Clin Endosc.  2017 Nov;50(6):578-584. 10.5946/ce.2016.129.

Risk Factors for the Presence of Symptoms in Peptic Ulcer Disease

Affiliations
  • 1Department of Internal Medicine, Konkuk University School of Medicine, Seoul, Korea. inksung@kuh.ac.kr

Abstract

BACKGROUND/AIMS
Peptic ulcer disease (PUD) is a common condition, but is difficult to detect in asymptomatic individuals. We aimed to investigate the prevalence of symptomatic and asymptomatic PUD during screening endoscopy and to identify risk factors for the presence of symptoms in patients with PUD.
METHODS
We investigated subjects who underwent a health inspection, including endoscopy of the upper gastrointestinal (GI) tract and a serum anti-Helicobacter pylori IgG assay, and who completed a self-report questionnaire about their symptoms.
RESULTS
Of the 12,852 subjects included in the study, 124 (1.0%) had symptomatic PUD and 309 (2.4%) had asymptomatic PUD. Old age, current smoking, and H. pylori infection were independent risk factors for symptomatic and asymptomatic PUD. Use of non-steroidal anti-inflammatory drugs (NSAIDs) was an independent risk factor only for symptomatic PUD (p=0.040). Compared to subjects with asymptomatic PUD, subjects with symptomatic PUD were more likely to have active-stage ulcers (p=0.002) and to drink more heavily (p=0.005).
CONCLUSIONS
Use of NSAIDs is a risk factor for symptomatic PUD, but not for asymptomatic PUD. Excessive alcohol consumption and active-stage ulcers in patients with PUD are related to the presence of gastroduodenal symptoms.

Keyword

Peptic ulcer; Anti-inflammatory agents, non-steroidal; Helicobacter pylori; Heavy drinking

MeSH Terms

Alcohol Drinking
Anti-Inflammatory Agents, Non-Steroidal
Endoscopy
Helicobacter pylori
Humans
Immunoglobulin G
Mass Screening
Peptic Ulcer*
Prevalence
Risk Factors*
Smoke
Smoking
Ulcer
Anti-Inflammatory Agents, Non-Steroidal
Immunoglobulin G
Smoke

Figure

  • Fig. 1. Flow chart of inclusion and exclusion of subjects. A total of 16,008 people who underwent a health inspection (gastroscopy, a self-report questionnaire, and a serum Helicobacter pylori IgG antibody test) at our center were investigated. Subjects younger than 17 years of age, subjects who underwent upper gastrointestinal (GI) surgery, subjects with adenoma or carcinoma in the upper GI tract, subjects who did not properly answer the questionnaire, subjects using proton pump inhibitors or histamine-2 receptor antagonists, and subjects previously diagnosed with functional dyspepsia were excluded from the study. If the results of the serum H. pylori IgG antibody test were equivocal and other H. pylori tests were not performed, subjects were excluded, because the presence of H. pylori infection could not be determined. Subjects without peptic ulcer disease (PUD) were categorized into the healthy control group. Among subjects diagnosed with PUD, subjects with ulcers in the scarring stage were excluded. The remaining subjects were categorized into the symptomatic or asymptomatic PUD group according to the presence of symptoms.


Cited by  1 articles

Clinical Significance of Risk Factors for Asymptomatic Peptic Ulcer Disease
Cheal Wung Huh, Byung-Wook Kim
Clin Endosc. 2017;50(6):514-515.    doi: 10.5946/ce.2017.159.


