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Journal ArticleDOI

Gastrointestinal toxicity of nonsteroidal antiinflammatory drugs.

TLDR
One hundred years have passed since Felix Hoffman reported the successful synthesis of acetylsalicylic acid as the first nonsteroidal antiinflammatory drug (NSAID) and numerous reports have corroborated this observation.
Abstract
One hundred years have passed since Felix Hoffman, working at Bayer Industries, reported the successful synthesis of acetylsalicylic acid as the first nonsteroidal antiinflammatory drug (NSAID).1,2 At the suggestion of Hermann Dreser, Bayer's chief pharmacologist at the time,3 the compound was called “aspirin” and was purported to represent a convenient mechanism for the delivery of salicylic acid in the treatment of rheumatic diseases, menstrual pain, and fever.2 Approximately 40 years elapsed before Douthwaite and Lintott4 provided endoscopic evidence that aspirin could cause gastric mucosal damage. Numerous reports have corroborated this observation,5–8 and the introduction of more potent agents . . .

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Citations
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Journal ArticleDOI

Oxidative Stress: An Essential Factor in the Pathogenesis of Gastrointestinal Mucosal Diseases

TL;DR: Unraveling the signaling events initiated at the cellular level by oxidative free radicals as well as the physiological responses to such stress is important to better understand disease pathogenesis and to develop new therapies to manage a variety of conditions for which current therapies are not always sufficient.

Guidelines for the management of rheumatoid arthritis: 2002 Update

TL;DR: The guideline reviewed in this month’s column describes the recommended care of patients who have been previously diagnosed with RA.
Journal ArticleDOI

Peptic ulcer disease

TL;DR: This work focuses on this revolution of understanding and management of peptic ulcer disease over the past 25 years, largely because of the increasingly widespread use of non-steroidal anti-inflammatory drugs (NSAIDs) and low-dose aspirin.
References
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Journal ArticleDOI

Up-regulation of cyclooxygenase 2 gene expression in human colorectal adenomas and adenocarcinomas

TL;DR: COX-2, but not COX-1, gene expression is markedly elevated in most human colorectal cancers compared with accompanying normal mucosa, and COx-2 expression seems to be increased in a subset of adenomas.
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Human cyclooxygenase-2 cDNA.

TL;DR: High-level induction of the hCox-2 transcript in mesenchymal-derived inflammatory cells suggests a role in inflammatory conditions and demonstrates that the Cox enzyme is encoded by at least two genes that are expressed and differentially regulated in a variety of cell types.
Journal ArticleDOI

Nitric oxide activates cyclooxygenase enzymes

TL;DR: It is demonstrated that NO enhances COX activity through a mechanism independent of cGMP and suggested that, in conditions in which both the NOS and COX systems are present, there is an NO-mediated increase in the production of proinflammatory prostaglandins that may result in an exacerbated inflammatory response.
Journal ArticleDOI

Systemic biosynthesis of prostacyclin by cyclooxygenase (COX)-2: the human pharmacology of a selective inhibitor of COX-2.

TL;DR: In this paper, the effects of celecoxib on indices of COX-1-dependent platelet thromboxane (Tx) A2 and on systemic biosynthesis of prostacyclin in vivo were examined.
Journal ArticleDOI

Differential inhibition of prostaglandin endoperoxide synthase (cyclooxygenase) isozymes by aspirin and other non-steroidal anti-inflammatory drugs.

TL;DR: Results demonstrate that the two PGH synthases are pharmacologically distinct and indicate that it may be possible to develop isozyme-specific cyclooxygenase inhibitors useful both for anti-inflammatory therapy and for delineating between the biological roles of the P GH synthase isozymes.
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