Surgical result of pterygium extended removal followed by fibrin glue-assisted amniotic membrane transplantation.

BACKGROUND/PURPOSE: To report the recurrence rate and cosmetic results of conjunctival wound edge and caruncle, and complications after pterygium extended removal followed by fibrin glue-assisted amniotic membrane transplantation. METHODS: A prospective interventional cohort study enrolled 57 (58 eyes) patients undergoing pterygium extended removal followed by fibrin glue-assisted amniotic membrane transplantation. All patients received postoperative follow-up for at least 12 months. Recurrence rate was graded from 1 to 4, and cosmetic results of conjunctival edge and caruncle were graded from 1 to 5. RESULTS: The cohort included 48 eyes with nasal pterygium, 5 eyes with temporal pterygium, and 5 eyes with double pterygium. There were 81.0% (n=47), 0% (n=0), 12% (n=7), and 7% (n=4) of eyes with Grades 1-4 recurrence, respectively. The cosmetic results of conjunctival wound edge and caruncle in cases with nasal pterygium showed 59.3% (n=32), 14.8% (n=8), 9.3% (n=5), 16.6% (n=9), and 0% (n=0) of eyes with Grades 1-5 morphology, respectively. Overall, 5.1% (n=3), 3.4% (n=2), 3.4% (n=2), 3.4% (n=2), 1.7% (n=1), 6.9% (n=4), and 1.7% (n=1) of patients suffered from postoperative pyogenic granuloma, transient diplopia, permanent motility restriction, steroid glaucoma, fat prolapse, subamniotic membrane hemorrhage, and early detachment of amniotic membrane, respectively. CONCLUSION: Pterygium extended removal followed by fibrin glue-assisted amniotic membrane transplantation results in low recurrence, satisfactory cosmetic results and a low incidence of additional complications.

Macular thickness and aging in retinitis pigmentosa.

PURPOSE: This study was designed to analyze macular tomography in patients of different ages with retinitis pigmentosa (RP) and correlate their visual function with macular thickness, which was measured by optical coherence tomography. METHODS: In all, 75 RP patients and 75 controls were stratified into three age groups and macular thickness was measured by optical coherence tomography. The tomography was subdivided into three circular zones, four quadrants, and nine areas for analysis. Ophthalmic examinations, which involved ophthalmoscopic examinations, dark adaptation tests, visual acuities, visual field examinations, electrooculography, and color sense discrimination tests, were performed. RESULTS: Macular thickness of the RP patients decreased in the middle age group (45- to 55-year old), whereas the oldest group showed an increased thickness. The thickness of the outer inferior area remained virtually unchanged, whereas the thickness of the inner temporal area showed the most fluctuation with age. In terms of circular sections, the most dramatic changes in macular thickness were observed in the fovea, and the aging effect decreased outward to the outer ring. Furthermore, the thickness of the fovea was more important than the thickness of the inner ring and the outer ring for electrooculography, visual acuity, and color sense discrimination in RP patients. CONCLUSIONS: In middle age RP patients, the macular thickness decreased, whereas an increased thickness was observed in patients older than 55 years. In addition, the inner temporal area was the most fragile, and the outer inferior area was the least affected in patients with RP.

Examining rhodopsin retention in endoplasmic reticulum and intracellular localization in vitro and in vivo by using truncated rhodopsin fragments.

