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Biomedical subjects

M A Kass

Publications and source records attributed to M A Kass.

At least 19 recordsLinked to original sources

Gonioscopic ab interno laser sclerostomy. A pilot study in glaucoma patients.

PURPOSE: The purpose of this study is to evaluate the safety and efficacy of gonioscopic ab interno laser sclerostomy (GLS) in patients with glaucoma. METHODS: The technique of GLS involves iontophoresis of methylene blue dye (1%) at the limbus to focally dye the sclera and to provide subsequent delivery of 10-microsecond pulsed laser energy to the dyed area through a goniolens. The laser emits at 660 nm, a wavelength that is maximally absorbed by the methylene blue dye. Patients were evaluated for fistula formation, intraocular pressure (IOP) reduction, and adverse sequelae. Thirty-eight treatments were performed in 35 eyes. RESULTS: Successful complete sclerostomies were achieved in 21 eyes (55%), which was associated with an acute mean reduction in IOP of 23 mmHg. Mean preoperative IOP for all patients was 35 mmHg, and 1 hour after treatment it was reduced to 18.5 mmHg. In 4 of the 38 treatments, there was no acute IOP reduction, and these eyes were judged as failures. The mean follow-up time was 8.2 months with a maximum follow-up of 15 months. By 9 months, 50% of patients had an IOP of 22 mmHg or lower. The number of antiglaucoma medications decreased from 3.1 to 1.7 for all eyes over the 15-month follow-up period. Hyphemas (13%) were the only major complication, and these resolved spontaneously. In only one case did the IOP increase after the procedure. CONCLUSION: The results of this trial indicate that GLS is technically feasible, and preliminary results of IOP control are promising.

Adult

MK-507 versus sezolamide. Comparative efficacy of two topically active carbonic anhydrase inhibitors.

Topical carbonic anhydrase inhibitors MK-507 and sezolamide hydrochloride (previously known as MK-417) were compared in a double-masked, randomized, placebo-controlled study in 82 patients with bilateral primary open-angle glaucoma or ocular hypertension. MK-507 was given every 8 or 12 hours, sezolamide every 8 hours, or placebo every 8 or 12 hours for 4 days. Both drugs lowered intraocular pressure (IOP) substantially. MK-507 was somewhat more active than sezolamide, with a peak mean IOP reduction of 26.2% for MK-507 versus 22.5% for sezolamide, although the difference between the treatments was not statistically significant. These drugs may have potential in the treatment of glaucoma.

Administration, Topical

MK-927: a topical carbonic anhydrase inhibitor. Dose response and duration of action.

The dose response to a single topical administration of the carbonic anhydrase inhibitor MK-927 was investigated in 24 patients with primary open angle glaucoma or ocular hypertension. Three concentrations of MK-927 (2%, 1%, and 0.5%) and placebo were administered in a two-center, double-masked, randomized, placebo-controlled, four-period crossover study. MK-927 at the 0.5% concentration appeared to be minimally effective in reducing intraocular pressure. A single topical dose of 1% MK-927 resulted in a significantly greater percent reduction in intraocular pressure for up to 6 hours when compared with treatment with placebo. Similarly, a single dose of 2% MK-927 significantly lowered intraocular pressure for 8 hours compared with treatment with placebo. The pressure reduction from baseline measured 23.7% and 11.3% at 8 hours after instillation of a single drop of 2% MK-927. The medication was well tolerated and appeared to lower intraocular pressure in a dose-dependent fashion.

Adult

Steady-state pattern electroretinogram following long term unilateral administration of timolol to ocular hypertensive subjects.

To determine whether long-term reduction of intraocular pressure leads to a corresponding preservation of the pattern electroretinogram (PERG), PERGs were studied in 21 patients with ocular hypertension who had received unilateral timolol therapy for a minimum of 6 years. The mean difference in intraocular pressure (IOP) between the placebo-treated and the timolol-treated eyes (over 6 years) was 2.4 mm Hg. Steady-state PERGs (16.0 rps) were obtained simultaneously in both eyes of each patient, with four check sizes (0.25, 0.5, 1.0 and 2.0 degrees). Significant (p less than 0.05) steady-state PERG deficits (i.e., amplitude more than two standard deviations below the mean value of age-matched controls) were observed in 16 eyes of 12 patients (10 placebo-treated and 6 timolol-treated eyes). The mean PERG amplitude did not differ significantly between the placebo-treated and timolol-treated eyes. However, a significant correlation (r = -0.423) in the IOP differences between the placebo-treated and timolol-treated eyes and the corresponding PERG amplitude differences was noted in three of the four test conditions (i.e. 0.25, 0.5, and 1.0 degrees). These results suggest that reducing IOP may preserve ganglion cell function in some patients with ocular hypertension.

Aged

Transscleral neodymium: YAG laser cyclocoagulation for uncontrolled glaucoma.

