Prevalence and diagnostic ability of β-zone parapapillary atrophy in open-angle glaucoma: a systematic review and meta-analysis.
Ontology highlight
ABSTRACT: Background
β-Zone parapapillary atrophy (β-PPA) is a common sign in patients with open-angle glaucoma (OAG). Some studies have suggested that β-PPA can aid in the diagnosis of OAG. We performed a systematic review and meta-analysis of the prevalence and diagnostic ability of β-PPA in OAG.Methods
We performed a literature search in PubMed, Web of Science, Embase and Google Scholar from inception to 1st November, 2021. Both hospital-based and population-based studies that reported details of β-PPA in OAG were included.Results
We screened 1404 articles from these databases and ultimately included 24 articles in our meta-analysis. The prevalence of β-PPA in OAG was 0.73 (95% CI 0.67 to 0.78). The results of subgroup analysis by country revealed prevalence rates of 0.83 (95% CI 0.78 to 0.88) in Japan, 0.85 (95% CI 0.64 to 0.97) in Korea, 0.64 (95% CI 0.55 to 0.73) in the USA, 0.61 (95% CI 0.58 to 0.63) in Germany and 0.57 (95% CI 0.39 to 0.74) in China. Fundus photography, Heidelberg retina tomography (HRT), Heidelberg retina angiography (HRA) + indocyanine green angiography (ICGA), Spectral domain optical coherence tomography (SD-OCT)and Swept source optical coherence tomography(SS-OCT) values were 0.65 (95% CI 0.58 to 0.71), 0.70 (95% CI 0.50 to 0.86), 0.78 (95% CI 0.61 to 0.91), 0.77 (95% CI 0.65 to 0.88) and 0.99(95% CI 0.87 to 1.00) respectively. The sensitivity and specificity of β-PPA as a diagnostic marker were 0.78 (95% CI 0.68 to 0.85) and 0.63 (95% CI 0.51 to 0.73), respectively.Conclusions
β-PPA is a potential diagnostic marker for OAG. However, a more detailed understanding of β-PPA characteristics is needed to improve the ability to predict OAG.
SUBMITTER: Zhou D
PROVIDER: S-EPMC8840052 | biostudies-literature | 2022 Feb
REPOSITORIES: biostudies-literature
Publications
Prevalence and diagnostic ability of β-zone parapapillary atrophy in open-angle glaucoma: a systematic review and meta-analysis.
Zhou Dengming D Cao Mengdan M Duan Xuanchu X
BMC ophthalmology 20220212 1
<h4>Background</h4>β-Zone parapapillary atrophy (β-PPA) is a common sign in patients with open-angle glaucoma (OAG). Some studies have suggested that β-PPA can aid in the diagnosis of OAG. We performed a systematic review and meta-analysis of the prevalence and diagnostic ability of β-PPA in OAG.<h4>Methods</h4>We performed a literature search in PubMed, Web of Science, Embase and Google Scholar from inception to 1st November, 2021. Both hospital-based and population-based studies that reported ...[more]
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Project description:Importanceβ-zone parapapillary atrophy (βPPA) has been reported as a risk factor for glaucoma onset and progression. Previous studies have shown that the prevalence of βPPA differs between individuals of African descent (AD) and European descent (ED).ObjectiveTo test whether the association between the presence and progression of βPPA vs visual field progression of glaucoma differs between these 2 ancestry groups.Design, setting, and participantsIn a prospective, multicenter, longitudinal cohort study, 634 individuals (1090 eyes) enrolled in the African Descent and Evaluation Study (ADAGES) with a diagnosis of glaucomatous optic neuropathy (GON) or ocular hypertension (OHT) and at least 2 disc stereophotographs were included. Two graders masked to clinical and ancestry data reviewed and graded the baseline and last disc stereophotographs for the presence of βPPA at baseline and βPPA