Abstract
Purpose: :
The hormonal form of vitamin D - 1a,25-dihydroxyvitamin D3 (VitD) was found to target genes in rat intestinal mucosa known to be involved in IOP reduction. We determined if VitD can alter IOP in nonhuman primates and the mechanism for this effect.
Methods: :
Normotensive monkeys were treated topically twice daily with 0.1-15µg (5µl) VitD to one eye, vehicle (propylene glycol) to the opposite eye. IOP (Goldmann applanation tonometry) was measured hourly for 6 hrs or more on day 3, and, for the 5µg dose, after days 8 and 12. Pupil diameter, serum calcium, mean arterial pressure (MAP) and heart rate (HR) were also measured. Aqueous humor formation was measured on day 3 by fluorophotometry. Outflow facility was measured after a single intracameral bolus injection of 1µg VitD or after twice daily topical treatment with 5µg for 2 days followed by intracameral bolus injection of 1µg on day 3. Retinal electrophysiology testing (scotopic and photopic flash intensity series and PERG) was conducted on days 10 or 11 of the 5µg bid treatments beginning 2 hr after treatment.
Results: :
IOP decreased dose-dependently and often bilaterally on day 3 of bid topical treatment, with a maximum reduction of 30% lasting 1-4 hr. No further reduction in IOP was achieved with prolonged treatment. Biomicroscopic examination was unremarkable at any time-point following topical administration. Aqueous humor formation and outflow facility were unchanged. There were no effects on serum calcium, MAP, HR, or pupil diameter. Electrophysiology results were unchanged in VitD treated eyes compared to baseline prior to the first treatment.
Conclusions: :
VitD lowers IOP in monkeys but the mechanism of action remains to be elucidated. Prolonged treatment (12 days) did not produce systemic or ocular toxicity effects. VitD has potential for development as an antiglaucoma agent.
Keywords: intraocular pressure