Two-Year Clinical Results After Selective Laser Trabeculoplasty for Normal Tension Glaucoma.
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ABSTRACT:
SUBMITTER: Lee JWY
PROVIDER: S-EPMC4915851 | biostudies-other | 2015 Jun
REPOSITORIES: biostudies-other
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Project description:This article aims to investigate the clinical results at 2 years after selective laser trabeculoplasty (SLT) for normal tension glaucoma (NTG). This prospective cohort study recruited NTG patients taking antiglaucoma medication. Subjects were excluded if they had previous glaucoma surgery/laser or corneal pathologies. All subjects underwent a 1-month washout. A single session of SLT was performed to 360° of the trabecular meshwork. Medication was resumed at 1 month to achieve a targeted 30% intraocular pressure (IOP) reduction from the post-washout/pre-SLT IOP. IOP was measured every 3 months and medication use was recorded at 3, 6, 12, and 24 months. Subjects with a secondary SLT or cataract extraction were excluded from IOP and medication analyses. At 24 months, 34 of the initial 45 right eyes were eligible for analyses. There were significant IOP reductions at all time intervals (except at 1 week) following SLT when compared to the prestudy (without medication) or pre-SLT (post-washout) IOP (P < 0.0001). Medications were likewise significantly reduced at all time intervals following SLT (P < 0.0001). At 24 months, the IOP was 11.5% lower than the prestudy IOP, 22.0% lower than the pre-SLT IOP, and medication use was reduced by 41.1% (P < 0.0001). Six out of 45 eyes (13.3%) required a secondary SLT. Absolute success (IOP reduction >20% from pre-SLT, without medication) was achieved in 11.1% (5/45). Reductions in IOP and medication use were evident at 2 years following SLT for the treatment of NTG whereas 11% remained medication free.The Clinical Trials Register of the University of Hong Kong HKCTR1847. The European Clinical Trials Database 2014-003305-15 (August 11, 2014).
| S-EPMC4616563 | biostudies-literature
Project description:BackgroundNormal tension glaucoma (NTG) is commonly treated with anti-glaucoma medications. Recently, selective laser trabeculoplasty (SLT) has been demonstrated to lower the intraocular pressure (IOP) and medication use in NTG. The purpose of this study was to investigate the efficacy of a single session of SLT for NTG at 1 year.MethodsThis prospective cohort study recruited NTG patients taking anti-glaucoma medication. Potential subjects were excluded if they had had previous glaucoma surgery or laser and also if intraocular surgery or additional SLT procedures were performed after the first treatment. All subjects underwent a 1-month washout. A 30% IOP reduction was set as the target IOP. A single session of SLT was performed to 360 degrees of the trabecular meshwork. At 1-month after SLT, medication was resumed to achieve the target IOP. The IOP was measured every 3 months, and the number of medications was recorded at 3, 6, and 12 months. Only the right eye was used for statistical analysis.ResultsIn 41 right eyes, the mean pre-study IOP was 14.3 ± 3.4 mmHg while on 1.5 ± 0.8 eye drops. The post-washout IOP was 16.2 ± 2.2 mmHg. A mean of 191.1 ± 26.3 SLT shots at 1.0 ± 0.07 mJ were applied. There was significant IOP reduction at all time intervals following SLT when compared to the post-washout IOP (P < 0.0001). The number of medications was significantly reduced at all time intervals following SLT when compared to the pre-study level (P < 0.0001). At 12 months, the mean IOP was 12.2 ± 2.2 mmHg while on 1.1 ± 0.9 eye drops.ConclusionsA single session of SLT for NTG achieved an additional 15% IOP reduction while using 27% less medication at 1 year compared to pre-study levels.Trial registrationThe Clinical Trials Register of the University of Hong Kong HKCTR1847 The European Clinical Trials Database 2014-003305-15 (August 11, 2014) ( https://www.clinicaltrialsregister.eu/ctr-search/search?query=2014-003305-15 ).