To determine the efficacy and safety of the procedure, we reviewed the records of 25 eyes of 25 patients who had received noncontact transscleral Nd:YAG laser cyclocoagulation for a variety of uncontrolled glaucomas. Thirteen to 35 pulses (mean, 22.7 pulses) had been placed 1 mm to 2 mm behind the limbus with an energy per pulse of 3.4 J to 8.2 J (mean 4.5 J). Follow-up ranged from 6 months to 23 months, with the exception of one eye, which had to be enucleated. Nine of the 25 eyes (36%) required one or two repeat treatments. Twelve (48%) had intraocular pressures at last follow-up of less than 21 mm Hg but greater than 4 mm Hg. Ten eyes (40%) developed moderate to severe pain transiently, and 10 (40%) developed substantial, but transient, inflammation. Transscleral Nd:YAG laser cyclocoagulation appears to be relatively effective and well tolerated.

Adolescent

Topical timolol administration reduces the incidence of glaucomatous damage in ocular hypertensive individuals. A randomized, double-masked, long-term clinical trial.

We conducted a randomized, double-masked, long-term clinical trial to determine whether topical timolol therapy was effective in delaying or preventing the onset of glaucomatous damage in moderate-risk ocular hypertensive subjects. In 62 patients, one eye was chosen randomly to receive timolol therapy twice daily while the fellow eye received placebo. During the course of the study, the mean +/- SD difference in intraocular pressure between the timolol-treated and the placebo-treated eyes was 2.3 +/- 2.6 mm Hg. Reproducible visual field loss developed in 4 timolol-treated eyes and 10 placebo-treated eyes. Progressive optic disc cupping was noted in 4 timolol-treated and 8 placebo-treated eyes. Using a computerized image analysis system, the mean +/- SD increase in optic disc pallor during the course of the study was 0.86% +/- 2.4% in the timolol-treated eyes as opposed to 1.80% +/- 3.6% in the placebo-treated eyes. This study provides evidence that lowering intraocular pressure by medical treatment reduces the incidence of glaucomatous damage in ocular-hypertensive individuals.

Administration, Topical

Timolol treatment prevents or delays glaucomatous visual field loss in individuals with ocular hypertension: a five-year, randomized, double-masked, clinical trial.

A 5-year, randomized, double-masked, clinical trial was conducted to determine whether treatment with topical timolol maleate was effective in preventing or delaying the onset of glaucomatous visual field loss in subjects with ocular hypertension. Sixty-five individuals considered to be at moderate risk for developing open-angle glaucoma were recruited for the study. In each patient, one eye was chosen randomly to receive timolol twice-daily while the fellow eye received diluent (placebo). Timolol administration reduced IOP from baseline in the treated eyes over the course of the study by a mean +/- SD of 4.9 +/- 3.4 mm Hg. Timolol administration also produced a mean +/- SD contralateral reduction of IOP from baseline in the untreated fellow eyes of 2.9 +/- 3.1 mm Hg. The mean +/- SD difference in IOP between the treated and untreated eyes during the study was 2.3 +/- 2.6 mm Hg. Over the course of the study reproducible visual field loss developed in 4 timolol treated eyes and 10 placebo treated eyes (P = .039, McNemar test). Clinical progressive optic disc cupping was noted in four treated and eight untreated eyes (P = .11, McNemar test). In the 42 subjects who completed a minimum 4-year follow-up, baseline and final optic disc photographs were analyzed using a computer image analysis system to determine changes in the area of disc pallor. The mean +/- SD increase in optic disc pallor was 0.86% +/- 2.4% in the timolol treated eyes and 1.80% +/- 3.6% in the placebo treated eyes. This difference was statistically significant (P = .04, paired t-test). This study provides evidence that medical treatment prevents or delays the onset of glaucomatous visual field loss and optic disc damage in individuals with ocular hypertension. The magnitude of the protective effect of timolol was partially obscured by the contralateral reduction of IOP in the placebo treated fellow eyes.

Adult

Intraocular pressure response to topical dexamethasone as a predictor for the development of primary open-angle glaucoma.

In a retrospective study we reviewed the records of 788 subjects who had been corticosteroid tested with 0.1% dexamethasone four times daily to one eye for six weeks. All subjects had normal kinetic visual fields and optic nerve heads in both eyes at the time of testing and were followed up for a minimum of five years. Some subjects had normal baseline intraocular pressures whereas others were considered to have ocular hypertension. Of 276 individuals who were high corticosteroid responders (intraocular pressure greater than 31 mm Hg during dexamethasone administration), 36 (13.0%) developed glaucomatous visual field loss during the follow-up period. Only nine of 261 individuals (3.4%) who were intermediate responders (intraocular pressure 20 to 31 mm Hg during dexamethasone administration) and none of 251 individuals who were low responders (intraocular pressure less than 20 mm Hg during dexamethasone administration) developed glaucomatous visual field loss. However, the ability of the intraocular pressure response to dexamethasone to predict the development of glaucomatous visual field loss was not as good as the predictive power of a multivariate model that included patient age, race, baseline intraocular pressure, baseline outflow facility, baseline cup/disk ratio, and systemic hypertension.

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