Gastrointestinal effects of nonsteroidal anti-inflammatory therapy

Jeffrey Raskin

Research output: Contribution to journalArticle

116 Citations (Scopus)

Abstract

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed for the treatment of many conditions including rheumatoid arthritis, osteoarthritis, gouty arthritis, the joint and muscle discomfort associated with systemic lupus erythematosus, and other musculoskeletal disorders. Yet, their benefits, which are believed to be a result of their ability to inhibit cyclooxygenase-2 (COX-2), are accompanied by considerable toxicity. NSAIDs' untoward effects are attributed to their inhibition of the constitutively expressed enzyme cyclooxygenase-1 (COX-1), with attendant suppression of the synthesis of prostanoids, substances that mediate key homeostatic functions. Side effects include suppression of hemostasis through inhibition of platelet aggregation, adverse effects in patients with heart failure and cirrhosis, and those with certain renal diseases, as well as complicating antihypertensive therapies involving diuretics or β-adrenoceptor blockade. Perhaps most importantly, NSAIDs disrupt the gastrointestinal mucosal- protective and acid-limiting properties of prostaglandins, frequently leading to upper gastrointestinal erosions and ulceration, with possible subsequent hemorrhage and perforation. These complications can be reduced through identification of patients at risk, with circumspect use of NSAIDs, careful functional monitoring, and, in the case of gastrointestinal toxicity, co- administration of such agents as misoprostol or omeprazole. However, these strategies introduce complexity into the treatment paradigm. Moreover, side effects and adverse events may be significantly reduced through the use of COX-2-specific inhibitors, new agents that alleviate pain and inflammation without the liability for adverse events caused by COX-1 inhibition.

Original languageEnglish
JournalAmerican Journal of Medicine
Volume106
Issue number5 B
DOIs
StatePublished - May 31 1999

Fingerprint

Anti-Inflammatory Agents
Cyclooxygenase 1
Prostaglandins
Gouty Arthritis
Pharmaceutical Preparations
Gastrointestinal Agents
Misoprostol
Aptitude
Omeprazole
Cyclooxygenase 2 Inhibitors
Cyclooxygenase 2
Therapeutics
Hemostasis
Platelet Aggregation
Diuretics
Osteoarthritis
Systemic Lupus Erythematosus
Adrenergic Receptors
Antihypertensive Agents
Rheumatoid Arthritis

ASJC Scopus subject areas

  • Nursing(all)

Cite this

Gastrointestinal effects of nonsteroidal anti-inflammatory therapy. / Raskin, Jeffrey.

In: American Journal of Medicine, Vol. 106, No. 5 B, 31.05.1999.

Research output: Contribution to journalArticle

@article{6b476a4604bf4d52b2ade2b14873ca4f,
title = "Gastrointestinal effects of nonsteroidal anti-inflammatory therapy",
abstract = "Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed for the treatment of many conditions including rheumatoid arthritis, osteoarthritis, gouty arthritis, the joint and muscle discomfort associated with systemic lupus erythematosus, and other musculoskeletal disorders. Yet, their benefits, which are believed to be a result of their ability to inhibit cyclooxygenase-2 (COX-2), are accompanied by considerable toxicity. NSAIDs' untoward effects are attributed to their inhibition of the constitutively expressed enzyme cyclooxygenase-1 (COX-1), with attendant suppression of the synthesis of prostanoids, substances that mediate key homeostatic functions. Side effects include suppression of hemostasis through inhibition of platelet aggregation, adverse effects in patients with heart failure and cirrhosis, and those with certain renal diseases, as well as complicating antihypertensive therapies involving diuretics or β-adrenoceptor blockade. Perhaps most importantly, NSAIDs disrupt the gastrointestinal mucosal- protective and acid-limiting properties of prostaglandins, frequently leading to upper gastrointestinal erosions and ulceration, with possible subsequent hemorrhage and perforation. These complications can be reduced through identification of patients at risk, with circumspect use of NSAIDs, careful functional monitoring, and, in the case of gastrointestinal toxicity, co- administration of such agents as misoprostol or omeprazole. However, these strategies introduce complexity into the treatment paradigm. Moreover, side effects and adverse events may be significantly reduced through the use of COX-2-specific inhibitors, new agents that alleviate pain and inflammation without the liability for adverse events caused by COX-1 inhibition.",
author = "Jeffrey Raskin",
year = "1999",
month = "5",
day = "31",
doi = "10.1016/S0002-9343(99)00112-6",
language = "English",
volume = "106",
journal = "American Journal of Medicine",
issn = "0002-9343",
publisher = "Elsevier Inc.",
number = "5 B",

