Abstract:
:The high concentrations of pro-inflammatory prostaglandins (PGs) produced in the joint during the initial stage of inflammation can be decreased by inhibiting their biosynthesis with nonsteroidal anti-inflammatory drugs (NSAIDs). The commonly encountered gastrointestinal intolerance in human subjects treated with NSAIDs is generally attributed to inhibition of PG synthesis in gastric mucosa, where the natural role of locally biosynthesized PGs is to protect the mucosa from necrosis upon exposure to noxious agents. The action of an ideal NSAID should therefore be tissue specific, i.e., it should inhibit PG formation at the sites of inflammation but not in gastric mucosa, where PGs are needed for cytoprotection. We believe that etodolac, a new, structurally distinct NSAID, meets this criterion, inhibiting PG synthesis in a tissue-specific fashion. Experimental data supporting this interpretation were obtained in rats by demonstrating that daily administration of orally effective anti-inflammatory doses of etodolac had no significant effect on gastric mucosal PGE2 or prostacyclin levels (measured as the stable metabolite, 6-keto-PGF1 alpha). In contrast, naproxen, piroxicam, and aspirin caused a statistically significant PG depletion. The results obtained in rats thus support the view that the favorable gastrointestinal safety profile of etodolac in human patients may be attributable to selective sparing of the cytoprotective PGs in gastric mucosa.
journal_name
Clin Rheumatoljournal_title
Clinical rheumatologyauthors
Dvornik D,Lee DKdoi
10.1007/BF02214106subject
Has Abstractpub_date
1989-03-01 00:00:00pages
16-24eissn
0770-3198issn
1434-9949journal_volume
8 Suppl 1pub_type
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journal_title:Clinical rheumatology
pub_type: 杂志文章,评审
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pub_type: 临床试验,信件
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pub_type: 杂志文章,meta分析
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pub_type: 杂志文章,已发布勘误
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journal_title:Clinical rheumatology
pub_type: 杂志文章
doi:10.1007/s10067-004-0937-0
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journal_title:Clinical rheumatology
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journal_title:Clinical rheumatology
pub_type: 信件
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journal_title:Clinical rheumatology
pub_type: 杂志文章
doi:10.1007/BF02031970
更新日期:1990-06-01 00:00:00
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journal_title:Clinical rheumatology
pub_type: 杂志文章
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更新日期:1995-07-01 00:00:00
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pub_type: 杂志文章
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