417776. PMID 28452210.
  15. "" (PDF).

Template:WS Template:WH


Template:WH Template:WS