Dyspepsia risk factors
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
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
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. [1][2][3][4][5][6][7][8]
Common risk factors
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
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 types I (MEN-I), antral G cell hyperplasia, basophilic leukemias, short bowel syndrome
References
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.