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Glaucoma Incidence and Treatment From the Association for Research in Vision and Ophthalmology (ARVO) Annual Meeting, Fort Lauderdale, Florida, USA, 29 April - 4 May 2001 Acute Angle Closure Glaucoma in Singapore Dr Friedman presented data from the Singapore Case-control Study of Acute Angle Closure Glaucoma. In this study, performed to identify new risk factors for acute angle closure glaucoma, the contra-lateral eyes of 65 patients with acute angle closure glaucoma presenting to the Singapore National Eye Center from March 1999 to November 2000 were examined. Detailed slit lamp, ultrasound biomicro-scopy, and Scheimpflug evaluations were performed. 220 population-based controls, frequency-matched for age and sex, were examined using the same techniques. Provocative tests, including repeat testing in a dark room and after administration of pilocarpine were also performed. The mean anterior chamber depth was 2.6 mm for controls versus 1.9 mm for patients (p < 0.001). Limbal anterior chamber depth (van Herick) demonstrated moderate screening effectiveness with more than 90% sensitivity and 60% specificity using a cut off of one-quarter corneal thickness. The ultrasound biomicroscopy angle measurements were all significantly less for patients than for controls (p < 0.001), but none had ideal screening characteristics. Scheimpflug measurement of the angle clearly separated patients from controls, with the best images occurring after pilocarpine instillation. Scheimpflug imaging is a quick and easily performed test that distinguishes the contralateral eyes of individuals with acute angle closure glaucoma from healthy eyes. Pilocarpine provocative tests may further improve the performance of Scheimpflug imaging. Finally, traditional measures of anterior chamber depth and limbal anterior chamber depth also distinguished patients from controls. Dr Friedman concluded that a screening strategy that combines a simplified examination of the limbal anterior chamber depth with a Scheimpflug assessment of the angle may allow for large-scale screening without a slit lamp.
Incidence of Open Angle Glaucoma in Melbourne A random cluster of 3271 participants (83% of eligible residents) aged 40 years or older were examined to determine the incidence of open angle glaucoma in Melbourne, Australia. Baseline examinations were conducted from 1992 to 1994 and follow-up data were collected from 1997 to 1999. Each participant underwent a standardised ophthalmic examination, including intra-ocular pressure measurements, visual fields, cup disc ratios, and paired stereo photographs of the optic disc, both at baseline and at follow-up. Glaucoma was assessed by a consensus group of 6 ophthalmologists, including 2 glaucoma specialists. Glaucoma was diagnosed as possible, probable, or definite. The overall incidence of probable and definite open angle glaucoma was 0.95% (95% CL, 1.55, 3.59) and any open angle glaucoma was 2.57% (95% CL, 0.60, 1.30). The incidence of glaucoma increased significantly with increased age (p < 0.001). The incidence of probable and definite glaucoma increased from 0% of partici-pants aged 40 to 49 years to 5.5% of participants aged 80 years and older. The incidence of any type of glaucoma increased from 0.3% of participants aged 40 to 49 years to 11% of participants aged 80 years and older. There was no relationship with gender. In Conclusion The incidence of open angle glaucoma increases significantly with age. Glaucoma is a major cause of visual loss and will become more important as the population ages and the number of elderly people increase.
