Dyspepsia risk factors

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

## Overview[edit | edit source]

Common risk factors for the development of dyspepsia include, Helicobacter pylori infection, chronic use of NSAIDs, family history of peptic ulcer disease, emotional stress, increased intake of high-fiber diet, overconsumption of caffeine, high-fat and greasy foods. Less common risk factors for the development of dyspepsia include tobacco, alcohol consumption, psychological stress and Zollinger-Ellison syndrome.

## Risk Factors[edit | edit source]

Risk factors for the development of dyspepsia can be divided into common and less common risk factors, which include the following:[1][2][3][4][5][6][7][8]

### Common risk factors[edit | edit source]

Common risk factors in the development of dyspepsia include:

* Helicobacter pylori infection
* Chronic use of NSAIDs
* Family history of peptic ulcer
* Eating meals too quickly
* Emotional stress while eating
* Overabundance of high-fiber foods
* Overconsumption of caffeine
* Spicy, high-fat, and greasy foods
* Too much food at meals

### Less common risk factors[edit | edit source]

Less common risk factors in the development of dyspepsia include:

* Tobacco
* Alcohol
* Psychological stress
* Nosocomial stress ulcers due the to the use of mechanical ventilation for more than 48 hours, and coagulopathy
* Rare conditions associated with gastric acid hypersecretion such as:
* Zollinger-Ellison syndrome, mastocytosis, or a retained antrum following partial gastrectomy
* Gastrinoma or multiple endocrine neoplasia type I (MEN-I), antral G cell hyperplasia, basophilic leukemias, short bowel syndrome

## References[edit | edit source]

1. ↑ Huang JQ, Sridhar S, Hunt RH (2002). "Role of Helicobacter pylori infection and non-steroidal anti-inflammatory drugs in peptic-ulcer disease: a meta-analysis". Lancet. 359 (9300): 14–22. doi:10.1016/S0140-6736(02)07273-2. PMID 11809181.
2. ↑ Ballinger A, Smith G (2001). "COX-2 inhibitors vs. NSAIDs in gastrointestinal damage and prevention". Expert Opin Pharmacother. 2 (1): 31–40. doi:10.1517/14656566.2.1.31. PMID 11336566.
3. ↑ Holvoet J, Terriere L, Van Hee W, Verbist L, Fierens E, Hautekeete ML (1991). "Relation of upper gastrointestinal bleeding to non-steroidal anti-inflammatory drugs and aspirin: a case-control study". Gut. 32 (7): 730–4. PMC 1378985. PMID 1855677.
4. ↑ Laporte JR, Carné X, Vidal X, Moreno V, Juan J (1991). "Upper gastrointestinal bleeding in relation to previous use of analgesics and non-steroidal anti-inflammatory drugs. Catalan Countries Study on Upper Gastrointestinal Bleeding". Lancet. 337 (8733): 85–9. PMID 1670734.
5. ↑ Wachirawat W, Hanucharurnkul S, Suriyawongpaisal P, Boonyapisit S, Levenstein S, Jearanaisilavong J, Atisook K, Boontong T, Theerabutr C (2003). "Stress, but not Helicobacter pylori, is associated with peptic ulcer disease in a Thai population". J Med Assoc Thai. 86 (7): 672–85. PMID 12948263.
6. ↑ Rosenstock S, Jørgensen T, Bonnevie O, Andersen L (2003). "Risk factors for peptic ulcer disease: a population based prospective cohort study comprising 2416 Danish adults". Gut. 52 (2): 186–93. PMC 1774958. PMID 12524398.
7. ↑ Stack WA, Atherton JC, Hawkey GM, Logan RF, Hawkey CJ (2002). "Interactions between Helicobacter pylori and other risk factors for peptic ulcer bleeding". Aliment. Pharmacol. Ther. 16 (3): 497–506. PMID 11876703.
8. ↑ Everhart JE, Byrd-Holt D, Sonnenberg A (1998). "Incidence and risk factors for self-reported peptic ulcer disease in the United States". Am. J. Epidemiol. 147 (6): 529–36. PMID 9521179.

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