More than 100 mutations of rhodopsin have been identified to be associated with retinitis pigmentosa (RP), and mostly autosomal-dominant RP (ADRP). The majority of rhodopsin-associated ADRP is caused by protein misfolding and ER retention. In this study, we aimed to evaluate rhodopsin folding, exiting the ER and intracellular localization through expression of the rhodopsin fragments in COS-1 cells as well as in the transgenic zebrafish. We cloned human rhodopsin cDNA, which was then divided into the N-terminal domain, the C-terminal domain, and the fragment between the N- and C-terminal domains, and examine their intracellular expression in vitro and in vivo. We introduced a point mutation, either F45L or G51V, into this fragment and observed the intracellular localization of these mutants in COS-1 cells and in the zebrafish. The results revealed all of the truncated rhodopsin fragments except for the C-terminal domain and the full-length rhodopsin which had some plasma membrane localization, formed aggregates nearby or within the ER in COS-1 cells; however, the N-terminally truncated rhodopsin fragment, the C-terminal domain, and the full-length rhodopsin could traffic to the ROS in the zebrafish. Besides, the F45L mutation and the G51Vmutation in the rhodopsin fragment between the N- and C-terminal domains produced different effects on the aggresome formation and the intracellular distribution of the mutants both in vivo and in vitro. This current study provides new information about the mutant rhodopsin as well as in treatment of the RP in humans in the future.

A six-week, parallel, randomized, double-blind study comparing the efficacy and safety of the 0.5% timolol/2.0% MK-507 combination b.i.d. to the concomitant administration of 0.5% timolol b.i.d. and 2.0% MK-507 b.i.d.

This was a 6-week, parallel, randomized, double-blind study comparing the efficacy and safety of the 0.5% timolol/2.0% MK-507 combination b.i.d. to the concomitant administration of 0.5% timolol b.i.d. and 2.0% MK-507 b.i.d. Patients with ocular hypertension or open-angle glaucoma from 21 to 85 years of age were enrolled in this study. Each of them should have intraocular pressure (IOP) of 20 mmHg or more in the study eye after they completed the wash-out period. The patients enrolled were randomly assigned to either combination (0.5% timolol/2.0% MK-507 b.i.d. and placebo b.i.d.) or concomitant (0.5% timolol b.i.d. and 2.0% MK-507 b.i.d.) treatment. During the study, no systemic or topical medication affecting IOP other than test drugs were allowed. A total of 20 randomized patients were included in the intention-to-treat population for analysis of data. The ten were assigned to the combination treatment and others were assigned to the concomitant treatment. There was no statistically significant difference between the two study treatments in terms of gender distribution, average age, and average IOP at the trough and the peak before starting the test medications. Mean reduction of the IOP from baseline to the final visit at the trough was 5.04 mmHg in the combination treatment and was 2.73 mmHg in the concomitant treatment. Mean reduction of the IOP at the peak was 2.19 mmHg in the combination treatment and was 2.53 mmHg in the concomitant treatment. There were no statistically significant differences in the above analyses between the two treatments. Safety evaluation was carried out, and number of adverse events in each treatment group did not differ substantially. Ocular signs and symptoms were evaluated in each visit, and all of the between-treatment values were not different significantly, either. Laboratory tests were performed, and showed no significant differences between pre- and post-treatment periods. None of these was found to be clinically serious, either. We concluded that the 0.5% timolol/2.0% MK-507 combination b.i.d. is equivalent in the efficacy of lowering IOP as well as safety compared to the concomitant administration of 0.5% timolol b.i.d. and 2.0% MK-507 b.i.d. in patients with ocular hypertension or open-angle glaucoma.

The efficacy of brimonidine in preventing intraocular pressure elevation in the provocative test for primary angle-closure glaucoma.

The purpose of this study was to evaluate the efficacy of 0.2% brimonidine tartrate in preventing intraocular pressure (IOP) elevation in the dark-prone provocative test for primary angle-closure glaucoma (PACG). Twenty-two eyes from 22 patients with angle-closure glaucoma were enrolled in this study. Each of the selected eyes had previously tested positive in a recent dark-prone test. One drop of 0.2% brimonidine tartrate was then instilled in each eye 2 hours prior to a second dark-prone test. An IOP elevation of greater than 8 mmHg was regarded as a positive result. The IOP elevation in the first dark-prone test was 11.91 +/- 5.17 (range: 5.7 - 27.3) mmHg, while the IOP only increased 5.70 - 2.96 (range: 2.9 - 12.2) mmHg in the second dark-prone test that was pre-treated with 0.2% brimonidine tartrate (p < 0.001). A significant difference was also noted in the pre-test IOP (15.59 +/- 3.86 mmHg vs. 13.33 +/- 3.65 mmHg, p = 0.008) as well as in the post-test IOP (27.62 +/- 7.27 mmHg vs. 19.03 +/- 3.50 mmHg, p < 0.001) in the two sequential dark-prone tests. All but three of the initially positive dark-prone tests (86.46%) converted to negative tests after pre-treatment with brimonidine. There was a significant effect of 0.2% brimonidine tartrate in the prevention of IOP elevation in PACG patients previously found to test positive in the dark-prone provocative test.