progression (development or enlargement). Mixed-effects linear models were tested with visual field mean deviation as a dependent variable and time (alone and with interaction terms) as independent variables. ADAGES enrollment began in January 2003 and ended in July 2006; follow-up ended in 2016.ExposuresDisc stereophotographs.Main outcomes and measuresProgression of βPPA in AD and ED individuals.ResultsIn 634 patients, a total of 814 eyes of AD (395 eyes) and ED (419) patients with GON and 276 eyes of AD (106) and ED (170) patients with OHT who were enrolled in ADAGES were analyzed. There were 336 (53.0%) women in the study; mean (SD) age was 61.9 (12.7) years. In the OHT group, the association between βPPA at baseline and visual field progression was not significantly different between AD and ED eyes (β = 0.071; 95% CI, -0.016 to 0.158; P = .11), nor was the association between βPPA progression and visual field progression (β = 0.020; 95% CI, -0.465 to 0.506; P = .93). In the GON group, ED eyes with baseline βPPA progressed faster than did AD eyes with baseline βPPA (β = -0.124; 95% CI, -0.241 to -0.007; P = .04), although the association between βPPA progression and visual field progression did not differ significantly between race groups (β = -0.101; 95% CI, -0.323 to 0.119; P = .37).Conclusions and relevanceRace had a significant effect on the association between baseline βPPA and rates of visual field progression in eyes with GON. Progression of βPPA was not associated with faster visual field progression in either racial group.
| S-EPMC5710265 | biostudies-literature
Project description:PurposeTo investigate the differences in the frequency of optic disc hemorrhage (DH) and prevalence of beta-zone parapapillary atrophy (βPPA) between individuals of African descent (AD) and European descent (ED).DesignProspective, multicenter, observational cohort.ParticipantsA total of 1950 eyes of 1172 participants of the African Descent and Glaucoma Evaluation Study (ADAGES).MethodsStereoscopic disc photographs of subjects with and without glaucomatous optic neuropathy (GON) followed during the first 13 years of the ADAGES underwent masked review searching for DH and βPPA. A total of 928 eyes (non-GON, 581; GON, 347) of 551 AD patients (non-GON, 334; GON, 217) and 1022 eyes (non-GON, 568; GON, 454) of 611 ED patients (non-GON, 334; GON, 277) were included. We compared the number of eyes with detected DH at any time during follow-up and eyes with βPPA between the AD and ED groups. The analyses were then adjusted for clinical parameters using multivariable logistic regression.Main outcome measuresDifferences in frequency of DH and prevalence of βPPA.ResultsA total of 9395 stereoscopic disc photographs were reviewed. More ED eyes experience DH than AD eyes (49/1022 [4.8%] vs. 10/928 eyes [1.1%], respectively; P < 0.001), whereas βPPA had higher prevalence in AD eyes (675 eyes [72%] vs. 659 eyes [64%]; P < 0.001). In the final multivariable model, after controlling for confounders, AD eyes were less likely to have at least 1 detected DH than ED eyes (odds ratio [OR], 0.21; 95% CI, 0.10-0.45; P < 0.001) but were more likely to have βPPA than ED eyes (OR, 1.55; 95% CI, 1.12-2.14; P = 0.008).ConclusionsSubjects of ED are at higher risk for developing DH compared with AD subjects, whereas AD subjects have greater prevalence of βPPA. These findings suggest that there are structural differences within the optic nerve complex between these groups. Further research is needed to determine whether racial differences in the frequency of DH and prevalence of βPPA affect the likelihood of glaucomatous progression.
