A man in his late 50s with recently diagnosed chronic lymphocytic leukaemia (CLL) developed rapidly progressive bilateral, painless vision loss. Despite significant visual impairment, initial fundus examination, optical coherence tomography and neuroimaging were largely unremarkable. Further investigation revealed visual field defects, optic nerve dysfunction on visual evoked potentials and cerebrospinal fluid (CSF) infiltration by leukaemic cells, confirming bilateral leukaemic optic neuropathy (LON). The patient was treated with high-dose intravenous methylprednisolone followed by ibrutinib, resulting in marked visual recovery and normalisation of visual fields. Temporary discontinuation of ibrutinib due to neutropenia led to symptom recurrence and persistent central nervous system infiltration, which improved after treatment was resumed. This case highlights the diagnostic challenges of LON, particularly when ophthalmic and imaging findings are initially normal, and underscores the importance of CSF analysis and prompt CLL-directed therapy to prevent irreversible visual loss and achieve favourable outcomes.

Dry age-related macular degeneration (AMD) is a leading cause of blindness, characterized by progressive loss of retinal pigment epithelium (RPE) and subsequent photoreceptor degeneration. Current experimental models, including sodium iodate-induced injury, fail to fully recapitulate the chronic, age-related progression of the human disease. Although RIP3-mediated necroptosis has been strongly implicated in RPE cell death, its direct contribution to retinal degeneration in vivo remains unclear. To address this limitation, we generated two RIP3 transgenic mouse lines with distinct patterns of RIP3 overexpression. While RIP3-Tg mice exhibit systemic RIP3 overexpression, RIP3-Tg-RPE mice display additional RPE-specific overexpression beyond the levels observed in RIP3-Tg mice. We then evaluated these transgenic lines, along with wild-type controls, for age-driven retinal degeneration by using optical coherence tomography (OCT), behavior-based visual function assays, and molecular profiling of inflammation and cell death. First, RIP3-Tg mice exhibited gradual retinal thinning, progressive visual decline, and sustained upregulation of pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6) over 6-15 months, recapitulating the slow progression of dry-AMD. Second, RIP3-Tg-RPE mice, which exhibit further RPE-specific increases in RIP3 expression, showed markedly accelerated retinal degeneration, with significant structural and functional deficits evident as early as 2 months of age. These findings indicate that ectopic RIP3 expression in the RPE contributes to inflammatory responses and subsequent retinal degeneration. Collectively, our results highlight RIP3 as a potential contributing factor in the progression of retinal degeneration and introduce biologically relevant transgenic models that capture both slow and accelerated disease progression. These models provide a valuable platform for investigating disease mechanisms and developing therapeutic strategies targeting necroptosis in dry-AMD.

Background Chronic rhinosinusitis (CRS) is a persistent inflammatory condition of the nasal cavity and paranasal sinuses lasting more than 12 weeks despite appropriate medical treatment. Its symptoms include nasal congestion, nasal drainage, facial pain, and loss of smell. The diagnosis of rhinosinusitis is essential to managing the condition effectively. Endoscopy and CT of the paranasal sinuses (CT-PNS) are two main imaging methods used to diagnose the condition. Endoscopy enables direct visualization of the nasal cavity, whereas CT provides detailed imaging of the paranasal sinuses. Neither imaging method is sufficient on its own, but each has advantages and disadvantages for the diagnostic process. Understanding these differences is essential to establishing an optimal diagnostic procedure for patients with CRS. Materials and methods This is a cross-sectional observational study conducted in patients with CRS in the department of otorhinolaryngology OPD with a sample size of 70. Patients were selected based on inclusion and exclusion criteria. The procedure was explained, and informed consent was obtained. They underwent diagnostic nasal endoscopy (DNE) and plain CT-PNS, and the findings were documented for comparison. Results CT positivity (88.6%) was higher than DNE positivity (82.9%), and dual positivity was observed in 77.1% of patients. The diagnostic validity of DNE showed a sensitivity of 87.1%, a specificity of 50.0%, a positive predictive value of 93.1%, and an accuracy of 82.9%. There was a statistically significant association between modalities, though the correlation between severity scores was weak and not significant. Conclusions DNE and CT-PNS are used to assess CRS, although they are complementary. DNE is highly effective as an initial, office-based diagnostic modality with good sensitivity and predictive value. In contrast, CT-PNS is necessary for overall evaluation, assessment of posterior sinus involvement, and operative planning.