Molecular Genetic Basis of Primary Congenital Glaucoma in India Dr Panicker presented a study to determine the possible molecular genetic defects underlying primary congenital glaucoma in India and to identify the pathogenic mutations causing this type of childhood blindness. Five consanguineous pedigrees with a clinically well characterised primary congenital glaucoma phenotype were recruited for genetic study. Leukocyte DNA was obtained from patients and controls and the coding regions of the primary candidate gene CYP1B1 were screened for mutations using polymerase chain reaction followed by direct sequencing, and sequence and restriction fragment analyses. Five distinct mutations were found in the coding regions of CYP1B1 gene in 8 affected members of 5 consanguineous pedigrees, of which 3 were novel. These included novel frameshift, missense, and known mutations. The frameshift mutation was homozygous, whereas the missense mutations were either homozygous or heterozygous. All are disease-causing mutations since all mutant alleles cosegregated with disease phenotype absent in the healthy population, and mutant residues were conserved. Based on 4 novel restriction enzyme assays, the segregation of mutant alleles in pedigrees and the healthy population were determined. Sequence alignment indicated conservation of mutated residues. Pseudo-dominant inheritance was noted in 1 family, whereas the other families showed an autosomal recessive mode of inheritance. A frameshift mutation identified by Dr Panicker and colleagues resulted in one of the most devastating primary con-genital glaucoma phenotypes known to date. In addition, several polymorphisms of this gene were found, one of which is novel. In Summary This is the first report describing the primary genetic defect underlying primary congenital glaucoma in India. Novel mutations identified in India will help in the under-standing of the molecular pathogenesis of this disorder. Novel diagnostic methods are helpful for fast mutation detection, carrier testing, and genetic counselling for at-risk individuals, and also for population screening. The data derived from this study may help in developing genotype-phenotype correlation.
Risk Factors for Progression of Ocular Hypertension to Primary Open Angle Glaucoma As a multifactorial disease, glaucoma may be associated with pressure-dependent and pressure-independent factors. Ocular hypertension may develop into primary open angle glaucoma (POAG) in many patients. Dr Landers described a study comparing patients with ocular hypertension with patients with POAG for pressure-dependent and pressure-independent risk factors. A high prevalence of any factor(s) could indicate a contribution to the pro-gression from ocular hypertension to POAG. 438 patients with POAG and with 301 with ocular hypertension were randomly selected and data on age and intraocular pressure at the time of diagnosis, gender, family history of glaucoma, systemic hypertension, diabetes, Raynaud's phenomenon, migraine, and myopia were collected. Multivariate analysis showed that older age at the time of diagnosis (¿2 = 73.10; 5 df; p < 0.001), myopia (odds ratio [OR], 1.5 [1.02 - 2.2]; p < 0.05), family history of glaucoma (OR, 1.6 (1.1 - 2.3); p < 0.01), and a high intraocular pressure (¿2 = 13.55; 4 df; p = 0.009) were found to be more prevalent among patients with POAG. No other significant differences could be found between the 2 groups. In Conclusion Patients with ocular hypertension may be at higher risk of developing POAG if they have myopia, a family history of glaucoma, or are of older age at the time of diagnosis.
Influence of Latanoprost on Aqueous Humor Flow Dr Vobig described a randomised double-masked clinical study of 42 eyes of 21 patients with primary open angle glaucoma and ocular hypertension. Fluorophotometry and pneumotonography were performed to investigate the effect of latanoprost 0.005% or placebo on aqueous humor flow and total outflow facility in glaucomatous eyes. Patients were given either latanoprost or placebo once in the evening. Fluorophoto-metry (Fluorotron Master II, Ocumetrics, USA) and pneumotonography (Model 30 Classic Pneumatonometer, Mentor, USA) was performed in 20 eyes of 10 patients (latanoprost group) and 22 eyes of 11 patients (placebo group). Patients with an intraocular pressure (IOP) higher than 28 mm Hg at baseline were excluded. Fluorophotometry, tonography, and IOP were measured at baseline and after 1 and 2 weeks of treatment. Data for right and left eyes were separately analysed using the student's paired t test. All patients com-pleted the protocol and IOP significantly decreased by 25% after 2 weeks' treatment with latanoprost (p < 0.01; Table 1). Fluorophotometry measurements showed no difference in aqueous flow over time in both groups. However, the total outflow facility increased significantly in the latanoprost-treated eyes after 2 weeks (p = 0.03; Table 1). Table 1. Reduction in intraocular pressure and increase in total outflow facility from baseline for patients receiving latanoprost for 2 weeks.
In Conclusion In accordance with the literature, Dr Vobig and colleagues found a mean 25% decrease in IOP after 2 weeks' treatment with latano-prost. The significant increase in total outflow facility in the latanoprost-treated eyes and the decrease in IOP took place at constant aqueous flow rates. Dr Vobig concluded that the decrease in IOP with latanoprost therapy is due to an increase in uveoscleral outflow.
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