The effect of topical clonidine on intraocular pressure.
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Adult↗
Biomedical subjects
M A Kass
Publications and source records attributed to M A Kass.
The effect of a generic drug law on the retail cost of antiglaucoma medications.
The passage of the Missouri generic drug law in 1979 did not increase the dispensing of generic antiglaucoma medications, nor did it reduce retail prices. In 1976 and in 1980, antiglaucoma medications purchased with generic prescriptions were no less expensive than medications purchased with brand-name prescriptions. Almost all generic prescriptions were filled with brand-name products. A wide range of prices (approximately twofold) was noted from pharmacy to pharmacy for each drug. The retail cost of antiglaucoma medication increased approximately 35% between March and April 1976 and July and August 1980. This was less than the increase in the Consumer Price Index for the urban United States during the same period.
Costs and Cost Analysis↗
Amorphous coating in open-angle glaucoma.
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Glaucoma↗
Acetazolamide and urolithiasis.
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Acetazolamide↗
Systemic factors in patients with low-tension glaucoma.
Nineteen patients (38 eyes) with low-tension glaucoma were compared with 53 subjects (106 eyes) with ocular hypertension. Comparable for age and sex, the 2 groups were assessed with respect to haematological and biochemical criteria, physical activity, and medical history. Statistical analyses of the differences between the 2 groups highlighted the importance of diastolic ophthalmodynamometry levels, prediagnosis exercise habits, cardiovascular disease status, and possibly systolic blood pressure. Patients with low-tension glaucoma suffered a higher prevalence of multiple abnormalities of these systemic factors than did their ocular hypertensive counterparts. There were no significant differences between the 2 groups with respect to the many other factors examined.
Adult↗
Flurbiprofen and intraocular pressure.
Systemic or topical administration of corticosteroids may produce a rise in intraocular pressure (IOP). Nonsteroidal anti-inflammatory drugs (NSAI drugs) are alternate therapy for ocular inflammatory disease. Flurbiprofen, a new NSAI drug, was tested in double-masked fashion to delineate its effect on IOP. Flurbiprofen did not alter IOP in known high corticosteroid responders nor did it block corticosteroid-induced ocular hypertension.
Adult↗
Prostaglandin and thromboxane synthesis by microsomes of inflamed rabbit ciliary body--iris.
Microsomes of albino rabbit ciliary body--iris were prepared 6 hr, 24 hr, 3 days, 7 days, and 28 days after intravitreal injection of 10 micrograms of Shigella endotoxin. The microsomal preparations were incubated for 15 min with [1-14C]arachidonic acid. Prostaglandin and thromboxane products (cyclo-oxygenase products) were identified by thin-layer chromatography and quantified by scintillation counting. Synthesis of prostaglandin F2 alpha (PGF2, PGD2, 6-keto-PGF1 alpha (a stable metabolite of PGI2) and thromboxane B2 (TXB2) (a stable metabolite of TXA2) was increased 24 hr, 3 days, and 7 days after endotoxin injection. The greatest increase was in TXB2 synthesis. Cyclo-oxygenase product synthesis returned to normal levels by 28 days. Ciliary body--iris microsomes prepared 15 min after paracentesis synthesized increased amounts of all cyclo-oxygenase products assayed, most notably TXB2 and PGE2. Ciliary body--iris microsomes from albino rabbit treated with topical 1% nitrogen mustard or pigmented rabbits treated with subcutaneous alpha-melanocyte--stimulating hormone (20 micrograms/kg) synthesized normal amounts of cyclo-oxygenase products.
Animals↗
Timolol and epinephrine: a clinical study of ocular interactions.
In a crossover design study, we assessed effects on intraocular pressure, pupillary diamter, pulse rate, and blood pressure over six hours of one drop of 0.5% timolol maleate and 2% epinephrine hydrochloride in one eye. Both eyes of each patient had been pretreated for one week with twice-daily applications pf epinephrine or timolol, respectively. In random sequence, 20 patients (40 eyes) participated in both phases of the study. Pretreatment with timolol significantly reduced the ocular hypotensive effect of epinephrine (from 15.3% to 4.6%); epinephrine pretreatment did not affect the pressure reduction of timolol. Pretreatment with timolol enhanced the mydriatic effect of epinephrine (from 35.8% to 71.9% pupillary dilation); pretreatment with epinephrine resulted in an apparent mydriatic effect for timolol.