| S-EPMC4417344 | biostudies-literature
Project description:Normal-tension glaucoma (NTG) is a multifactorial optic neuropathy which, similar to open-angle glaucomas, is characterized by progressive retinal ganglion cell death and glaucomatous visual field loss. The major distinction of NTG from open-angle glaucomas is that the intraocular pressure (IOP) does not exceed the normal range. Missing the major risk factor and target of therapy, the elevated IOP, NTG poses a clinical challenge. Several insightful reviews have been published on the pathophysiology of NTG describing the possible underlying mechanisms. The current literature available also suggests that a significant percentage of patients with NTG (as high as 21%) have a family history of glaucoma, indicating a genetic predisposition to the disease. These facts strengthen the indication that NTG remains an enigmatic process. The aim of this review was to summarize the vascular, mechanical and genetic components considered to be responsible for NTG development and to discuss the mechanisms through which they are involved in the pathogenesis of NTG.
| S-EPMC6307418 | biostudies-literature
Project description:Normal-tension glaucoma (NTG) is a common cause of vision loss.To investigate the role of TANK binding kinase 1 (TBK1) gene duplications in NTG to gain insights into the causes of glaucoma that occurs at low intraocular pressure (IOP).In this multicenter case-control study, we investigated patients who met the criteria for NTG, including glaucomatous optic neuropathy, visual field defects, and maximum recorded untreated IOP of 21 mm Hg or less, and matched controls. Participants (N?=?755) were recruited from Southampton, United Kingdom (180 patients and 178 controls), Rochester, Minnesota (65 patients and 12 controls), New York, New York (96 patients and 16 controls), and Iowa City, Iowa (208 controls).Detection of TBK1 gene duplications and comparison of the extent of the identified DNA that is duplicated with prior TBK1 copy number variations associated with NTG.A TBK1 gene duplication was detected in 1 of 96 patients (1.0%) from New York and none of the controls. Analysis of duplication borders with comparative genome hybridization demonstrated that this patient has a novel duplication that has not been previously reported. No gene duplications were detected in any of the other cohorts of patients or controls.Duplication of the TBK1 gene is a rare cause of NTG. The identification of another case of NTG attributed to TBK1 gene duplication strengthens the case that this mutation causes glaucoma.
| S-EPMC4372533 | biostudies-literature
Project description:Importance:Mutations in the myocilin (MYOC) gene are the most common molecularly defined cause of primary open-angle glaucoma that typically occurs in patients with high intraocular pressures (IOP). One MYOC mutation, p.Gln368Ter, has been associated with as many as 1.6% of primary open-angle glaucoma cases that had a mean maximum recorded IOP of 30 mm Hg. However, to our knowledge, the role of the p.Gln368Ter mutation in patients with normal-tension glaucoma (NTG) with an IOP of 21 mm Hg or lower has not been investigated. Objective:To evaluate the role of the p.Gln368Ter MYOC mutation in patients with NTG. Design, Setting, and Participants:In this case-control study of the prevalence of the p.Gln368Ter mutation in patients with NTG, cohort 1 was composed of 772 patients with NTG and 2152 controls from the United States (Iowa, Minnesota, and New York) and England and cohort 2 was composed of 561 patients with NTG and 2606 controls from the Massachusetts Eye and Ear Infirmary and the NEIGHBORHOOD consortium. Genotyping was conducted using real-time polymerase chain reaction that was confirmed with Sanger sequencing, the imputation of genome-wide association study data, or an analysis of whole-exome sequence data. Data analysis occurred between April 2007 and April 2018. Main Outcomes and Measures:Comparison of the frequency of the p.Gln368Ter MYOC mutation between NTG cases and controls with the Fisher exact test. Results:Of 6091 total participants, 3346 (54.9%) were women and 5799 (95.2%) were white. We detected the p.Gln368Ter mutation in 7 of 772 patients with NTG (0.91%) and 7 of 2152 controls (0.33%) in cohort 1 (P = .03). In cohort 2, we detected the p.Gln368Ter mutation in 4 of 561 patients with NTG (0.71%) and 10 of 2606 controls (0.38%; P = .15). When the cohorts were analyzed as a group, the p.Gln368Ter mutation was associated with NTG (odds ratio, 2.3; 95% CI, 0.98-5.3; P = .04). Conclusions and Relevance:In cohorts 1 and 2, the p.Gln368Ter mutation in MYOC was found in patients with IOPs that were 21 mm Hg or lower (NTG), although at a frequency that is lower than previously detected in patients with higher IOP. These data suggest that the p.Gln368Ter mutation may be associated with glaucoma in patients with normal IOPs as well as in patients with IOPs that are greater than 21 mm Hg.
