Background: Although nasolacrimal duct probing is the standard treatment for congenital nasolacrimal duct obstruction (CNLDO) among children, the optimal timing of this procedure has been a topic of debate. The aim of the study was to analyze the clinical efficacy of nasolacrimal duct probing among patients with CNLDO symptoms at various ages. Methods: An 8-year retrospective study involved 2434 patients (3009 eyes), who underwent nasolacrimal duct probing conducted under topical anesthesia in the operating theatre. The study group consisted of 1148 girls (47.2%) and 1286 boys (52.8%) from 2 weeks to 41 months (average age was 8 ± 5.6 months). The participants were divided into nine age groups: 0–2 months, 3–6 months, 7–9 months, 10–12 months, 13–15 months, 16–18 months, 19–21 months, 22–24 months and over 24 months. Results: Bilateral obstruction was present among 575 (23.6%) children and was associated with a higher percentage of unsuccessful procedures compared to patients with unilateral obstruction (16.9% vs 10.2%, p < 0.001 Chi-square test). The success rate of the initial probing was 87.2% for all children and it was shown that it decreased with age. In the above age groups, it was 87.9%; 91.4%; 89.6%; 86%; 76.3%; 71.3%; 70.3%; 70.2%; 65.4%, respectively. Conclusions: Probing is a safe and effective procedure. However, age at the time of the initial intervention and bilateral surgery constitute significant risk factors for failed probing. Probing between 7 and 9 months appears to be reasonable treatment strategy for children without recurrent infections. Early surgical intervention may be considered for patients with additional signs.
Myopia is an evolving global health challenge, with estimates suggesting that by 2050 it will affect half of the world's population, becoming the leading cause of irreversible vision loss. Moreover, myopia can lead to various complications, including the earlier onset of cataracts. Given the progressive aging of the population and the increase in life expectancy, this will contribute to a rising demand for cataract surgery, posing an additional challenge for healthcare systems. The pathogenesis of nuclear and posterior subcapsular cataract (PSC) development in axial myopia is complex and primarily involves intensified liquefaction of the vitreous body, excessive production of reactive oxygen species, impaired antioxidant defense, and chronic inflammation in the eyeball. These factors contribute to disruptions in mitochondrial homeostasis, abnormal cell signaling, lipid peroxidation, protein and nucleic acid damage, as well as the induction of adverse epigenetic modifications. Age-related and oxidative processes can cause destabilization of crystallins with subsequent protein accumulation, which finally drives to a lens opacification. Moreover, an altered redox status is one of the major contributors to the pathogenesis of PSC. This review aims to summarize the mechanisms known to be responsible for the accelerated development of cataracts in axial myopia and to enhance understanding of these relationships.
Background: Long-term use of topical, especially benzalkonium chloride (BAC)-preserved, antiglaucoma medications can cause a negative impact on the ocular surface. The aim of the study was to assess the effect of topical carbonic anhydrase inhibitors (CAIs) on selected oxidative stress biomarkers in the tear film. Methods: The patients were divided into four sex-matched groups: group C (n = 25) – control group – subjects who did not use topical antiglaucoma medications, group DL (n = 14) – patients using preservative-free dorzolamide, group DL + BAC (n = 16) – patients using topical BAC-preserved dorzolamide, group BL + BAC (n = 17) – patients using BAC-preserved brinzolamide. Subjects in all the study groups have been using the eye drops two times daily for 6–12 months. The oxidative stress biomarkers in the tear film samples were measured: total protein (TP) concentration, advanced oxidation protein products (AOPP) content, total sulfhydryl (-SH) groups content, the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), as well as Total Oxidant Status (TOS), Total Antioxidant Response (TAR), and Oxidative Stress Index (OSI). Results: The advanced oxidation protein products content, Total Oxidant Status as well as superoxide dismutase and catalase activities in the group DL + BAC and BL + BAC were higher in comparison with the group C. The total sulfhydryl groups content was lower in the group DL + BAC and BL + BAC when compared to group C. Oxidative Stress Index was higher in the groups DL + BAC and BL + BAC in comparison with the groups DL and C. Conclusions: Use of topical benzalkonium chloride-preserved carbonic anhydrase inhibitors increases oxidative stress in the tear film.