Aged↗
Prognostic significance of optic disk cupping in ocular hypertensive patients.
The stereoscopic photographs of 102 patients with increased intraocular pressure (IOP) and normal visual fields were graded for cup:disk ratio. All patients were followed up for a five-year period, during which time 27 patients developed glaucomatous visual field loss and 75 patients did not. The patients who subsequently developed glaucomatous visual field loss had significantly larger cup:disk ratios than did the patients who did not develop glaucomatous visual field loss. Patients with a mean IOP greater than or equal to 28 mm Hg and a vertical contour cup:disk ratio greater than or equal to 0.6 had a 100% incidence of the development of glaucomatous visual field loss as compared to a 2% incidence in those with a mean IOP less than 28 mm Hg and a vertical cup:disk ratio less than 0.6. Disk:cup asymmetry and progressive increase in the area of the disk occupied by the cup was more common in the group that developed glaucomatous visual field loss.
Aged↗
Dipivefrin: current concepts.
Pro-drugs are agents that require biotransformation prior to exhibiting pharmacologic activity. Dipivefrin (dipivalyl epinephrine or DPE) is an epinephrine pro-drug produced by the addition of two pivalic acid groups to the parent compound. This creates a more lipophilic molecule which penetrates the cornea more readily than epinephrine. Enzymes in ocular tissues convert dipivefrin into its active form, epinephrine. In concentrations approximately one-tenth that of epinephrine, topically applied dipivefrin therefore produces: (1) similar intra-ocular concentrations of epinephrine; (2) similar reductions in intra-ocular pressure (IOP); (3) similar degrees of mydriasis; and (4) fewer extraocular and systemic side effects. For reasons that are discussed, dipivefrin should probably not be used in conjunction with anticholinesterases. Dipivefrin offers the same risk of cystoid macular oedema as does epinephrine. Dipivefrin is a safe, effective, and well-tolerated alternative to epinephrine in the treatment of elevated IOP. It is particularly useful for patients who cannot tolerate epinephrine.
Absorption↗
New broad spectrum anti-glaucoma drop.
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Glaucoma↗
Timolol plus maximum-tolerated antiglaucoma therapy.
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Adult↗
Timolol maleate: efficacy and safety.
A randomized, double-masked trial of various concentrations of timolol maleate ophthalmic solution (0.1%, 0.25%, 0.5%, and 1.0%) vs placebo demonstrated that all concentrations of timolol effectively lowered intraocular pressure (IOP). A 0.5% solution of timolol was as effective in reducing IOP as the 1.0% concentration. Blood pressure, visual acuity, and pupillary diameter were not altered significantly by any concentration of timolol tested during this study. There was a dose-dependent decrease in resting pulse rate with increasing concentrations of timolol. No objective signs of drug intolerance were found on external ocular examination, nor were any subjective symptoms elicited on questioning the subjects. Timolol applied topically twice daily in concentrations of 0.1% to 0.5% appeared to be an effective and safe ocular hypotensive agent.
Adult↗
Multivariate analysis of the risk of glaucomatous visual field loss.
In a retrospective study, 92 patients with ocular hypertension, ie, intraocular pressure of 21 mm Hg or higher, and no evidence of glaucomatous visual field defects, were observed for five years. Visual field defects developed in one or both eyes of 33 patients during the five-year follow-up period, while none were detected in the remaining 59. Values for suspected risk factors, determined at the outset of the follow-up period, were subjected to a multivariate analysis with use of linear discriminant analysis and a multiple logistic function. Models of risk providing maximum separation of the two patient groups (visual field loss vs no visual field loss) found that the risk factors having the greatest significance for prediction of visual field loss included vertical estimates of cup/disc ratio, mean IOP during the period of observation, a positive family history of glaucoma, and age. Factors having the lowest predictive values included IOP response to topical dexamethasone, plasma cortisol suppression, and a history of systemic hypertension.