Ocular hypotensive effect and safety of brinzolamide ophthalmic solution in open angle glaucoma patients.

BACKGROUND AND PURPOSE: Brinzolamide is a new topical carbonic anhydrase inhibitor for intraocular pressure (IOP) control. It has high inhibitory activity against human carbonic anhydrase II, which is the key isoenzyme regulating aqueous humor production. We conducted this study to compare the ocular hypotensive effect and safety of 1% brinzolamide versus that of 0.5% timolol twice daily. METHODS: In a double-masked design, 50 open angle glaucoma patients who had a baseline IOP between 20 to 30 mm Hg were randomized to receive either 1% brinzolamide ophthalmic solution or 0.5% timolol twice daily. After completing a 2-week pre-study screening period, patients were scheduled to receive 6 weeks of treatment. Visual acuity, IOP, slit-lamp biomicroscopy, corneal thickness, refraction status, blood pressure, heart rate, and treatment-related signs and symptoms were evaluated at follow-up visits. The eye selected for treatment was the one with the higher baseline IOP, or the right eye if the IOPs were the same in both eyes. The fellow eye served as control. RESULTS: 48 patients completed the study, and there were 24 patients in each group. A significant decrease in mean IOP was found after 6 weeks of treatment in both the brinzolamide group (-17.0%) and the timolol group (-19.7%), with no significant between-group difference in the control of IOP. The central corneal thickness of treatment eyes, measured by ultrasound pachometry, had not changed after 6 weeks of brinzolamide treatment. The study medications were generally well tolerated and no serious adverse reactions occurred during the 6-week study period. CONCLUSION: When used twice a day, topical brinzolamide is as effective as 0.5% timolol in lowering IOP in patients with open angle glaucoma.

Retinitis pigmentosa reduces the risk of proliferative diabetic retinopathy: a nationwide population-based cohort study.

PURPOSE: To study the association between retinitis pigmentosa (RP) and the progression of diabetic retinopathy (DR). METHODS: Using the Longitudinal Health Insurance Database 2000 of Taiwan, we identified individuals with an initial diagnosis for RP during the period of 1997-2008. A non-RP comparison group, 10-fold frequency matched by sex, age, index year and the year of diabetes diagnosed, were randomly selected from the same database. The occurrence of DR was observed for all subjects until the end of 2009. The Kaplan-Meier curves were used to illustrate the cumulative probability of developing DR for the RP group and comparison groups. The hazard ratio (HR) of DR for the RP group relative to the comparison group was estimated using Cox proportional hazards model after adjusting for potential confounders. RESULTS: The Kaplan-Meier curves were not statistically significant different between the RP group and the comparison group. However, the RP group had a higher cumulative probability of developing DR during the first six to seven years. The cumulative probability kept increasing and became higher in the comparison group but remained unchanged in the RP group. The HR for the RP patients comparing with the comparison group was 0.96 (95% confidence interval (CI) = 0.43-2.14). Stratified by severity, RP was associated with a non-statistically significant reduced risk of proliferative DR (PDR) (HR = 0.70, 95% CI = 0.16-3.14). The HR for non-proliferative DR (NPDR) was 1.08 (95% CI = 0.40-2.86). CONCLUSION: In this study, RP was not statistically significant associated with the incidence of DR.