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Lee M. Jampol, MD; Shelly Jain; Bogdan Pudzisz; Robert N. Weinreb, MD

Arch Ophthalmol. 1994;112(7):891-894.

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

Prostaglandins ARE 20-carbon metabolites of arachidonic acid that are biosynthesized by ocular tissues and are involved in human intraocular inflammation.¹ They are released in response to ocular trauma, including surgery.² When released in large concentrations following trauma, intraocular surgery, or in association with uveitis, they may contribute to the disruption of the blood-aqueous barrier, miosis, and cystoid macular edema (CME). By inhibiting the cyclooxygenase pathway of prostaglandin biosynthesis, a major metabolic pathway of arachidonic acid, nonsteroidal antiinflammatory drugs (NSAIDs) may be useful in patients undergoing cataract surgery.³ Inhibitors of the lipoxygenase pathway, another major pathway of arachidonic acid metabolism, also are being evaluated.

The US Food and Drug Administration (FDA) has approved several topical NSAIDs, each primarily a cyclooxygenase inhibitor, for clinical use in ophthalmology, but these approvals have been limited solely to specific indications. For example, flurbiprofen sodium (Ocufen) and suprofen (Profenal) are only approved for . . . [Full Text PDF of this Article]

Author Affiliations
Chicago, Ill; San Diego, Calif

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