To compare the safety, efficacy, and perioperative outcomes of radiofrequency ablation (RFA) and endovenous microwave ablation (EMA), each combined with foam sclerotherapy, versus traditional high ligation and stripping (HL/S) for symptomatic lower extremity varicose veins. The primary endpoint was the change in Venous Clinical Severity Score (VCSS) from baseline to 12 months postoperatively. This multicenter retrospective study analyzed 305 patients from two hospitals, divided into three groups: RFA + sclerotherapy (n = 102), EMA + sclerotherapy (n = 101), and HL/S (n = 102). Perioperative outcomes (operation time, blood loss, hospital stay), postoperative pain (Visual Analog Scale, VAS), inflammatory markers (CRP, IL-6), dorsal foot venous pressure, coagulation parameters, complication rates, Venous Clinical Severity Score (VCSS), and Chronic Venous Insufficiency Quality of Life Questionnaire (CIVIQ-20) scores were assessed and compared up to 12 months postoperatively. Both minimally invasive groups demonstrated superior perioperative outcomes compared to HL/S, including shorter operation times, less blood loss, and reduced hospital stays. Postoperative pain scores were significantly lower in the RFA and EMA groups, with RFA showing the lowest early pain levels. Inflammatory markers (CRP, IL-6) and coagulation activation (D-dimer, fibrinogen) were significantly lower in the ablation groups, with RFA values being the lowest. Complication rates were lower in the RFA (34.3%) and EMA (41.6%) groups versus HL/S (58.8%). However, no significant differences were observed among the three groups in long-term VCSS, CIVIQ-20 scores, or recurrence rates at 12 months. RFA and EMA combined with sclerotherapy are safe and effective minimally invasive alternatives to HL/S, offering advantages in faster recovery, less pain, reduced inflammatory response, and fewer complications. While perioperative benefits favor thermal ablation, all three techniques provide comparable long-term symptomatic relief and quality-of-life improvement.

This case illustrates that a pituitary tumor can be masked by coexisting glaucoma, and that early differential diagnosis using optical coherence tomography (OCT), Central 24-2 threshold visual field testing, and magnetic resonance imaging (MRI) to facilitate timely surgical intervention might avoid irreversible vision loss. A 73-year-old female was initially diagnosed with cataracts and glaucoma and monitored by retinal nerve fiber layer (RNFL) measurements using OCT, with readings of 97 μm in the right eye and 85 μm in the left eye in 2010. This case was followed continuously by the author for over 17 years. Although her intraocular pressure remained well controlled, her left eye RNFL progressively declined, dropping to 72 μm in 2022 and further to 62 μm in 2025. Visual field testing in 2016 revealed bitemporal defects, including a glaucomatous arcuate defect, which became increasingly pronounced by 2020 and, by 2025, demonstrated severe defects in the left eye, inconsistent with controlled glaucoma. MRI in 2025 confirmed a 2.2 cm adenoma compressing the optic chiasma with left optic nerve atrophy. In retrospect, review of the chart revealed early warning signs of a brain lesion, and the tumor was unfortunately identified only after significant vision loss had already occurred, underscoring that early diagnosis and timely surgery can prevent and sometimes reverse vision loss. Any atypical glaucoma presentation or inexplicable change in a patient with controlled glaucoma should therefore be carefully evaluated to exclude pituitary or other intracranial tumors, particularly through diligent visual field review and optic nerve examination. Glaucoma is fundamentally an optic nerve disease, and multidisciplinary cooperation is essential: neurologists managing pituitary tumor patients should refer them to ophthalmologists to rule out coexisting glaucoma, while ophthalmologists encountering unusual glaucoma cases should refer patients to primary care physicians or neurologists to exclude intracranial pathology. This report aims to remind clinicians of this rare but well-documented condition and highlight early diagnostic clues to prevent the pituitary tumor from being masked by a narrow specialty focus.

Wolfram syndrome is a rare autosomal recessive disorder caused by pathogenic variants in the WFS1 gene and characterized by early-onset, insulin-dependent diabetes mellitus, optic atrophy, sensorineural hearing loss, arginine vasopressin deficiency, and progressive neurodegeneration driven by chronic endoplasmic reticulum (ER) stress; no proven disease-modifying therapy currently exists. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) augment glucose-dependent insulin secretion and, in preclinical models, preserve β-cell mass, attenuate ER stress, and confer neuroprotection - properties of particular therapeutic relevance to Wolfram syndrome.