| S-EPMC4921256 | biostudies-literature
Project description:PURPOSE:To evaluate whether automated assessment of beta zone parapapillary atrophy (?PPA) area can differentiate between glaucomatous and healthy eyes of varying axial lengths (AL). DESIGN:Cross-sectional study. METHODS:?PPA was automatically identified in glaucoma and healthy eyes with enhanced-depth imaging optical coherence tomography (OCT) optic nerve head (ONH) radial B-scans. Associations with AL and the presence of glaucoma were assessed. Manually delineated ?PPA on individual OCT ONH B-scans of 35 eyes from the Diagnostic Innovations in Glaucoma Study served to validate the automated method. RESULTS:One hundred fifty-three glaucoma eyes (mean ± standard deviation) (visual field mean deviation, -5.0 ± 6.4 dB and mean AL, 25.1 ± 1.1 mm) and 73 healthy eyes (visual field mean deviation, 0.1 ± 1.4 dB and mean AL, 24.1 ± 1.1 mm) were included. In multivariable analysis, larger ?PPA area was significantly associated with a diagnosis of glaucoma after controlling for age, central corneal thickness, and AL. Moreover, in multivariable analysis, the odds of having glaucoma were doubled for each 0.2 mm2 larger ?PPA area. The age- and AL-adjusted area under the receiver operating characteristic curve (95% confidence interval) of ?PPA area for differentiating between glaucoma and healthy eyes was 0.75 (0.68-0.81). Agreement for the location of the Bruch membrane opening and the location of retinal pigment epithelium tips was stronger between the automated technique and each individual observer than it was between the 2 observers. CONCLUSIONS:Larger ?PPA area, as determined by automated OCT assessment, is significantly associated with a diagnosis of glaucoma, even after adjusting for age and AL, and may aid in differentiating healthy from glaucomatous eyes.
| S-EPMC6173207 | biostudies-literature
Project description:A substantial fraction of glaucoma has a genetic basis. About 5% of primary open angle glaucoma (POAG) is currently attributed to single-gene or Mendelian forms of glaucoma (ie glaucoma caused by mutations in myocilin or optineurin). Mutations in these genes have a high likelihood of leading to glaucoma and are rarely seen in normal subjects. Other cases of POAG have a more complex genetic basis and are caused by the combined effects of many genetic and environmental risk factors, each of which do not act alone to cause glaucoma. These factors are more frequently detected in patients with POAG, but are also commonly observed in normal subjects. Additional genes that may be important in glaucoma pathogenesis have been investigated using quantitative traits approaches. Such studies have begun to identify genes that control the magnitude of important quantitative features of glaucoma that may also be important risk factors for POAG, such as central corneal thickness. Each of these different approaches to study glaucoma genetics is providing new insights into the pathogenesis of POAG.
| S-EPMC3171270 | biostudies-literature
Project description:The total RNA from control and POAG optic nerve lamina cribrosa region was isolated and subjected to analysis on U133A 2.0 affymetrix microarray chip. The results from these two analysis was compared to determine whether PAD II RNA level is altered. Purpose of the study. This study was done to determine which RNA transcripts undergo significant changes in the optic nerve between normal and cadaver primary open-angle glaucoma donors. Using donor tissues from NDRI we have performed proteomic analyses (which will be published shortly), we intend a comparison between the proteomic and RNA changes for select proteins in our study. Sample Collection and Preparation of Labeled Copy RNA; The total RNA from optic nerve was obtained using TRIZOL (Invitrogen Inc., Carlsbad, CA) with modification of recommended protocols. The optic nerve from donor eyes were carefully excised and minced into small pieces first using a scissor and then a scalpel. Prior to use tissue was washed with DEPC water and all solutions were prepared in DEPC water. The minced tissue was placed in a glass homogenizer with 1 ml TRIZOL per 100 mg of tissue and homogenized in a