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Abstract #19114 Published in IGR 3-1
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 K; Ota I; Ibaraki N; Akura J; Ichihashi S; Shibuya Y; Maekubo K; Miyake SArchives of Ophthalmology 2001; 119: 387-394
OBJECTIVE: To investigate the effects of timolol maleate with preservative and its preserved (PV) and non-preserved vehicles (NPV) (benzalkonium chloride) on the blood-aqueous barrier and angiographic cystoid macular edema (CME) in early postoperative pseudophakia. PATIENTS AND METHODS: Patients with ocular hypertension, normal tension glaucoma, and primary open-angle glaucoma who underwent surgery for cataracts. The study included a double-masked trial for timolol, PV, and NPV and a single-masked trial on the effect of diclofenac sodium and fluorometholone acetate on all three. The patients were divided into six groups, each of which were simultaneously administered the following different combinations of compounds: timolol and diclofenac (group A), timolol and fluorometholone (group B), PV and diclofenac (group C), PV and fluorometholone (group D), NPV and diclofenac (group E), and NPV and fluorometholone (group F). The six groups were then compared using a laser flare cell meter to determine the degree of disruption of the blood-aqueous barrier and fluorescein angiography to investigate angiographic CME. The differences in mean daily fluctuations in intraocular pressure were compared on the preoperative baseline day and for five weeks postoperatively. Twice daily administration of 0.5% timolol maleate or the vehicles was started two days before surgery, and continued until five weeks after surgery. Diclofenac or fluorometholone drops were instilled in the eyes four times preoperatively, on the day of surgery, and three times daily for five weeks postoperatively. RESULTS: The flare amount was higher on the third and seventh days in group B than in group D, but was the same after the seventh day. The incidence of angiographic CME was the same between both groups. These two factors were significantly lower in group F. These two factors were also significantly lower in the three groups that received diclofenac instead of fluorometholone, with no difference among these groups. The intraocular pressure decline was significant in groups that received timolol compared with groups that received PV or NPV. CONCLUSIONS: Timolol and its preservative, benzalkonium chloride, cause disruption of the blood-aqueous barrier in early postoperative pseudophakia and increased incidence of angiographic CME. The concurrent administration of nonsteroidal anti-inflammatory drug such as diclofenac prevents these adverse effects without interfering with the drop in intraocular pressure caused by timolol. The addition of benzalkonium chloride to timolol contributes considerably to these adverse effects. CLINICAL RELEVANCE: The present results suggest the cause of similar complications produced by other anti-glaucoma eyedrops containing similar preservatives.
Dr K. Miyake, Shohzankai Medical Foundation, Miyake Eye Hospital, 1070-Kami 5, Higashiozone-cho, Nagoya 462-0823, Japan
Classification:
11.3.4 Betablocker (Part of: 11 Medical treatment > 11.3 Adrenergic drugs)
