At the present time,
corticosteroids are still the most effective class of drugs for the treatment of ocular
inflammation. However, since their prolonged use may result in severe ocular side effects, it would be therapeutically beneficial to develop nonsteroidal anti-inflammatory drugs that have similar or greater efficacy than
steroids, but do not share their ocular side effects. Several currently available non-steroidal drugs have been used clinically as prophylactic or therapeutic agents for the following: 1. Prevention of pupillary constriction during intraocular surgery (
cataract extraction). 2. Prevention of postoperative
inflammation, i.e., incidence of anterior chamber cellular reaction and aqueous flare (breakdown of blood-aqueous barrier) and IOP rise following
cataract surgery,
intraocular lens implantation, and
argon laser trabeculoplasty. 3. Prevention of
contact lens induced
corneal neovascularization. 4. Improvement of
lens opacity (
bendazac). 5. Prevention of
cystoid macular edema following intraocular surgery. Treatment over long-term period may be effective; postoperative treatment is ineffective. 6. Prevention of conjunctival
hyperemia. Some prophylactic ocular uses such as prevention of surgical
miosis or postoperative
fluorescein leakage have been reported to be successful. However, it is unclear whether the reported success reflected the pharmacological effects due to inhibition of the AA cascade - and hence, reflects the role of some
eicosanoids in surgical
miosis or postoperative
fluorescein leakage - or reflect the effects of these drugs on unexplored physiological or pharmacological mechanisms. For example, pretreatment with
flurbiprofen to prevent surgical
miosis was based on the assumption that PGs are potent miotic agents in all mammals, including humans. It remains to be established however, whether the small reduction in the extent of
pupillary miosis is due to prevention of PG synthesis by this
drug or to the prevention of the synthesis of other AA products, such as
prostacyclin and
thromboxane or possibly to some entirely different mechanism. Prevention of post-surgical
fluorescein leakage by prophylactic pre and/or post surgical treatment with a variety of
nonsteroidal anti-inflammatory agents is also assumed to be due to inhibition of intraocular PG synthesis, although the possibility that it is due to prevention of the synthesis of
prostacyclin or TxA2 has not been ruled out. Even more important, it has not been demonstrated that prevention of this post operative
fluorescein leakage reflects the prevention or inhibition of true CME and associated loss of visual acuity.(ABSTRACT TRUNCATED AT 400 WORDS)