| S-EPMC6512256 | biostudies-literature
Project description:ImportanceGlaucoma has been dichotomically classified as open or closed angle, and accordingly, distinct therapies have been administered. In this study, the issue of narrow-angle normal-tension glaucoma (NTG), which may be an intermediate-stage or hybrid-stage disease entity, was addressed.ObjectiveTo determine whether anterior chamber (AC) angle width plays any role in NTG progression.Design, setting, and participantsRetrospective analysis of prospectively collected data at Seoul National University Hospital between January 2004 and December 2009. Fifty-two eyes of narrow-angle NTG and 52 wide-angle NTG eyes matched for age, untreated intraocular pressure, and mean deviation of visual field. Nonindentation gonioscopy was used to grade AC angles: narrow angle was defined as a partially invisible (invisible in ≥90° and <180°) pigmented posterior trabecular meshwork, and wide angle was defined as a fully visible pigmented posterior trabecular meshwork. Data were analyzed in September 2017.Main outcomes and measuresOptic disc/retinal nerve fiber layer defect and visual field progression.ResultsOf the narrow-angle NTG cohort, the mean (SD) age was 49.5 (9.1) years and 15 individuals (28.8%) were women; of the wide-angle NTG cohort, the mean (SD) age was 48.7 (9.5) years and 19 (36.5%) were women. All participants were Korean. Over the course of the mean (SD) 7.6 (0.4)-year follow-up period, 25 of 52 narrow-angle eyes (48.1%) and 13 of 52 wide-angle eyes (25.0%) showed structural progression (odds ratio [OR], 2.78; 95% CI, 1.21-6.37; P = .02). Meanwhile, 21 of 52 narrow-angle eyes (40.3%) and 9 of 52 wide-angle eyes (17.3%) showed functional progression (OR, 3.24; 95% CI, 1.31-8.00; P = .009). The cumulative probability of both structural and functional progression was significantly greater in the narrow-angle than in the wide-angle group (mean [SD] 5-year survival rates, 0.56 [0.07] vs 0.83 [0.05]; P = .006 and 0.60 [0.07] vs 0.87 [0.05]; P = .007, respectively). The baseline diurnal intraocular pressure's SD was approximately 1.38-times greater in the narrow-angle than in the wide-angle group (1.8 [0.6] vs 1.3 [0.3] mm Hg; mean difference, 0.52; 95% CI, 0.32-0.72; P < .001). For the follow-up intraocular pressure fluctuation, the narrow-angle group showed an approximately 1.75-times greater SD (2.1 [0.5] vs 1.2 [0.3] mm Hg; mean difference, 0.93; 95% CI, 0.77-1.09; P < .001).Conclusions and relevanceNarrow-angle NTG showed a greater probability of disease progression than did wide-angle NTG. Further studies determining whether augmented or differentiated treatment strategies would be beneficial for patients with narrow-angle NTG are warranted.
| S-EPMC6439780 | biostudies-literature
Project description:Although primary open-angle glaucoma (OAG) generally occurs in older individuals and manifests in eyes with elevated intraocular pressure (IOP), it may also occur in young patients or in eyes with an IOP that always measures within the statistically normal range. Recent advances in optical coherence tomography angiography have enabled noninvasive visualization of the vasculature around the optic disc. In this study, we investigated the clinical features of young Korean patients with OAG and compared the peripapillary vessel density of patients with normal-tension glaucoma (NTG) to those with high-tension glaucoma (HTG). The peripapillary vessel density was reduced in eyes with HTG compared with that in normal subjects (HTG: 23.18?±?2.06% vs. normal subjects: 24.74?±?1.88%, P value?=?0.013). In contrast, the peripapillary vessel density of eyes with NTG was comparable with that of normal eyes (NTG: 23.98?±?2.30% vs. normal subjects: 24.74?±?1.88%, P value?=?0.505). These findings suggest that young patients with HTG show greater peripapillary microvascular attenuation than healthy subjects or young patients with NTG, indicating that different levels of the initial untreated IOP may have different effects on the peripapillary vessel density in young patients with OAG.