Purpose: The aim of this study was to evaluate changes in the thickness of the peripapillary retinal nerve fiber layer (pRNFL) in children with a diagnosis of juvenile idiopathic arthritis (JIA) who were positive for human leukocyte antigen (HLA)-B27, treated for the first episode of unilateral acute anterior uveitis (AAU). Materials and Methods: This retrospective study included 41 children (aged 5 to 14 years; mean age 8.32 ± 2.4 years) with HLA-B27 positivity and unilateral JIA-AAU, and 40 healthy children. Optical coherence tomography (OCT) imaging was performed during active inflammation and subsequent noninflammatory phases (6 months after the resolution of inflammatory symptoms in the anterior segment of the eye). Results: There was a marked difference in mean pRNFL thickness between eyes with AU in the active phase, unaffected fellow eyes and the control group (110.22 ± 5.95 μm, 102.39 ± 4.39 μm and 95.83 ± 8.84 μm, respectively; p < 0.001). The thickness of pRNFL in eyes with AU in the active phase in all sectors was greater compared to unaffected fellow eyes (p < 0.001) and normal eyes (p < 0.001). In addition, it was demonstrated that pRNFL thickness was significantly increased in the superior and temporal sectors in the unaffected fellow eyes compared to the control group (128.73 ± 13.16 μm vs. 121.48 ± 13.35 μm and 71.37 ± 4.02 μm vs. 64.98 ± 9.12 μm, respectively). Even during the inactive phase, eyes with AU, compared to the healthy control group, had significantly greater pRNFL thickness in the inferior sector (129.78 ± 11.98 μm vs. 122.3 ± 14.59 μm; p = 0.018), along with the temporal sector (70.88 ± 5.48 μm vs. 64.98 ± 9.12 μm; p = 0.001). Conclusions: An increase in pRNFL thickness in children with unilateral JIA-AAU who were positive for HLA-B27 antigen can be observed in both eyes compared to healthy controls, and this change may persist even after the inflammatory symptoms have resolved. Measurements of pRNFL thickness resulting from JIA-AU-associated glaucoma should be performed during quiescent periods to avoid subclinical changes in pRNFL thickness caused by inflammation. However, when reviewing the results, it should be noted that changes in pRNFL parameters may be present despite evidence of a resolution of inflammation.
Background: Mowat-Wilson syndrome (MWS) is extremely rare multisystemic autosomal dominant disorder caused by mutations in the Zinc Finger E-Box Binding Homeobox 2 (ZEB2) gene. Ocular pathologies are one of the symptoms that appear in the clinical picture of MWS individuals, but not many have been described so far. Pathologies such as optic nerve or retinal epithelium atrophy, iris or optic disc coloboma as well as congenital cataracts have been most frequently described until now. Therefore, we would like to report the first case of bilateral developmental cataract in a 9-year-old girl with MWS who underwent successful cataract surgery with intraocular lens implantation. Case Presentation: A 9-year-old girl, diagnosed with p.Gln694Ter mutation in ZEB2 gene and suspicion of MWS was referred to the Children’s Outpatient Ophthalmology Clinic for ophthalmological evaluation. Her previous assessments revealed abnormalities of the optic nerve discs. The patient was diagnosed with atrophy of the optic nerves, convergent strabismus, and with-the-rule astigmatism. One year later, during the follow-up visit, the patient was presented with decreased visual acuity (VA), developmental total cataract in the right eye and a developmental partial cataract in the left eye. This resulted in decreased VA confirmed by deteriorated responses in visual evoked potential (VEP) test. The girl underwent a two-stage procedure of cataract removal, first of one eye and then of the other eye with artificial lens implants. In the 2 years following the operation, no complications were observed and, most remarkably, VA improved significantly. Conclusions: The ZEB2 gene is primarily responsible for encoding the Smad interaction protein 1 (SIP1), which is involved in the proper development of various eye components. When mutated, it results in multilevel abnormalities, also in the proper lens formation, that prevent the child from normal vision development. This typically results in the formation of congenital cataracts in children with MWS syndrome, however, our case shows that it also leads to the formation of developmental cataracts. This is presumably due to the effect of the lack of SIP1 on other genes, altering their downstream expression and is a novel insight into the importance of the SIP1 in the occurrence of ocular pathologies. To the best of our knowledge, this is the first case of bilateral developmental cataract in the context of MWS. Moreover, a novel mutation (p.Gln694Ter) in the ZEB2 gene was found corresponding to this syndrome entity. This report allows us to gain a more comprehensive insight into the genetic spectrum and the corresponding phenotypic features in MWS syndrome patients.
We report a case of a 25-year-old woman with sudden and painless diminution in vision and central scotoma in her left eye (LE). She was a smoker and had been taking combined oral contraceptive (COC) pills for 1 year. On admission, the best-corrected visual acuity (BCVA) was 1,5/50 in the LE.