Reference

1. Milosavljevic T, Kostić-Milosavljević M, Jovanović I, Krstić M. Complications of peptic ulcer disease. Dig Dis. 2011; 29:491–493.
Article
2. Al Dhahab H, McNabb-Baltar J, Al-Taweel T, Barkun A. State-of-the-art management of acute bleeding peptic ulcer disease. Saudi J Gastroenterol. 2013; 19:195–204.
Article
3. Wolfe MM, Lichtenstein DR, Singh G. Gastrointestinal toxicity of nonsteroidal antiinflammatory drugs. N Engl J Med. 1999; 340:1888–1899.
Article
4. Hopkins RJ, Girardi LS, Turney EA. Relationship between Helicobacter pylori eradication and reduced duodenal and gastric ulcer recurrence: a review. Gastroenterology. 1996; 110:1244–1252.
Article
5. Atherton JC, Cao P, Peek RM Jr, Tummuru MK, Blaser MJ, Cover TL. Mosaicism in vacuolating cytotoxin alleles of Helicobacter pylori. Association of specific vacA types with cytotoxin production and peptic ulceration. J Biol Chem. 1995; 270:17771–17777.
6. Hunt RH, Yuan Y. Acid-NSAID/aspirin interaction in peptic ulcer disease. Dig Dis. 2011; 29:465–468.
Article
7. Yamaoka Y, Ojo O, Fujimoto S, et al. Helicobacter pylori outer membrane proteins and gastroduodenal disease. Gut. 2006; 55:775–781.
Article
8. Potamitis GS, Axon AT. Helicobacter pylori and Nonmalignant Diseases. Helicobacter. 2015; 20 Suppl 1:26–29.
9. Thorat MA, Cuzick J. Prophylactic use of aspirin: systematic review of harms and approaches to mitigation in the general population. Eur J Epidemiol. 2015; 30:5–18.
Article
10. Sasaki H, Nagahara A, Hojo M, et al. Ten-year trend of the cumulative Helicobacter pylori eradication rate for the ‘Japanese eradication strategy’. Digestion. 2013; 88:272–278.
Article
11. Kim JH, Kim HY, Kim NY, et al. Seroepidemiological study of Helicobacter pylori infection in asymptomatic people in South Korea. J Gastroenterol Hepatol. 2001; 16:969–975.
Article
12. Lau JY, Sung J, Hill C, Henderson C, Howden CW, Metz DC. Systematic review of the epidemiology of complicated peptic ulcer disease: incidence, recurrence, risk factors and mortality. Digestion. 2011; 84:102–113.
Article
13. Choi HS, Lee SY, Kim JH, et al. Combining the serum pepsinogen level and Helicobacter pylori antibody test for predicting the histology of gastric neoplasm. J Dig Dis. 2014; 15:293–298.
14. Halder SL, Locke GR 3rd, Schleck CD, Zinsmeister AR, Talley NJ. Influence of alcohol consumption on IBS and dyspepsia. Neurogastroenterol Motil. 2006; 18:1001–1008.
Article
15. Kim HM, Cho JH, Choi JY, et al. NSAID is inversely associated with asymptomatic gastric ulcer: local health examination data from the Korean National Health Insurance Corporation. Scand J Gastroenterol. 2013; 48:1371–1376.
Article
16. Yap PR, Goh KL. Non-steroidal anti-inflammatory drugs (NSAIDs) induced dyspepsia. Curr Pharm Des. 2015; 21:5073–5081.
Article
17. D’Elios MM, Andersen LP. Inflammation, immunity, and vaccines for Helicobacter pylori. Helicobacter. 2009; 14 Suppl 1:21–28.
18. Tahara T, Arisawa T, Shibata T, et al. Association of endoscopic appearances with dyspeptic symptoms. J Gastroenterol. 2008; 43:208–215.
Article
19. Li LF, Chan RL, Lu L, et al. Cigarette smoking and gastrointestinal diseases: the causal relationship and underlying molecular mechanisms (review). Int J Mol Med. 2014; 34:372–380.
Article
20. Lee SP, Sung IK, Kim JH, Lee SY, Park HS, Shim CS. The effect of emotional stress and depression on the prevalence of digestive diseases. J Neurogastroenterol Motil. 2015; 21:273–282.
Article
21. Ford AC, Bercik P, Morgan DG, Bolino C, Pintos-Sanchez MI, Moayyedi P. Characteristics of functional bowel disorder patients: a cross-sectional survey using the Rome III criteria. Aliment Pharmacol Ther. 2014; 39:312–321.
Article
22. Oshima T, Miwa H. Epidemiology of functional gastrointestinal disorders in Japan and in the world. J Neurogastroenterol Motil. 2015; 21:320–329.
Article
23. Bode G, Brenner H, Adler G, Rothenbacher D. Dyspeptic symptoms in middle-aged to old adults: the role of Helicobacter pylori infection, and various demographic and lifestyle factors. J Intern Med. 2002; 252:41–47.
Article
24. Stone MA, Barnett DB, Mayberry JF. Lack of correlation between self-reported symptoms of dyspepsia and infection with Helicobacter pylori, in a general population sample. Eur J Gastroenterol Hepatol. 1998; 10:301–304.
Article
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