Dyspepsia causes
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahad Hasan, M.D.[2] Kiran Singh, M.D. [3] Ajay Gade MD[4]]
Overview
Dyspepsia is a symptom complex of epigastric pain or burning, postprandial fullness, and early satiation arising from the gastroduodenal region. Its causes are divided into two groups:[1]
- Organic (secondary) dyspepsia: a structural, systemic, metabolic, infectious, or drug-related cause is identified, and symptoms resolve when it is treated.
- Functional dyspepsia (FD): no explanatory disease is found on evaluation.
Approximately 80% of patients with dyspepsia have no structural explanation and are classified as FD.[2][3] History and examination cannot reliably distinguish organic from functional dyspepsia, and no accurate biomarker exists.[2][3] The most common organic contributors are gastroesophageal reflux disease, peptic ulcer disease, and NSAID/aspirin use. Myocardial ischemia is the key extra-luminal cause that must not be missed.
Causes
Life-threatening Causes
- Myocardial ischemia can present as epigastric pain that mimics dyspepsia, particularly in women, older adults, and patients with diabetes mellitus.
- The 2021 AHA/ACC chest pain guideline explicitly lists the upper abdomen as a location of ischemic pain and notes that among outpatients presenting with chest pain, approximately 10–20% have a gastrointestinal cause, which can mimic myocardial ischemia; symptoms alone do not reliably distinguish the two.[4]
- Use a low threshold for ECG and troponin testing in these situations:
- Pain that is exertional or radiates.
- Pain accompanied by diaphoresis or dyspnea.
- Patients at higher cardiovascular risk.
Organic Causes
Among organic causes, erosive esophagitis, gastric ulcer, and duodenal ulcer are the principal clinically significant findings in primary-care patients undergoing prompt endoscopy for uninvestigated dyspepsia.[5] In an updated meta-analysis of 15 studies (41,763 participants), erosive esophagitis was the most common abnormality (pooled 11.0%; 95% CI 8.9–13.2%), followed by peptic ulcer (4.4%; 95% CI 2.5–6.7%); more than 85% of examinations were completely normal and gastroesophageal cancer was rare (<0.4%). Notably, only peptic ulcer — and specifically duodenal ulcer — was significantly more common in dyspeptic than non-dyspeptic patients (OR 1.61; 95% CI 1.08–2.39); erosive esophagitis was equally prevalent in both groups (OR 0.89).[6]
| Category | Cause | Key points |
|---|---|---|
| Luminal | Gastroesophageal reflux disease | Erosive esophagitis is the most common endoscopic abnormality in dyspepsia (~11%), though its prevalence is no higher than in non-dyspeptic controls. Heartburn is not itself a dyspeptic symptom, but it frequently coexists with dyspepsia and does not exclude FD.[6][3] |
| Luminal | Peptic ulcer disease (with or without Helicobacter pylori infection) | The only endoscopic finding significantly more common in dyspeptic than in non-dyspeptic patients (OR 1.61; duodenal ulcer OR 2.06). Dyspepsia is the presenting symptom in ~81% of patients with peptic ulcer, but only ~8% of patients presenting with dyspepsia in primary care have an ulcer at endoscopy.[6][7] |
| Drugs | NSAIDs and aspirin (best established) | Other implicated agents:
The AGA technical review also lists alendronate, orlistat, acarbose, digitalis, and potassium supplements as theoretical causes. Supporting data for drugs other than NSAIDs are lacking.[8][9] |
| Luminal (malignant) | Gastric or esophageal cancer | Rare (<0.5% of dyspepsia). Its possibility is the reason for endoscopy based on age and alarm features. |
| Motility | Gastroparesis | Overlaps clinically with FD; approximately 18–30% of FD patients have (usually mild) delayed gastric emptying, and gastroparesis and FD are increasingly regarded as a spectrum rather than distinct disorders, so the distinction is imperfect (see Pathophysiology).[2][10][11] |
| Pancreaticobiliary | Symptomatic gallstone disease, sphincter of Oddi dysfunction, biliary dyskinesia, gallbladder cancer | Suspect when typical biliary pain or jaundice is present. |
| Pancreaticobiliary | Chronic pancreatitis, pancreatic cancer | — |
| Hepatic | Hepatocellular carcinoma | — |
| Inflammatory | Crohn's disease (gastroduodenal) | — |
| Infectious | Parasitic infection (Giardia lamblia, Strongyloides, anisakiasis) | — |
| Infiltrative | Eosinophilic gastroenteritis, sarcoidosis, amyloidosis | — |
| Vascular | Chronic mesenteric ischemia (intestinal angina) | — |
Helicobacter pylori-Associated Dyspepsia
- Under the Kyoto consensus, H. pylori gastritis is an organic (infectious) disease and is not part of FD.[1][2]
- Classification depends on the response to eradication:
- Sustained symptom remission for ≥6 months after successful eradication defines H. pylori-associated dyspepsia.
- Persistent or recurrent symptoms after eradication reclassify the patient as FD.
- Most H. pylori-positive dyspeptic patients are not cured by eradication. Roughly 91% remain symptomatic, and the overall number needed to treat is about 14.[12]
Post-infection Dyspepsia
- Acute infectious gastroenteritis (bacterial, viral, or parasitic) is an established cause of new-onset dyspepsia, termed post-infection FD.
