DESIGN: Prospective, longitudinal study.
METHODS: Sixty-five NTG patients who were followed up for 5 years are included in this study. All the enrolled patients underwent baseline 24-h IOP and BP monitoring via 2-hourly measurements in their habitual position and were followed up for over 5 years with reliable VF tests. Modified Anderson criteria were used to assess VF progression. Univariable and multivariable analyses using Cox's proportional hazards model were used to identify the systemic and clinical risk factors that predict progression. Kaplan-Meier survival analyses were used to compare the time elapsed to confirmed VF progression in the presence or absence of each potential risk factor.
RESULTS: At 5-year follow-up, 35.4% of the enrolled patients demonstrated visual field progression. There were statistically significant differences in the mean diastolic blood pressure (p 43.7 mmHg (log rank = 0.018).
CONCLUSION: Diastolic parameters of BP and OPP were significantly lower in the NTG patients who progressed after 5 years. Low nocturnal DOPP is an independent predictor of glaucomatous visual field progression in NTG patients.
METHODS: This is a cross-sectional study involving 27 patients with symptoms of OSAS seen at a tertiary institutional center and 25 normal controls performed between June 2015 and June 2016. All patients and controls underwent a polysomnography (PSG) test and were diagnosed with OSAS based on the apnea-hypopnea index (AHI). Patients are those with OSAS symptoms and had AHI > 5, whereas controls are staffs from the ophthalmology clinic without clinical criteria for OSAS and had PSG result of AHI
METHODS: Patients with newly diagnosed AAC were identified prospectively over a 12-month period (November 2011 to October 2012) by active surveillance through the Scottish Ophthalmic Surveillance Unit reporting system. Data were collected at case identification and at 6 months follow-up.
RESULTS: There were 114 cases (108 patients) reported, giving an annual incidence of 2.2 cases (95% CI 1.8 to 2.6) or 2 patients (95% CI 1.7 to 2.4) per 1 00 000 in the whole population in Scotland. Precipitating factors were identified in 40% of cases. Almost one in five cases was associated with topical dilating drops. Best-corrected visual acuity (BCVA) at presentation ranged from 6/6 to perception of light. The mean presenting intraocular pressure (IOP) was 52 mm Hg (SD 11). Almost 30% cases had a delayed presentation of 3 or more days. At 6 months follow-up, 75% had BCVA of 6/12 or better and 30% were found to have glaucoma at follow-up. Delayed presentation (≥3 days) was associated with higher rate of glaucoma at follow-up (22.6% vs 60.8%, p<0.001), worse VA (0.34 vs 0.74 LogMAR, p<0.0001) and need for more topical medication (0.52 vs 1.2, p=0.003) to control IOP.
CONCLUSION: The incidence of AAC in Scotland is relatively low compared with the Far East countries, but in line with previous European data. Almost one in five cases were associated with pupil dilation for retinal examination.
METHODS: RGCs were isolated and cultured, and monoclonal antibodies (anti-rat Thy-1, Brn3a and RBPMS) were examined by immunocytochemistry. An overexpression vector MALAT1-RNA activation (RNAa), gene knockout vector MALAT1-RNA interference (RNAi), and control vector MALAT1-negative control (NC) were constructed. A chronic high intraocular pressure (IOP) rat model of glaucoma was established by episcleral vein cauterization. The RGCs were divided into the RGC control, RGC pressure, RGC pressure + MALAT1-NC, RGC pressure + MALAT1-RNAi and RGC pressure + MALAT1-RNAa groups. Sixty Sprague-Dawley (SD) rats were randomly divided into the normal, high IOP, high IOP + MALAT1-NC, high IOP + MALAT1-RNAa and high IOP + MALAT1-RNAi groups. qRT-PCR and western blotting were used to detect the expression levels of LncRNA-MALAT1 and PI3K/Akt. Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) and flow cytometry were used to detect RGC apoptosis.
RESULTS: Immunocytochemistry revealed that the cultured RGCs reached 90% purity. Compared with the RGC pressure + MALAT1-NC group, the RGC pressure + MALAT1-RNAa group exhibited elevated expression levels of MALAT1, lower total protein levels of PI3K and Akt and decreased RGC apoptosis, while these expression levels were reversed in the RGC pressure + MALAT1-RNAi group. RGC numbers and PI3K/Akt expression levels in the high IOP model groups were lower than those in the normal group. In the high IOP + MALAT1-RNAa group, the mRNA and protein expression levels of PI3K/Akt were reduced but higher than those in the other three high IOP model groups. Additionally, RGC numbers in the high IOP + MALAT1-RNAa group were lower than those in the normal group but higher than those in the other three high IOP model groups.
CONCLUSION: Our study provides evidence that LncRNA-MALAT1 could inhibit RGC apoptosis in glaucoma through activation of the PI3K/Akt signaling pathway.
METHODS: This was a cross-sectional comparative study comparing primary angle closure glaucoma (PACG) patients (Group A) with primary angle closure and primary angle closure suspect (Group B). Group A was treated with topical pressure-lowering drugs; Group B was not. Data on ocular diagnosis and details of treatment were obtained from medical records. Ocular surface disease incidence was assessed using the Ocular Surface Disease Index (OSDI) questionnaire and from clinical signs using Schirmer's test, tear break-up time and corneal fluorescein stain. Predictive Analytic Software 20 and STATA analysis software were used for statistical analyses.
RESULTS: Group A demonstrated a higher rate of OSD (OSDI 52.3%, Schirmer's test 70.5%, tear break-up time (TBUT) 75%, corneal staining 77.3%) compared to Group B (OSDI 39.0%, Schirmer's test 73.2%, TBUT 58.5% and cornea staining 14.6%) except for Schirmer's test. There was a significant difference in mean score of OSDI (p=0.004), TBUT (p=0.008) and cornea staining (p<0.001) between two groups. Primary angle closure glaucoma treated with more than two medications and for more than three years had worse ocular surface disease parameters but without statistical significant difference.
CONCLUSION: Ocular surface disease is common in PACG patients treated with topical pressure-lowering drugs. Topical pressure-lowering drugs caused significant OSD symptoms and signs except for tear production in PACG patients. Thorough evaluation of ocular surface disease is important to ensure appropriate treatment and intervention in PACG patients.