PurposeTo investigate the influences of smartphone use on ocular symptoms, status of the tear film, and oxidative stress indices in the tears and at the ocular surface.MethodsEighty healthy volunteers were enrolled in the study. Subjective symptoms and asthenopia were evaluated using the ocular surface disease index (OSDI), visual analogue scale (VAS), and computer vision syndrome (CVS) score before and after smartphone or computer display (control) use. The status of the tear film was evaluated using fluorescein film break-up time (FBUT), non-invasive keratograph break up time (NIKBUT), Schirmer score, keratoepitheliopathy (KEP), and tear meniscus height (TMH). Oxidative stress markers in the tear film including hexanoyl lysine (HEL), 4-hydroxy-2-nonenal (4-HNE), malondialdehyde (MDA), and 8-oxo-2’-deoxyguanosine (8-OHdG) in the tear film were measured using ELISA. Reactive oxygen species (ROS) at the ocular surface were measured through 2’,7’-dichloro-dihydrofluorescein diacetate. All measurements were conducted at baseline, and after use for 1 and 4 h.ResultsAll parameters showed no significant group-wise differences at baseline. Scores of OSDI, VAS, fatigue, burning sensation, and dryness showed significant increases after 1 and 4 h of smartphone use compared with those at baseline (all P < 0.05). The smartphone group showed higher OSDI, fatigue, burning, and dryness scores than the control group at 4 h. Smartphone use showed significantly decreased FBUT and NIBUT at 4 h than those at baseline (P < 0.01). In the smartphone group, the concentration of HEL significantly increased at 4 h compared with that at baseline and 1 h (P < 0.01). Both groups showed increased ROS with higher value in the smartphone group versus the control group at 4 h (P < 0.01).ConclusionsSmartphone use could not only aggravate subjective symptom indices such as the OSDI, VAS, and CVS but also induce tear film instability and oxidative stress indices in the tears and at the ocular surface.
PurposeWe aimed to examine the clinical features and prognosis of ocular ischemic syndrome and to investigate the risk factors for the development of neovascular glaucoma (NVG).MethodsThe medical records from 25 patients (25 eyes) who were diagnosed with ocular ischemic syndrome were retrospectively analyzed. We recorded the length of time between symptom onset and diagnosis, visual acuity, intraocular pressure, clinical findings of the anterior and posterior segments of the eye, fluorescein angiography, systemic diseases, smoking history, and the extent of any ipsilateral carotid artery stenosis. The risk factors for NVG in patients with ocular ischemic syndrome were investigated.ResultsThe mean age was 67.9 ± 12.5 years, and 21 men and 4 women were included in this study. At initial examination, the mean logarithm of the minimum angle of resolution (logMAR) was 2.02 ± 1.26, and the mean intraocular pressure was 21.0 ± 10.3 mmHg. Among 25 eyes of the 25 patients, NVG occurred in 17 eyes after a mean period of 12.6 ± 14.0 months. The length of time between symptom onset and diagnosis (p = 0.025) and the extent of ipsilateral carotid artery stenosis (p = 0.032) were identified as significant risk factors for NVG. At the final follow-up, the mean logMAR visual acuity was 3.13 ± 1.24, showing a poor prognosis regardless of whether NVG occurred.ConclusionsOverall, the prognosis for ocular ischemic syndrome is very poor. The risk of NVG increases with the length of time between symptom onset and diagnosis, as well as with the severity of ipsilateral carotid artery stenosis.
Mucin or lipid-targeting agents combined with aqueous supplements in patients with refractory EDE with short TBUT might improve subjective symptoms and TBUT. Of this, targeting whole tear film layers was most effective in improving ocular symptoms and tear film quality.
