A comparative study of two methods of optic disc evaluation in patients of glaucoma.

INTRODUCTION: Glaucoma is a progressive disorder and requires serial evaluation in order to monitor disease progression and optimize therapy. OBJECTIVE: The objective of this study was to determine the correlation between each of cup/disc (C/D) ratio and the disc damage likelihood scale (DDLS) with retinal nerve fiber layer (RNFL) and global indices in Humphrey field analyzer II (HFA II). DESIGN: Cross-sectional study. MATERIALS AND METHODS: A total of 50 patients diagnosed with primary open angle glaucoma were examined to grade DDLS score and C/D ratio. The average (avg) RNFL was obtained using the Fast RNFL protocol on optical coherence tomography (OCT) (4.0.2 Carl Zeiss). HFA II Swedish Interactive Threshold Algorithm Standard 24-2 visual fields were obtained within 1 month of clinical examination. The correlation of C/D ratio with avg RNFL thickness, Mean deviation and Pattern standard deviation was calculated by Pearson correlation coefficient (r). Similar coefficients were obtained for DDLS. RESULTS: The P value for the difference in the r between C/D ratio with RNFL (-0.628) and DDLS with RNFL (-0.8369) was significant (P < 0.01) when correlation of C/D, DDLS with RNFL was considered. CONCLUSION: The DDLS shows stronger correlation with structural changes in OCT than C/D ratio. The disc diameter and rim width increases the value of clinical optic disc examination.

Acute primary angle closure in a patient with high myopia: a case report.

Primary angle closure in a high myopic patient is rare. Here is presented a report of one such patient who presented with acute primary angle closure in one eye. Conservative management followed by laser iridotomy was effective in the treatment of this patient.

A study on central corneal thickness and optic disc size in patients with primary open angle glaucoma.

The aim of the study was to evaluate a possible relationship between central corneal thickness (CCT) and optic disc area in patients with primary open angle glaucoma (POAG). Patients with POAG and age matched control group underwent routine ocular examination along with optic nerve head evaluation by Stratus optical coherence tomography (OCT) and CCT measurement by ultrasound pachymetry. Pearson's coefficient was calculated in both groups to find out correlation between these two parameters. In this series 90 eyes of 45 control subjects and 94 eyes of 47 POAG patients were studied. In the control group 40% were female, 60% male and among the POAG patients 34% female, 66% male. Mean CCT in control subjects was 566.98 micron (SD = 19.36, n = 90) and in POAG patients was 526.61 micron (SD = 29.93, n = 94). There was a significant difference in two groups (p = 0.0002). Disc area in control group had mean of 2.32mm(2) (SD = 0.305, n = 90) and in POAG group 2.982mm(2) (SD = 0.566, n = 94). Statistically significant difference was found among the two groups (p = 0.0). CCT was inversely correlated with optic disc size. In control subjects, r = -0.141, but it was not statistically significant (p = 0.092). In POAG group, r = -0.256 and the correlation was statistically significant (p = 0.0063). CCT was significantly less in POAG patients compared to control subjects. Mean disc area was significantly higher among the POAG group compared to control subjects. CCT was inversely correlated with disc area in both groups, but was statistically significant in POAG patients.

Primary role of CYP1B1 in Indian juvenile-onset POAG patients.

PURPOSE: CYP1B1, a member of the cytochrome P450 superfamily of enzymes, has been implicated in primary congenital glaucoma (PCG). Recent studies suggest a role of CYP1B1 in primary open-angle glaucoma (POAG) as a modifier locus. The purpose of the study was to further investigate the potential role of CYP1B1 in POAG patients. METHODS: Two hundred unrelated Indian POAG patients and 100 unrelated ethnically matched controls were enrolled in this study. The coding sequence of CYP1B1 was amplified by polymerase chain reaction (PCR) from genomic DNA, followed by direct DNA sequencing to identify the allelic variants. RESULTS: Six mutations were identified in nine patients and none of the controls examined. One novel mutation (R523T) was detected in the homozygous condition while three reported (W57C, E229K, and R368H) and two novel mutations (S515L and D530G) were found in the heterozygous state. The homozygous mutation of a conserved residue, detected in a familial juvenile onset POAG (JOAG) patient (lacking MYOC or OPTN mutations), cosegregated with the disease locus in an autosomal recessive mode of transmission. All the novel mutations (R523T, S515L and D530G) were detected in a region of CYP1B1 that did not harbor any of the 34 point mutations implicated in PCG. In addition, six previously reported (p.R48G, p.A119S, p.V432L, p.D449D, p.N453S, and 372-12C>T in intron 1) and four novel (p.V395V, p.P400P, p.V518A, and c.2016C>G in the 3'-UTR) single nucleotide polymorphism (SNPs) were also observed in POAG patients and controls. CONCLUSIONS: Our observation suggests that on rare occasions CYP1B1 may be primarily responsible for JOAG by possible monogenic association, and this observation emphasizes the importance of screening for mutation in this gene of JOAG patients that are determined not to harbor mutations in previously characterized candidate genes and loci for POAG.