 |
|
Latanoprost Accelerates Disruption of the Blood-Aqueous Barrier and the Incidence of Angiographic Cystoid Macular Edema in Early Postoperative Pseudophakias
Kensaku Miyake, MD;
Ichiro Ota, MD;
Kumiko Maekubo, MD;
Satomi Ichihashi, MD;
Sampei Miyake, MD
Arch Ophthalmol. 1999;117:34-40.
Objective To study the effect of latanoprost, a prostaglandin analog, on the blood-aqueous barrier and angiographic cystoid macular edema (CME) formation in early postoperative pseudophakias.
Patients and Methods Included in the study were eyes with ocular hypertension, normal-tension glaucoma, or primary open-angle glaucoma undergoing surgery for cataract. The study consisted of a randomized double-masked trial for latanoprost and an open-label controlled trial for determining the effects of diclofenac sodium or fluorometholone eyedrop use on latanoprost or its placebo. We compared 4 groups of eyes with concurrent application of latanoprost and diclofenac (group A), latanoprost and fluorometholone (group B), latanoprost placebo and diclofenac (group C), and latanoprost placebo and fluorometholone (group D). A laser flare cell meter was used to determine the severity of blood-aqueous barrier disruption, and fluorescein angiography was performed to determine angiographic CME formation. Mean diurnal intraocular pressure differences were compared on the preoperative baseline day and in the fifth postoperative week. Latanoprost (0.005%) or its placebo was given once a day starting 2 days before surgery until the fifth postoperative week. Diclofenac or fluorometholone eyedrops were given 4 times a day before surgery on the day of surgery and 3 times a day until the fifth postoperative week.
Results In group B compared with group D, the amount of flare 3 days and 1 and 2 weeks after surgery and the incidence of angiographic CME in the fifth postoperative week were significantly higher. These 2 factors were significantly higher in group B than in group A (P<.05) and in group D than in group C (P<.01). There was no significant difference in these factors between groups A and C. The intraocular pressure decline was significant in groups A and B compared with groups C and D (P<.05), but there was no significant difference between groups A and B and between groups C and D.
Conclusions Latanoprost therapy enhances disruption of the blood-aqueous barrier and increases the incidence of angiographic CME formation in early postoperative pseudophakias. Because administration of nonsteroidal eyedrops such as diclofenac seems to prevent the adverse effects of latanoprost therapy while maintaining its effect to lower intraocular pressure, we suggest their concurrent application.
From the Shohzankai Medical Foundation, Miyake Eye Hospital, Nagoya, Japan. The authors do not have any commercial interest in the products mentioned in the article.
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
|
Use of ocular hypotensive prostaglandin analogues in patients with uveitis: does their use increase anterior uveitis and cystoid macular oedema?
Chang et al.
Br. J. Ophthalmol. 2008;92:916-921.
ABSTRACT
| FULL TEXT
Blood-Aqueous Barrier Changes After the Use of Prostaglandin Analogues in Patients With Pseudophakia and Aphakia: A 6-Month Randomized Trial
Arcieri et al.
Arch Ophthalmol 2005;123:186-192.
ABSTRACT
| FULL TEXT
Human Lens Epithelial Cell Damage and Stimulation of Their Secretion of Chemical Mediators by Benzalkonium Chloride Rather Than Latanoprost and Timolol
Goto et al.
Arch Ophthalmol 2003;121:835-839.
ABSTRACT
| FULL TEXT
Effect of non-steroidal anti-inflammatory ophthalmic solution on intraocular pressure reduction by latanoprost
Kashiwagi and Tsukahara
Br. J. Ophthalmol. 2003;87:297-301.
ABSTRACT
| FULL TEXT
Enhanced Disruption of the Blood-Aqueous Barrier and the Incidence of Angiographic Cystoid Macular Edema by Topical Timolol and Its Preservative in Early Postoperative Pseudophakia
Miyake et al.
Arch Ophthalmol 2001;119:387-394.
ABSTRACT
| FULL TEXT
Latanoprost May Trigger the Biosynthesis of Endogenous Prostaglandins in Early Postoperative Pseudophakias
Camras and Miyake
Arch Ophthalmol 1999;117:1265-1266.
FULL TEXT
|
