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Gillian J McLellan, Allyson A Gosling, Julie A Kiland, Lauren E Rutkowski, Norman Matthew Ellinwood; Steroid-induced ocular hypertensive response in a spontaneous feline glaucoma model. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):3268.
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Increase in intraocular pressure (IOP) is a recognized adverse effect of sustained corticosteroid (CCS) therapy in susceptible individuals and steroid-induced ocular hypertension (SIOH) may ultimately cause glaucomatous damage. The purpose of our study was to determine the incidence and magnitude of the SIOH response in a spontaneous large animal glaucoma model.
5 cats with recessively inherited symmetric glaucoma, homozygous for a mutation in LTBP2, and 5 normal adult cats were used in this randomized study. IOP had been measured weekly in all cats at the same time each morning for at least 3mths prior to initiating the study. Over the course of the study, IOP was measured by a single, masked observer using rebound tonometry each morning, 5 days per week. One eye of each cat was randomly selected for treatment BID with a single drop of 0.1% dexamethasone alcohol solution for 4 wks, and then with 1% prednisolone acetate suspension for an additional 3wks. The contralateral eye was treated BID with balanced salt solution and served as a control. On conclusion of this treatment phase, IOP data were collected as above until a return to baseline was documented. A positive SIOH response was defined as a consistent >15% or >25% increase in IOP in the treated eye relative to the control eye over 2wks of the treatment phase in normal and glaucomatous cats, respectively.
Mean (SD) IOP was 31.4 (6.4)mmHg in LTBP2 mutant cats and 15.6(1.2)mmHg in normal cats in the pre-treatment phase. The SIOH response to CCS was highly variable between individuals. Response rate was higher in cats with pre-existing aqueous outflow abnormalities (4/5) than in normal cats (2/5). In normal cats, the increase in IOP was considered clinically insignificant (maximal increase relative to control eye = 6.4mmHg). In contrast, marked elevation in IOP (maximal increase= 56mmHg) was documented in glaucomatous cats. No difference in response rate or magnitude was observed between CCS treatments. IOP had returned to baseline values within 11 days.
Incidence rate and inter-individual variability in the SIOH response in cats is comparable to that seen in the human population and is accentuated in cats with pre-existing glaucoma. This spontaneous model represents a valuable opportunity to study the pathophysiological mechanisms responsible for differing susceptibility to SIOH and glaucoma.
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