ObjectivesAmiodarone is widely used to treat arrhythmia. However, amiodarone is known for its severe toxicity to the liver, lungs, and thyroid. Amiodarone causes liver damage ranging from asymptomatic serum aminotransferase elevation to hepatic failure requiring liver transplantation. Although amiodarone toxicity has been reported, its simultaneous multi-organ toxicity is not well-known. Here, we introduce a novel case of multi-systemic amiodarone toxicity involving the liver, lungs, thyroid, and eyes.Case PresentationA 61-year-old woman visited the emergency room due to general weakness, nausea, visual disturbance, heat intolerance, and a non-productive cough. The patient had been using clopidogrel and amiodarone due to underlying atrial fibrillation. The total level of bilirubin was 0.71 mg/dL, aspartate aminotransferase was 358 U/L, alanine aminotransferase was 177 U/L, and prothrombin time was 27.1 s. Computed tomography showed diffuse increased liver intensity and scattered hyperattenuated nodular consolidations in both lungs. Transthoracic needle lung biopsy revealed fibrinoid interstitial inflammation with atypical change of type II pneumocytes and intra-alveolar foamy macrophages. In addition, the thyroid-stimulating hormone level was <0.008 μIU/mL, and free thyroxine was 4.67 ng/dL. The thyroid scan showed diffuse homogenous intake of technetium-99 m pertechnetate in both thyroid lobes. The ophthalmologic exam detected bilateral symmetrical corneal deposits in a vortex pattern. With these findings, we could diagnose amiodarone-induced hepatic, pulmonary, thyroid, and ophthalmologic toxicity. Liver function was restored after cessation of amiodarone, and thyroid function was normalized with methimazole administration. However, due to aggravated lung consolidations, systemic steroid treatment was administered, and improvement was seen 1 week after, at the follow-up exam. As her symptoms improved, she was discharged with a plan of steroid administration for 3 to 6 months.ConclusionsThis case implies the possibility of multi-systemic amiodarone toxicity. Thus, the toxicity of amiodarone to multiple organs must be monitored. Prompt cessation of the drug should be considered upon diagnosis.
Introduction: To determine the short-term real-world safety and efficacy of intravitreal brolucizumab injections in Korean patients with neovascular age-related macular degeneration (nAMD). Methods: This multicenter retrospective study involved 294 eyes (treatment naïve 20 eye (6.8%) and non-treatment naïve 274 eyes (93.2%)) of 290 patients from 13 hospitals or retinal centers in South Korea. Patients with nAMD who received brolucizumab injection(s) between April 1 and November 30, 2021, with a follow-up ≥1 month, were included. Primary outcomes were safety, incidence of intraocular inflammation (IOI), and potential risk factors. The secondary outcome was efficacy, i.e., change in best-corrected visual acuity (BCVA) and optical coherence tomography-measured macular thickness and retinal fluid. Results: The mean age was 71.63±8.66. The follow-up period was 2.38±0.79 months. The mean number of brolucizumab injections during the follow-up was 1.52±0.58. The overall incidence of IOI was 13.9% (n=41 eyes). Most IOI cases were of anterior uveitis (8.8%, 26 eyes), followed by retinal vasculitis (2.4%, seven eyes) and occlusive retinal vasculitis (0.3%, one eye). Most eyes showed IOI resolution (n=40, 97.5%) and BCVA restoration (n=39, 95.1%) with or without corticosteroid treatment during the follow-up. Age, sex, IOI history, or other anti-vascular endothelial growth factor injection histories were not associated with the occurrence of IOI. However, only thin subfoveal choroidal thickness (SFCT) was associated with the occurrence of IOI (odds ratio=0.995, p=0.020). BCVA at 1 month improved from baseline (Baseline 0.518±0.356 vs. 1 month 0.503±0.383, p=0.023), but the improvement was not maintained. Anatomical improvement was significant after 3 months. Conclusion: IOI was well-controlled with or without steroid treatment. Most IOI eyes (95.1%) were restored to the level of vision before IOI occurrence and occlusive vasculitis was rare. In the short term, brolucizumab injection effectively improved vision at 1 month and dried retinal fluid for 3 months.
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