Glaucoma↗
Dipivefrin and epinephrine treatment of elevated intraocular pressure: a comparative study.
Every 12 hours 0.1% dipivefrin was administered to one eye and 2% epinephrine hydrochloride was administered to the fellow eye of 42 patients with primary open-angle glaucoma or ocular hypertension in a randomized, double-masked study lasting three months. Dipivefrin produced similar percent reductions in intraocular pressure (18.6%) to epinephrine (21.0%), as well as similar increases in outflow facility and pupil diameter. A significantly lower incidence of burning and stinging after drug instillation was noted with dipivefrin therapy. This study supported the contention that dipivefrin is an effective and safe alternative to epinephrine therapy for the reduction of elevated intraocular pressure.
Adult↗
Efficacy and patient acceptance of pilocarpine gel.
Fifteen patients with symmetrically increased intraocular pressure (IOP) participated in a single-masked random 30-day clinical trial comparing 4% pilocarpine hydrochloride gel applied at bedtime to one eye with 4% pilocarpine hydrochloride drops instilled four times daily in the fellow eye. Both forms of pilocarpine reduced IOP significantly at 8 A.M., 12 noon, and 4 P.M. (P less than .01). At these times there was no significant difference in effect between the two forms of pilocarpine (P greater than .05). The mean IOP of eyes treated with gel showed no significant difference from the pretreatment value at 10 P.M. (P = .37), whereas at this time eyes treated with drops did maintain a significant IOP reduction (P = .02). At 10 P.M. pilocarpine drops reduced IOP significantly more than did pilocarpine gel (P = .002). Pupil diameter was affected by the gel and drops in a similar pattern to that of IOP. Patients tolerated the gel with few side effects and were pleased by the convenience of administration once daily.
Administration, Topical↗
Prostaglandin and thromboxane synthesis by microsomes of rabbit ocular tissues.
Microsomes of albino rabbit ocular tissues were incubated with (1-14C)-arachidonic acid for 15 min at 37 degrees C. Thin-layer chromatography revealed that ciliary body-iris microsomes were capable of synthesizing prostaglandin F2alpha (PGF2alpha), PGE2, PGD2, thromboxane B2(TXB2), and 6-keto-PGF1alpha. Indomethacin 14 micrometer in the incubation medium essentially abolished all prostaglandin synthesis detectable by this method. Imidazole 10 mM in the incubation medium inhibited only TXB2 synthesis. Ciliary body-iris microsomes were incubated for 2 min at 0 degrees C with PGH2. The products of this reaction were superfused over spiral strips of rabbit aorta and produced the strong contractions typical of TXA2. Addition to imidazole to the incubation medium blocked the formation of the contracting substance. Incubation of ciliary body-iris microsomes with (1-14C)--8,11,14-eicosatrienoic acid produced PGF1alpha, PGD1, and PGE1 but no evidence of any thromboxane product or 6-keto-PGF1alpha. Conjunctival and corneal microsomes synthesized prostaglandins, although less effectively than ciliary body-iris microsomes, when incubated with (1-14C)-arachidonic acid. Microsomes of sclera, retina-choroid, and lens synthesized little, if any, prostaglandins.
8,11,14-Eicosatrienoic Acid↗
Increased corneal thickness simulating elevated intraocular pressure.
A 17-year-old girl had intraocular pressure readings of 30 to 40 mm Hg in both eyes, with normal visual fields and optic nerve heads. Medical treatment was unsuccessful in lowering the IOP measurements substantially. The central corneal thickness was 0.90 mm in each eye in the absence of corneal edema. Cannulation of the left anterior chamber revealed an IOP of 11 mm Hg, while the Perkins' and Schiŏtz' tonometers gave readings of 35 and 34 mm Hg, respectively. Previously, elevated tonometry readings had been obtained by Goldmann's, Perkins', Schiŏtz', MacKay and Marg's, pneumatic tonometer and air puff tonometer. This suggested that measurement of central corneal thickness be performed in cases in which IOP recordings do not correspond to other clinical findings.
Adolescent↗