NSAIDs and the gastrointestinal tract

Abstract

NSAIDs incur significant gastrointestinal (GI) side effects. The complication risk increases with history of peptic ulcer or older age. Helicobacter pylori infection and cardioprotective aspirin have independent and additive risks in the presence of NSAID use. NSAID enteropathy is increasingly recognized. Cardiovascular and GI risk stratification and H. pylori infection testing should be done before initiating NSAIDs. An NSAID combined with a proton pump inhibitor (PPI) is comparable to cyclooxygenase (COX)-2 inhibitors for gastroprotection, but for high-risk patients, COX-2 plus PPI should be considered. Aspirin and COX-2 inhibitors are associated with reduced colon adenoma risk, but higher dose and longer duration of treatment with aspirin appears effective. Hence, patients at high risk of colorectal cancer (with significant family or personal history of premalignant adenoma) must be identified, and cardiovascular and GI risk must be assessed before using these agents as chemopreventive drugs.

Etiological factors of duodenal and gastric ulcers

“…Meta-analyses have shown that Hp eradication therapy was effective for healing and prevention of recurrence of PUs in Hp-positive patients and that treatment of Hp infection was more effective than antisecretory non-eradicating therapy (with or without long-term maintenance therapy) in preventing recurrent bleeding (15). Hp eradication has been associated with decreased risk of gastric cancer in patients with PUD (16). In our study, Hp was also correlated with inflammatory activity.…”

Targeting specific cell signaling transduction pathways by dietary and medicinal phytochemicals in cancer chemoprevention

“…The intake of non-steroidal anti-inflammatory drugs (NSAIDs) correlated with a reduced incidence of oesophagus, colon and rectum, stomach cancer (Langman et al, 2000;Reddy et al, 1996;Steinbach et al, 2000). NSAIDs have shown undisputable promise as chemopreventive agents, however major concerns over their cardiovascular toxicity, gastrointestinal side effects, liver and renal adverse effects (Bresalier et al, 2005;Gupta and Eisen, 2009;Knights et al, 2009;Nussmeier et al, 2005, Solomon et al, 2005Ulrich et al, 2006) have shifted interest on natural inflammatory agents that can reverse/and or halt the process of carcinogenesis with limited cytotoxicity ( Table 2). The implication of inflammatory processes and oxidative stress on carcinogenesis indicate the therapeutic benefit of natural anti-inflammatory agents which exert their activity mostly through the antioxidative property.…”

The Etiological Factors of Duodenal and Gastric Ulcers

“…The risk is increased with older age and history of PUD. Helicobacter pylori infection and cardioprotective acetylsalicylic acid have additive risks in the presence of NSAID use (16). The development of PUD was observed earlier in the combined H pylori and NSAID group than in patients with only NSAID use and this suggests a synergic effect between the two risks factors in the development of PUD (3).…”