}

TY - JOUR

T1 - Gastrointestinal effects of nonsteroidal anti-inflammatory therapy

AU - Raskin, Jeffrey

PY - 1999/5/31

Y1 - 1999/5/31

N2 - Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed for the treatment of many conditions including rheumatoid arthritis, osteoarthritis, gouty arthritis, the joint and muscle discomfort associated with systemic lupus erythematosus, and other musculoskeletal disorders. Yet, their benefits, which are believed to be a result of their ability to inhibit cyclooxygenase-2 (COX-2), are accompanied by considerable toxicity. NSAIDs' untoward effects are attributed to their inhibition of the constitutively expressed enzyme cyclooxygenase-1 (COX-1), with attendant suppression of the synthesis of prostanoids, substances that mediate key homeostatic functions. Side effects include suppression of hemostasis through inhibition of platelet aggregation, adverse effects in patients with heart failure and cirrhosis, and those with certain renal diseases, as well as complicating antihypertensive therapies involving diuretics or β-adrenoceptor blockade. Perhaps most importantly, NSAIDs disrupt the gastrointestinal mucosal- protective and acid-limiting properties of prostaglandins, frequently leading to upper gastrointestinal erosions and ulceration, with possible subsequent hemorrhage and perforation. These complications can be reduced through identification of patients at risk, with circumspect use of NSAIDs, careful functional monitoring, and, in the case of gastrointestinal toxicity, co- administration of such agents as misoprostol or omeprazole. However, these strategies introduce complexity into the treatment paradigm. Moreover, side effects and adverse events may be significantly reduced through the use of COX-2-specific inhibitors, new agents that alleviate pain and inflammation without the liability for adverse events caused by COX-1 inhibition.

AB - Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed for the treatment of many conditions including rheumatoid arthritis, osteoarthritis, gouty arthritis, the joint and muscle discomfort associated with systemic lupus erythematosus, and other musculoskeletal disorders. Yet, their benefits, which are believed to be a result of their ability to inhibit cyclooxygenase-2 (COX-2), are accompanied by considerable toxicity. NSAIDs' untoward effects are attributed to their inhibition of the constitutively expressed enzyme cyclooxygenase-1 (COX-1), with attendant suppression of the synthesis of prostanoids, substances that mediate key homeostatic functions. Side effects include suppression of hemostasis through inhibition of platelet aggregation, adverse effects in patients with heart failure and cirrhosis, and those with certain renal diseases, as well as complicating antihypertensive therapies involving diuretics or β-adrenoceptor blockade. Perhaps most importantly, NSAIDs disrupt the gastrointestinal mucosal- protective and acid-limiting properties of prostaglandins, frequently leading to upper gastrointestinal erosions and ulceration, with possible subsequent hemorrhage and perforation. These complications can be reduced through identification of patients at risk, with circumspect use of NSAIDs, careful functional monitoring, and, in the case of gastrointestinal toxicity, co- administration of such agents as misoprostol or omeprazole. However, these strategies introduce complexity into the treatment paradigm. Moreover, side effects and adverse events may be significantly reduced through the use of COX-2-specific inhibitors, new agents that alleviate pain and inflammation without the liability for adverse events caused by COX-1 inhibition.

UR - http://www.scopus.com/inward/record.url?scp=0033620703&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033620703&partnerID=8YFLogxK

U2 - 10.1016/S0002-9343(99)00112-6

DO - 10.1016/S0002-9343(99)00112-6

M3 - Article

C2 - 10390123

AN - SCOPUS:0033620703

VL - 106

JO - American Journal of Medicine

JF - American Journal of Medicine

SN - 0002-9343

IS - 5 B

ER -