- In a meta-analysis, the pooled odds ratio for FD after gastroenteritis was 2.18 (95% CI 1.70–2.81). Risk was highest within 12 months and declined thereafter.[13]
- Post-infection FD has a prevalence of approximately 10%.[14]
- Post-infection onset is associated with weight loss, early satiety, and increased duodenal eosinophils.[10]
Functional Dyspepsia
- FD accounts for the large majority of dyspepsia and is a disorder of gut-brain interaction.[2]
- Its mechanisms are covered in the Pathophysiology microchapter:
- Impaired gastric accommodation
- Visceral hypersensitivity
- Delayed gastric emptying
- Low-grade duodenal microinflammation
- Psychological comorbidity
- Associations that increase FD risk are covered in the Risk Factors microchapter; they are not organic causes. They include:
- Female sex
- Smoking
- NSAID use
- H. pylori status
- High body mass index
- Anxiety and depression
Areas of Uncertainty
- H. pylori-associated dyspepsia: The construct is contested. The same consensus that defines it reclassifies non-responders as FD, and because most eradicated patients remain symptomatic, the entity is small and its long-term validity is debated.[12]
- FD and gastroparesis: The two may be overlapping or interchangeable syndromes rather than distinct entities, which blurs delayed gastric emptying as a discrete cause.
- Post-infection FD: The magnitude and durability of risk vary widely across studies. The mechanism (residual immune activation vs. change in the duodenal microbiome) is unsettled.[13][14]
References
- ↑ 1.0 1.1 Stanghellini V, Chan FK, Hasler WL, Malagelada JR, Suzuki H, Tack J, Talley NJ (2016). "Gastroduodenal Disorders". Gastroenterology. 150 (6): 1380–1392. doi:10.1053/j.gastro.2016.02.011. PMID 27147122.
- ↑ 2.0 2.1 2.2 2.3 2.4 Ford AC, Mahadeva S, Carbone MF, Lacy BE, Talley NJ (2020). "Functional dyspepsia". Lancet. 396 (10263): 1689–1702. doi:10.1016/S0140-6736(20)30469-4. PMID 33049222 Check
|pmid=value (help). - ↑ 3.0 3.1 3.2 Wauters L, Dickman R, Drug V, et al. (2021). "United European Gastroenterology (UEG) and European Society for Neurogastroenterology and Motility (ESNM) consensus on functional dyspepsia". Neurogastroenterol Motil. 33 (9): e14238. doi:10.1111/nmo.14238.
- ↑ Gulati M, Levy PD, Mukherjee D, et al. (2021). "2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain". J Am Coll Cardiol. 78 (22): e187–e285. doi:10.1016/j.jacc.2021.07.053.
- ↑ Thomson AB, Barkun AN, Armstrong D, et al. (2003). "The prevalence of clinically significant endoscopic findings in primary care patients with uninvestigated dyspepsia: the Canadian Adult Dyspepsia Empiric Treatment – Prompt Endoscopy (CADET-PE) study". Aliment Pharmacol Ther. 17 (12): 1481–1491. doi:10.1046/j.1365-2036.2003.01646.x.
- ↑ 6.0 6.1 6.2 Nasseri-Moghaddam S, Mousavian AH, Kasaeian A, et al. (2023). "What Is the Prevalence of Clinically Significant Endoscopic Findings in Subjects With Dyspepsia? Updated Systematic Review and Meta-Analysis". Clin Gastroenterol Hepatol. 21 (8): 1739–1749. doi:10.1016/j.cgh.2022.05.041.
- ↑ Vakil N (2024). "Peptic Ulcer Disease: A Review". JAMA. 332 (21): 1832–1842. doi:10.1001/jama.2024.19094.
- ↑ Talley NJ, Vakil NB, Moayyedi P (2005). "American Gastroenterological Association technical review on the evaluation of dyspepsia". Gastroenterology. 129 (5): 1756–1780. doi:10.1053/j.gastro.2005.09.020.
- ↑ Bytzer P (2010). "Dyspepsia as an adverse effect of drugs". Best Pract Res Clin Gastroenterol. 24 (2): 109–120. doi:10.1016/j.bpg.2009.11.006.
- ↑ 10.0 10.1 Törnblom H, Carbone F, Hasler WL, et al. (2026). "Gastroduodenal disorders". Gastroenterology. 170 (6): 1240–1260. doi:10.1053/j.gastro.2026.01.038.
- ↑ Shin A (2024). "Disorders of gastric motility". Lancet Gastroenterol Hepatol. 9 (11): 1052–1064. doi:10.1016/S2468-1253(24)00231-2.
- ↑ 12.0 12.1 Broeders B, Carbone F, Balsiger LM, et al. (2023). "Review article: Functional dyspepsia—a gastric disorder, a duodenal disorder or a combination of both?". Aliment Pharmacol Ther. 57 (8): 851–860. doi:10.1111/apt.17414. Vancouver style error: initials (help)
- ↑ 13.0 13.1 Pike BL, Porter CK, Sorrell TJ, Riddle MS (2013). "Acute gastroenteritis and the risk of functional dyspepsia: a systematic review and meta-analysis". Am J Gastroenterol. 108 (10): 1558–1563. doi:10.1038/ajg.2013.147.
- ↑ 14.0 14.1 Brown G, Hoedt EC, Keely S, et al. (2022). "Role of the duodenal microbiota in functional dyspepsia". Neurogastroenterol Motil. 34 (11): e14372. doi:10.1111/nmo.14372.