Nonsteroidal Anti-inflammatory Drugs and Abdominal Pain

Abstract

1. David N. Collier, MD, PhD 1. Brody School of Medicine at East Carolina University Greenville, NC 1. Cassie Billings, PharmD 1. Pitt County Memorial Hospital Greenville, NC Acute Renal Failure Associated with Non-Steroidal Anti-Inflammatory Drugs in Healthy Children. Krause I, Cleper R, Einstein B, Davidovits M. Pediatr Nephrol. 2005;20 :1295– 1298[OpenUrl][1][CrossRef][2][PubMed][3] Analgesic-antipyretic and Anti-inflammatory Agents and Drugs Employed in the Treatment of Gout. In: Hardman JG, Limbird LE, Gilman AG, eds. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 10th ed. New York, NY: McGraw-Hill; 2001:687– 731 Non-steroidal Anti-inflammatory Drugs and Exacerbations of Asthma in Children. Body R, Potier K. Emerg Med J. 2004;21 :713– 724[OpenUrl][4][Abstract/FREE Full Text][5] The Effectiveness of Five Strategies for the Prevention of Gastrointestinal Toxicity Induced by Non-steroidal Anti-inflammatory Drugs: Systematic Review. Hooper L, Brown TJ, Elliot RA, et al. BMJ. 2004;329 :948[OpenUrl][6][Abstract/FREE Full Text][7] The Safety of Acetaminophen and Ibuprofen Among Children Younger Than Two Years Old. Lesko SM, Mitchell AA. Pediatrics. 1999;104 :e39[OpenUrl][8][Abstract/FREE Full Text][9] Nonsteroidal anti-inflammatory drugs (NSAIDs) are a chemically heterogeneous group of compounds that have analgesic, antipyretic, and anti-inflammatory properties. These effects are mediated primarily through inhibition of the cyclooxygenase enzymes (COX-1 and COX-2), which are involved in the production of prostaglandins (PGs) and thromboxanes (TXs). The COX-1 isoform is produced constitutively in a variety of tissues and organs, including the kidney, vascular endothelium, and gastric mucosa. In many tissues, expression of the COX- 2 isoform is induced by inflammatory mediators, but COX-2 also is produced constitutively in the brain, uterus, and kidneys. PGI2 and prostaglandins of the E family (PGEs) reduce the pain threshold of nociceptors, resulting in hyperalgia (the sensitization of afferent nerve endings to the effects of mechanical or chemical stimulation). 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