This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Citing articles on Web of Science (9)  • Contact me when this article is cited  Related Content  • Similar articles in JAMA  Social Bookmarking   What's this?

Robert F. Willkens, MD

JAMA. 1978;240(15):1632-1635.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

NONSTEROIDAL anti-inflammatory agents take their origin in antiquity, and despite their extensive proliferation, they remain empirical forms of therapy. The inflammatory reaction, once remembered by students of pathophysiology as a tetrad of Greek terms, is now defined as a series of interacting biochemical pathways that include inflammatory mediators, the complement cascade, the coagulation intermediates, and fixed and migrating reactive cells. The aim of treatment with anti-inflammatory agents as such is to control rather than eliminate the inflammatory response. Where the stimulus, or provocation, is recognized, it becomes relatively easy to turn off this reaction. Similarly, when a specific mediator or cell can be identified, such as histamine or the mast cell, agents directed at these elements of inflammation can intercept and modify the harmful effects of this reaction. Unfortunately, most of the disorders for which anti-inflammatory agents are useful have undefined causes, and treatment is directed at the overall response . . . [Full Text PDF of this Article]

Author Affiliations
From the Department of Medicine, Harborview Medical Center, University of Washington, Seattle.

Footnotes
Reprint requests to Department of Medicine, Harborview Medical Center, University of Washington, 325 Ninth Ave, Seattle, WA 98104 (Dr Willkens).

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?