| S-EPMC6914787 | biostudies-literature
Project description:Duplication of the TBK1 gene is associated with 1-2% of normal tension glaucoma, a common cause of vision loss and blindness that occurs without grossly abnormal intraocular pressure. We generated a transgenic mouse that has one copy of the human TBK1 gene (native promoter and gene structure) incorporated into the mouse genome (Tg-TBK1). Expression of the TBK1 transgene in the retinae of these mice was demonstrated by real-time PCR. Using immunohistochemistry TBK1 protein was predominantly localized to the ganglion cell layer of the retina, the cell type most affected by glaucoma. More intense TBK1 labelling was detected in the retinal ganglion cells (RGCs) of Tg-TBK1 mice than in wild-type littermates. Tg-TBK1 mice exhibit the cardinal sign of glaucoma, a progressive loss of RGCs. Hemizygous Tg-TBK1 mice (with one TBK1 transgene per genome) had a 13% loss of RGCs by 18 months of age (P?=?1.5 × 10-8). Homozygous Tg-TBK1 mice had 7.6% fewer RGCs than hemizygous Tg-TBK1 mice and 20% fewer RGCs than wild-type mice (P?=?1.9 × 10-5) at 6 months of age. No difference in intraocular pressures was detected between Tg-TBK1 mice and wild-type littermates as they aged (P?>?0.05). Tg-TBK1 mice with extra doses of the TBK1 gene recapitulate the phenotype of normal tension glaucoma in human patients with a TBK1 gene duplication. Together, these studies confirm the pathogenicity of the TBK1 gene duplication in human glaucoma and suggest that excess production of TBK1 kinase may have a role in the pathology of glaucoma.
| S-EPMC6075615 | biostudies-literature
Project description:ObjectivesTo evaluate the association between serum retinol concentration and normal-tension glaucoma (NTG).MethodsA total of 345 study subjects were recruited in a prospective cross-sectional study: 101 patients with NTG, 106 patients with high-pressure primary open-angle glaucoma (POAG) and 138 healthy control subjects. Serum retinol concentration in fasting blood samples was determined by ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). All study subjects were given complete ophthalmic examinations and diagnosed by two glaucoma sub-specialists.ResultsSerum retinol concentrations in NTG, POAG, and controls were 338.90 ± 103.23 ng/mL, 405.22 ± 114.12 ng/mL, and 408.84 ± 122.36 ng/mL respectively. NTG patients had lower serum retinol concentrations than POAG (p < 0.001) or healthy controls (p < 0.001). There was no statistical difference between the POAG and healthy controls (p = 0.780). Higher proportion of NTG patients (37.6%) than POAG (17.9%) or controls (21.7%) had serum retinol concentrations lower than 300 ng/mL. Serum retinol was positively correlated with optic nerve sheath diameter (ONSD) (r = 0.349, p = 0.001) in glaucoma patients and not associated with any other demographic features or ophthalmic biometric parameters in the NTG patients. Multivariate logistic regression showed that serum retinol (OR = 0.898, 95CI%: 0.851-0.947) was associated with incident NTG.ConclusionsNTG patients had lower serum retinol concentrations. Serum retinol uniquely associated with NTG makes it a new potential option for the diagnosis and treatment of the disease.
| S-EPMC9391421 | biostudies-literature
Project description:N-acetylcysteine (NAC) is widely used as a mucolytic agent and as an antidote to paracetamol overdose. NAC serves as a precursor of cysteine and stimulates the synthesis of glutathione in neural cells. Suppressing oxidative stress in the retina may be an effective therapeutic strategy for glaucoma, a chronic neurodegenerative disease of the retinal ganglion cells (RGCs) and optic nerves. Here we examined the therapeutic potential of NAC in two mouse models of normal tension glaucoma, in which excitatory amino-acid carrier 1 (EAAC1) or glutamate/aspartate transporter (GLAST) gene was deleted. EAAC1 is expressed in retinal neurons including RGCs, whereas GLAST is mainly expressed in Müller glial cells. Intraperitoneal administration of NAC prevented RGC degeneration and visual impairment in EAAC1-deficient (knockout; KO) mice, but not in GLAST KO mice. In EAAC1 KO mice, oxidative stress and autophagy were suppressed with increased glutathione levels by NAC treatment. Our findings suggest a possibility that systemic administration of NAC may be available for some types of glaucoma patients.
| S-EPMC6349904 | biostudies-literature