Korean J Gastroenterol.  2016 Jun;67(6):300-312. 10.4166/kjg.2016.67.6.300.

Nonsteroidal Anti-inflammatory Drug and Aspirin-induced Peptic Ulcer Disease

• Shim YK
• Kim N

• KMID: 2307756
• DOI: http://doi.org/10.4166/kjg.2016.67.6.300

Abstract

Despite decreasing Helicobacter pylori prevalence, the prevalence of peptic ulcer disease is increasing in the aged population, mainly due to increasing use of NSAIDs to manage pain and inflammation. In addition, low dose aspirin is employed as an anti-coagulant for those who have suffered or are at high risk of ischemic stroke and cardiovascular disease. However, NSAIDs and aspirin are injurious to mucosa of stomach and duodenum. NSAID-induced inhibition of mucosal prostaglandin synthesis is thought to be a major mechanism of gastrointestinal mucosal injury. The proportion of elderly has increased rapidly in Korea, with the proportion over 65 years old expected to be 24.3% in 2030. In this higher-risk population, the strategy to reduce the incidence of NSAID-related peptic ulcers and complications such as bleeding, obstruction and perforation is very important. Proton pump inhibitors (PPIs) with cyclooxygenase-2 inhibitor can be used for reducing the risk of NSAID-related ulcers and upper gastrointestinal (GI) complications. However, continuous use of PPI has several problems. In addition, NSAID-related problems in the lower GI tract have increased, in contrast to the decrease of NSAID-related upper GI disease. The aim of this review is to provide an evidence-based knowledge regarding the mechanism, complications of treatment, and prevention strategies for NSAID- or aspirin-related peptic ulcer disease in Korea.

Keyword

Non-steroidal anti-inflammatory agents; Aspirin; Peptic ulcer

MeSH Terms

Aged
Anti-Inflammatory Agents, Non-Steroidal
Aspirin
Cardiovascular Diseases
Cyclooxygenase 2
Duodenum
Helicobacter pylori
Hemorrhage
Humans
Incidence
Inflammation
Korea
Lower Gastrointestinal Tract
Mucous Membrane
Peptic Ulcer*
Prevalence
Proton Pump Inhibitors
Stomach
Stroke
Ulcer
Anti-Inflammatory Agents, Non-Steroidal
Aspirin
Cyclooxygenase 2
Proton Pump Inhibitors

Figure

• 

  Fig. 1. Two related isoforms of the COX and LOX enzyme pathway and the role of non-steroidal anti-inflammatory drug (NSAID). COX-1 is expressed constitutively. It regulates normal cellular processes such as gastric cytoprotection, vascular homeostasis, platelet aggregation, and kidney function. COX-2 is increased during states of inflammation or in response to mitogenic stimuli. Nonselective NSAID inhibits the COX-1 and COX-2 pathways. Selective COX-2 NSAIDs inhibit only the COX-2 pathway. When COX-1 and COX-2 are inhibited, its inhibitor, 5-LOX enzyme, is more activated and LTB4, C4 and D4 are more induced. COX, cylcooxygenase; PG, prostaglan-din; TX, thromboxane; LOX, lipoxyge-nase; LT, leukotriene; GI, gastrointestinal.

• 

  Fig. 2. Algorithm for long-term NSAID therapy according to a patient's gastrointestinal (GI) and cardiovascular (CV) risk factors. ASA, aspirin; ns-NSAID, non-specific NSAID; PPI, proton pump inhibitor. Adapted from the article of Scarpignato et al.81 (BMC Med 2015;13:55).

Reference

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