Pathologic myopia is a major cause of irreversible visual impairment worldwide and is characterized by excessive axial elongation accompanied by progressive retinal degeneration. Whether vision loss results primarily from passive retinal stretching or selective neurodegeneration remains unclear, hindering the development of effective neuroprotective and regenerative therapies. Here, we investigated retinal neuronal, vascular, and glial alterations in retinal pigment epithelium (RPE)-specific Lrp2 knockout (Best1-Cre/Lrp2[fl/fl] conditional knockout, CKO) model of pathologic myopia. The CKO mice were examined longitudinally using multimodal ocular imaging, electroretinography, optokinetic testing, fluorescein angiography, and quantitative immunohistochemistry analysis. CKO phenotype[+] mice developed early-onset, progressive axial elongation and high myopia, accompanied by fundus features closely resembling human pathologic myopia, including peripapillary and patchy chorioretinal atrophy. Retinal function was markedly impaired, with significant reductions in scotopic a-, b-, and c-wave amplitudes. Although axial elongation resulted in a 1.98-fold increase in retinal surface area and a 55.95% reduction in retinal thickness, quantitative correction for retinal expansion revealed selective neuronal loss rather than uniform retinal degeneration. Total numbers of rods, cones, horizontal cells, and GABAergic amacrine cells were reduced by 22, 40, 30, and 57%, respectively, together with a 66% loss of photoreceptor synaptic ribbons. In contrast, retinal ganglion cells and bipolar cells exhibited reduced density but preserved absolute cell numbers. These neuronal changes were accompanied by retinal and choroidal microvascular degeneration, Müller gliosis, microglial activation and subretinal accumulation, and RPE dysmorphology. Our findings demonstrate that axial elongation induces neuron subtype-specific degeneration rather than generalized retinal thinning. Our study identifies photoreceptors, horizontal cells, and inhibitory amacrine cells as particularly vulnerable populations and implicates impaired RPE support, neurovascular dysfunction, and chronic glial activation as key mechanisms driving myopic retinopathy. This study provides a mechanistic framework for developing targeted neuroprotective and regeneration-based therapies for pathologic myopia.

Ocular diseases are a significant public health problem worldwide and represent one of the leading causes of disability. The prevalence of visual impairment is steadily increasing, largely driven by the ageing population. Oxidative stress, chronic inflammation and neurodegenerative processes underlie the pathogenesis of many eye diseases, including age-related macular degeneration (AMD), diabetic retinopathy, glaucoma, and cataracts, contributing to progressive vision loss and functional impairment. Carotenoids such as lutein, zeaxanthin, meso-zeaxanthin, β-carotene, lycopene, and astaxanthin exhibit multidirectional biological effects, including antioxidant, anti-inflammatory, and neuroprotective properties. These compounds are selectively accumulated in the tissues of the eye, especially in the retina and macula, where they neutralise reactive oxygen species, modulate inflammatory pathways, stabilise mitochondrial function and support the survival and function of retinal ganglion cells and photoreceptors. The aim of our review was to provide a comprehensive review of current data regarding the mechanisms of action of carotenoids and their potential clinical significance in the prevention and treatment of retinal, optic nerve, lens, and eye surface diseases, including dry eye syndrome and Meibomian gland dysfunction. We identified results of available experimental and clinical research and outlined that an adequate supply of carotenoids in the diet or in the form of supplementation may support the protection of eye structures against oxidative and inflammatory damage, improve visual performance and potentially slow disease progression. However, high-quality prospective clinical trials are necessary to conclusively assess their therapeutic efficacy and establish evidence-based recommendations for clinical practice.

Age-related macular degeneration (AMD), characterized by pathologic choroidal neovascularization (CNV), is a leading cause of vision loss in the elderly. Vascular endothelial growth factor A (VEGFa) antagonists can prevent acute vision loss, but high treatment burden and loss of efficacy with chronic therapy highlight the need to explore alternative mechanisms. Recently, microRNA-34a (miR-34a) has emerged as a key regulator in aging and age-related diseases, but its role in neovascular AMD is unclear. In an injury-induced murine CNV model, we found miR-34a promoted pathological angiogenesis, without altering expression of Vegfa or its receptor Kdr, the canonical regulators of CNV. Mechanistically, miR-34a directly targets and inhibits the transcription factor KLF2, thereby upregulating the proangiogenic factors CXCR4 and CXCL12. Finally, we show miR-34a exacerbates CNV in aged mice and is expressed in CNV lesions excised from wet AMD patients. These findings establish a causal link between the age-related miR-34a and neovascularization in AMD.

Camurati-Engelmann Disease (CED) is a rare sclerosing bone dysplasia in which skull-base hyperostosis may result in neuro-ophthalmic complications. We report a 21-year-old woman with presumed CED and known bilateral choroidal osteomas who presented with bilateral optic nerve swelling. Neuroimaging demonstrated diffuse cranial hyperostosis with optic canal narrowing but no definitive optic nerve compression or venous sinus thrombosis. Lumbar puncture confirmed raised intracranial pressure with an opening pressure of 33 cm H2O. Optical coherence tomography revealed right eye subretinal fluid without choroidal neovascular membrane. Papilloedema improved initially with acetazolamide, but treatment was changed to oral furosemide due to intolerance to acetazolamide. There was continued visual decline in association with progressive subretinal fluid. Right eye intravitreal bevacizumab was ineffective, while fovea-sparing photodynamic therapy achieved resolution of subretinal fluid but was complicated by retinal pigment epithelial and photoreceptor loss. At 2.5-year follow-up, visual acuity was reduced in both eyes, with mild bilateral chronic papilloedema and enlargement of choroidal osteomas. This case illustrates multifactorial visual loss in CED with skull base hyperostosis arising from raised intracranial pressure and co-existing retinochoroidal pathology. This is the first documented case of CED with bilateral choroidal osteomas and highlights the role of multimodal imaging and multidisciplinary collaboration.