Related Experiment Videos

Comparative incidence of upper gastrointestinal bleeding associated with individual non-steroidal anti-inflammatory

M J Llorente Melero1, J M Tenías Burillo, A Zaragoza Marcet

  • 1Unit of Rheumatology, Lluís Alcanyís Hospital, Xátiva, Valencia, Spain. JOTEBU@mail.ono.es

Abstract

Insights

Choosing nonsteroidal anti-inflammatory drugs (NSAIDs) with preferential cyclo-oxygenase-2 (COX-2) inhibition can significantly reduce the risk of upper gastrointestinal bleeding (UGIB). This study highlights the varying GI toxicity among NSAIDs, emphasizing COX-2 preferential agents for safer use.

Area of Science:

  • Pharmacology
  • Gastroenterology
  • Clinical Medicine

Background:

  • Cyclo-oxygenase (COX) exists in two isoforms: COX-1 and COX-2.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibiting COX-1 are associated with gastrointestinal (GI) damage.
  • NSAIDs with a higher COX-2/COX-1 inhibition ratio may offer reduced GI toxicity.

Purpose of the Study:

  • To compare the incidence of upper gastrointestinal bleeding (UGIB) across specific NSAIDs.
  • To evaluate the role of "COX-2 preferential" inhibitors in mitigating GI toxicity.

Main Methods:

  • An observational study estimating NSAID-related UGIB incidence over four years.
  • Data collected from UGIB cases, NSAID sales, and community dosage information.
  • Rate ratios (RR) and 95% confidence intervals (CI) calculated, referencing NSAIDs with the lowest UGIB incidence.

Main Results:

  • UGIB incidence varied significantly among thirteen NSAIDs, ranging from 1.7 to 25.8 per 1,000 person-years.
  • "COX-1 preferential" inhibitors showed a 5.3 times higher RR of UGIB compared to "COX-2 preferential" inhibitors.
  • NSAIDs with "COX-1-COX-2 mixed" inhibition had a 2.2 times higher RR of UGIB.

Conclusions:

  • Significant differences in GI toxicity exist among specific NSAIDs.
  • Utilizing NSAIDs with "COX-2 preferential" inhibition could lead to a substantial decrease in UGIB cases.
  • This suggests a safer therapeutic approach by selecting NSAIDs with a favorable COX-2/COX-1 inhibition profile.

Related Concept Videos

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab (Humira),...
Drugs for Treatment of Ulcerative Colitis in IBD01:29

Drugs for Treatment of Ulcerative Colitis in IBD

Ulcerative colitis is a chronic inflammatory condition primarily affecting the colon and rectum. The primary drugs used in the treatment of ulcerative colitis are aminosalicylates. They exhibit anti-inflammatory and immunosuppressive properties. They modulate inflammatory mediators and inhibit the activity of nuclear factor κB (NF-κB). Aminosalicylates also reduce inflammation by inhibiting prostaglandin and leukotriene production and decreasing neutrophil chemotaxis and superoxide generation. 
Peptic Ulcer Disease IV: Management01:26

Peptic Ulcer Disease IV: Management

Medical treatment strategies for peptic ulcers encompass various methods. The primary goal of treatment is to diminish gastric acidity and strengthen mucosal defense mechanisms.
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current medication...
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...
Peptic Ulcer Disease III: Clinical Manifestations and Complications01:25

Peptic Ulcer Disease III: Clinical Manifestations and Complications

Duodenal UlcersDuodenal ulcers are the most common form of peptic ulcer disease, presenting with chronic, intermittent epigastric pain. Pain typically appears 2–3 hours after meals, especially when the stomach is empty, often waking patients at night. It is characteristically relieved by food or antacids (“pain–food–relief”). Some patients remain asymptomatic until complications like bleeding or perforation emerge, particularly with NSAID or anticoagulant use.Gastric UlcersGastric ulcers share...