glass homogenizer DUALL 20 (Kimble Kontes Glass Co, Vineland, NJ) with 10 strokes cycles each at room temperature and after freezing with liquid nitrogen for 1 min for 40 cycles. This RNA was extracted with chloroform, isoamylalcohol and precipitated with sodium citrate/sodium chloride and isopropanol. The final air-dried RNA precipitate was suspended in DEPC water and stored in â??80oC prior to use. RNA was prepared for hybridization according to the GeneChip Expression Analysis Technical Manual (Affymetrix, Santa Clara, CA). The hybridization was performed at Gene Expression Array Core Facility at Case Western Reserve University (www.geacf.net). The RNA sample was cleaned using a column from a Qiagen RNeasy kit, (part # 74104 ) in accordance with the manufacturerâ??s instructions. The volume of DEPC water used to elute the RNA from the Qiagen column was dictated by the nominal mass of the loaded RNA sample. Samples were eluted in 100ml of water, precipitated with 0.5 volume of 7.5M Ammonium Acetate and 2.5 volumes of 100% ethanol at -20oC for 1 hr and centrifuged for 10 min at room temperature. The pellet was drained and washed twice in 500µl of 70% ethanol. Supernatant was aspirated. The pellet was dried briefly (less than 1 min) in a speeedvac (Savant) and re-suspended in a small volume (~ 12â??15ml) of DEPC water. A small aliquot (2ml) of the sample was used for quantitation. Cleaned RNA samples were annotated as â??clnRNAâ?? and stored at -20oC. cDNA Synthesis; The protocol recommended by Affymetrix Inc. for cDNA synthesis was used at all times. The reaction was primed by annealing an oligo-dT primer coupled to a T7 RNA polymerase promoter to the RNA sample. Whenever possible, 8 mg of clnRNA were reverse transcribed using Superscript II reverse transcriptase in a 20ml reaction at 42oC for 1 hr. Second strand synthesis was carried out immediately in a total reaction volume of 150ml in the presence of E. coli DNA polymerase I, RNAse H and DNA ligase. The reaction mixture incubated for 2 hrs at 16oC and for a further 5 min in the presence of T4 DNA pol.. The reaction was terminated by the addition of EDTA. The sample was cleaned with a Qiagen cDNA clean-up column according to the manufacturers directions. The elution buffer volume was 14ml. The eluted samples were stored overnight at -20oC. In-Vitro Transcription (IVT) reaction; In a 0.5ml microfuge tube, complementary RNA (cRNA) was generated in an IVT reaction using a BioArray High Yield ENZO kit (Affymetrix). The 40ml reaction contained 10ml of cDNA sample and was incubated at 37oC in the heating block for 4-5hrs. Samples were mixed by flicking, pulse-centrifuged and returned to the incubator once every 40 minutes. Upon completion of the reaction, IVT samples were adjusted to a volume of 100ml with DEPC-treated water and cleaned using Qiagen RNA clean-up columns. Samples were eluted in 45ml of DEPC-treated water. A 2ml-aliquot was used for quantitation. Corrected concentrations of cRNA (minus the input clnRNA) were determined. A standard fragmentation reaction volume was 40ml in a 0.5 ml microfuge tube and used 20mg of overall IVT RNA in 1X fragmentation buffer (40mM Tris acetate, pH 8.1, 100mM KOAc, 30mM MgOAc). The reaction was incubated at 94oC for 35min in a heat block. After the 35 min incubation the fragmented samples were placed on ice. The standard hybridization cocktail volume was 300ml. 150ml of 2X hybridization buffer was added (final concentrations : 100mM MES, 1M [Na+], 20mM EDTA, 0.01% Tween 20) Herring sperm and acetylated BSA were added to a final concentration of 0.1 and 0.5mg/ml respectively. The amount of fragmentation reaction containing 15mg of cRNA was added to the cocktail and the remaining volume was made up with molecular biology grade water. A 15ml aliquot of a 20X mixture of in-vitro transcripts of bacterial genes BioB BioC BioD and cre as external controls (spikes) were added to the cocktail to give final concentrations of 1.5, 5, 25 and 100pM respectively. Control oligonucleotide (5ml) was added to a final concentration of 50pM. Array Hybridization; Sample Hyridization cocktails (300ml) were removed from storage at â??20oC and thawed in a 45oC temperature block. The samples were incubated at 45oC for 5 min, incubated at 45oC for 5 min and then centrifuged at 15,000g for 5 min. This study used commercially available Affymetrix HG U133A 2.0 arrays only. These are in situ synthesized, high density oligonucleotide arrays which can interrogate 22,777 gene entities. The part number is 900444 more detailed information may be found at www.affymetrix.com website. Meanwhile, the affymetrix chip arrays were taken from their storage at 4oC and allowed to come to room temperature. The chamber was filled with 1X hybridization buffer (final concentrations : 100mM MES, 1M [Na+], 20mM EDTA, 0.01% Tween 20). The chip was then preconditioned by incubation in the hybridization oven at 45oC for 10 min. The chip was removed and the chamber drained. Sample cocktails (200ml) were then introduced into the chamber of the chips. The ports were sealed with tough-spots stickers and placed in the hybridization oven and incubated at 45oC with rotation overnight. Next day (16hr later), the incubation was terminated and the chips removed from the oven. Samples were retrieved from the chips and stored again in a freezer at -20oC. The chips were filled with buffer A and placed in a module of Fluidics 400 wash station. The chips were subjected to the Affymetrix â??EuKws4 ver 2â?? programmed series of stringent post hybridization washes, staining and post-staining washes in accordance with Affy protocols. Upon completion of the wash series (approximately 2 hrs), the chips were removed from the Fluidics station. The chips were inspected. Chips were scanned using an Agilent Gene Array scanner 3000 driven by Affymetrix GCOS software. Generation of Expression Values; Microarray Suite, version 5 (Affymetrix), was used to generate *.cel files, and a computer program (Probe Profiler, ver. 1.3.11; Corimbia Inc., Berkeley, CA) developed specifically for the GeneChip system (Affymetrix) was used to convert intensity data into quantitative estimates of gene expression for each probe set. The software identifies informative probe pairs, and down-weights the signal contribution of probe pairs that are subject to differential cross-hybridization effects or that consistently produce no signal. The software also detects and corrects for saturation artifacts, outliers, and chip defects. A probability statistic was generated for each probe set. The probability is associated with the null hypothesis that the expression level of the probe set is equal to zero (background). Genes not significantly expressed above background in any of the samples (P > 0.05) were
2008-06-12 | E-GEOD-2387 | biostudies-arrayexpress
Project description:AimTo estimate the risk of blindness with primary angle-closure glaucoma (PACG) compared to primary open-angle glaucoma (POAG) in those population-based studies that reported blindness rates for both PACG and POAG.MethodA systematic search was performed in PubMed for articles published in English between 2000 and 2020 reporting the prevalence of POAG as well as PACG among various ethnic populations. A study was included if it was (1) population-based (2) had published prevalence and blindness rates for both PACG and POAG in the same cohort. (3) Glaucoma was defined as per the International Society for Geographical and Epidemiological Ophthalmology (ISGEO) criteria. The proportion of blindness for both POAG and PACG for each study and the cumulative proportion taking all the studies were calculated.ResultsWe included 23 studies with 78,434 participants. POAG was diagnosed in 1702 persons with 151 (8.9%) blind. There were 724 cases of PACG with 196 (27.0%) blind. The risk ratio of blindness in PACG to POAG varied from 0.73 to 10.6 among the studies. The cumulative risk ratio was 2.39 (95% confidence interval (CI); 1.99, 2.87). Risk ratios for studies including visual field restriction while defining blindness were similar to studies that did not (1.92 vs 2.64, P = 0.11). Risk ratios were also similar for studies that used greater than 2 instead of 3 or more quadrants of iridotrabecular contact to define angle closure (2.79 vs 2.25).ConclusionPrimary angle-closure disease is more likely to be associated with blindness.
| S-EPMC9582001 | biostudies-literature
Project description:ImportanceEarly diagnosis of open-angle glaucoma can lead to vision-saving treatment, and genetic variation is an increasingly powerful indicator in disease risk stratification.ObjectiveTo compare polygenic and monogenic variants in risk of glaucoma.Design, setting, and participantsClinical and genetic data were obtained for 2507 individuals from the Australian and New Zealand Registry of Advanced Glaucoma (ANZRAG) and 411 337 individuals in cross-sectional cohort studies including individuals of European ancestry in the UK Biobank. Recruitment to the UK Biobank occurred between 2006 and 2010, and data analysis occurred between September 2019 and August 2020.Main outcomes and measuresAssociation of monogenic and polygenic variants with glaucoma risk.ResultsIndividuals at high polygenic risk, defined as those in the top 5% of an unselected population, had a glaucoma risk (odds ratio [OR], 2.77; 95% CI, 2.58-2.98) comparable with the risk among individuals heterozygous for the MYOC p.Gln368Ter variant (OR 4.19; 95% CI, 3.25-5.31), which is the most common single-gene variant known to cause primary open-angle glaucoma. High polygenic risk was more than 6 times more common than MYOC p.Gln368Ter heterozygosity in ANZRAG (15.7% vs 2.6%) and more than 15 times more common in the general population (5.0% vs 0.32%). Within ANZRAG, high polygenic risk was associated with a mean (SD) age at glaucoma diagnosis that did not differ from the age at glaucoma diagnosis among individuals heterozygous for MYOC p.Gln368Ter (57.2 [14.2] vs 54.8 [13.6] years; P > .99).Conclusions and relevanceMonogenic and high polygenic risk were each associated with a more than 2.5-fold increased odds of developing glaucoma and an equivalent mean age at glaucoma diagnosis, with high polygenic risk more than 15 times more common in the general population.
| S-EPMC8283675 | biostudies-literature
Project description:Open-angle glaucoma is a multifactorial optic neuropathy characterized by progressive loss of retinal ganglion cells and their axons. It is an irreversible disease with no established cure. The only currently approved treatment is aimed at lowering intraocular pressure, the most significant risk factor known to date. However, it is now clear that there are other risk factors involved in glaucoma's pathophysiology. To achieve future improvements in glaucoma management, new approaches to therapies and novel targets must be developed. Such therapies may include new tissue targets for lowering intraocular pressure, molecules influencing ocular hemodynamics, and treatments providing neuroprotection of retinal ganglion cells. Furthermore, novel drug delivery systems are in development that may improve patient compliance, increase bioavailability, and decrease adverse side effects.
| S-EPMC4229725 | biostudies-literature
Project description:This study aimed to investigate the molecular mechanism responsible for primary open-angle glaucoma (POAG) progression. We analyzed microRNAs (miRNAs) expression profiling in aqueous humor (AH) of both POAG patients and normal controls, using a microarray-based approach. Subsequently, differentially expressed miRNAs (DEmiRNAs) were identified using Bayes moderated t-test. Next, DEmiRNAs target genes were predicted based on miRNA databases, followed by GO analysis and pathway analysis using DAVID. Furthermore, OAG-related genes analysis for target genes was carried out using CTD database, respectively. Finally, verification of DEmiRNAs expression levels was performed by RT-qPCR. A total of 40 significant DEmiRNAs were identified between control and POAG groups, including 24 up-regulated miRNAs and 16 down-regulated miRNAs. Further, the target genes of hsa-miR-206, including BMP2, SMAD4, ID2, and TNF, were mainly enriched in transforming growth factor-β (TGF-β) signaling pathway. While, target genes of hsa-miR-184, hsa-miR-34c-5p, hsa-miR-7-2-3p and hsa-miR-20b-3p, including BCL2, EPHB2, VEGFA, COL4A1, APC, and TGFBR1, were enriched in eye development. Moreover, FNDC3B, CAV2 and VEGF, target genes of hsa-miR-206 or hsa-miR-34c-5p, were the OAG-related genes. Ultimately, RT-qPCR analysis confirmed that mRNA levels of hsa-miR-206, hsa-miR-7-2-3p, and hsa-miR-20b-3p were increased, while those of hsa-miR-184 and hsa-miR-34c-5p were decreased in POAG compared with normal groups (P < 0.05). Hsa-miR-206, hsa-miR-184, hsa-miR-34c-5p, hsa-miR-7-2-3p and hsa-miR-20b-3p might play a significant role in the pathogenesis of POAG and hsa-miR-206 might be associated with the development of POAG by regulating TGF-β signaling pathway. These results might provide insight toward a better understanding of the pathogenesis of POAG.
2015-08-04 | GSE71639 | GEO
Project description:Long non-coding RNAs were associated with the development and progression of glaucoma. Our study aim to identify the potential genes in human trabecular meshwork related to primary open-angle glaucoma (POAG).
2019-09-28 | GSE138125 | GEO