Bilateral corneal edema in an alcoholic male.
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ABSTRACT:
SUBMITTER: Lee PY
PROVIDER: S-EPMC8259528 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:In this article, we report a case of bilateral severe reversible corneal edema caused by amantadine therapy.A 39-year-old women was referred to us for evaluation of bilateral corneal edema. Her past medical history was significant for multiple sclerosis, anorexia, and seizures. She developed painless progressive bilateral loss of vision for the past 6 months. She was evaluated by several ophthalmologists elsewhere who felt that the patient's visual loss was secondary to a nutritional deficiency as opposed to related to multiple sclerosis. She was started on vitamin B-12 medication without improvement in her symptoms. She was then evaluated by neuro-ophthalmology. The examination revealed severe bilateral corneal edema and was referred to our corneal service for further evaluation of her corneal condition. Our examination revealed best corrected visual acuity of 20/400 bilaterally. Corneal thickness was 940 microm in the right eye and 802 microm in the left. Color vision was intact. Conjunctivas were white bilaterally. Cornea evaluation revealed diffuse stromal edema and Descemet's folds and microcystic subepithelial edema with to guttae noted. Anterior chambers were deep and quiet. A specular microscopy revealed significant pleomorphism and polymegathism with an endothelial cell count of 1,504 cells in the right eye and 1,596 in the left eye.Review of the patient's medical information revealed therapy with amantadine 2 months prior to the appearance of the patient's symptoms as a means to control the patient's tremors. The patient experienced rapid resolution of the corneal edema within the next 2 months after discontinuation of the agent with recovery of best corrected visual acuity of 20/40 in the right eye and 20/30 in the left.In cases of unexplained corneal edema and in the absence of any identifiable ocular cause, a review of toxic effects of systemic medications should be performed. Early diagnosis may prevent irreversible endothelial damage. Amantadine can cause endothelial failure and needs to be considered as part of the differential diagnosis of corneal edema.
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Project description:Lymphatic vessels play a crucial role in systemic immune response and regulation of tissue fluid homeostasis. Corneal lymphangiogenesis in bacterial keratitis has not been studied. In this study, we investigated the mechanism and the role of corneal lymphangiogenesis in a murine bacterial keratitis model using Pseudomonas aeruginosa. We first demonstrated that corneal lymphangiogenesis was enhanced mainly in the late stage of bacterial keratitis, contrary to corneal angiogenesis that started earlier. Corresponding to the delayed lymphangiogenesis, expression of the pro-lymphangiogenic factors VEGF-C and VEGFR-3 increased in the late stage of bacterial keratitis. We further found that F4/80 and CD11b positive macrophages played an essential role in corneal lymphangiogenesis. Notably, macrophages were specifically involved in corneal lymphangiogenesis in the late stage of bacterial keratitis. Finally, we demonstrated the beneficial role of corneal lymphangiogenesis in ameliorating the clinical course of bacterial keratitis. Our study showed that bacterial activity was not directly involved in the late stage of keratitis, while corneal lymphangiogenesis reduced corneal edema and clinical manifestation in the late stage of bacterial keratitis. These findings suggest that the process of lymphangiogenesis in bacterial keratitis ameliorates corneal inflammation and edema in the late stage of bacterial keratitis.
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Project description:We present a patient with recurrent mantle cell lymphoma (MCL) who was treated with zanubrutinib, a Bruton's tyrosine kinase inhibitor. He subsequently developed bilateral cystoid macular edema (CME) in both eyes. This is the first report of CME in a patient with MCL who was treated with zanubrutinib. CME was refractory to topical corticosteroid therapy, but sub-Tenon's steroid injections and holding off zanubrutinib managed to decrease the CME. Treatment managed to prevent further vision loss but did not restore lost vision. The prompt ophthalmic exam is recommended for patients on zanubrutinib with decreased vision.
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Project description:PURPOSE:The optical density of the cornea can be evaluated quantitatively by "densitometry" using a rotating Scheimpflug camera. Densitometry allows evaluation of corneal opacity in the anterior segment of the eye by quantitative measurement of scattering light. In the present investigation, we evaluate quantitatively minimal subclinical corneal edema after cataract surgery using densitometry. METHODS:Fifty four eyes of 34 patients who underwent cataract surgery were enrolled. Measurement of corneal density was performed using Pentacam® before and on days 1, 3 and 7 after surgery. RESULTS:Densitometry scores increased from 18.12?±?1.76 before cataract surgery to 21.03?±?3.84 on day 1 (P?<?0.001) and 19.90?±?2.46 on day 3 (P?=?0.018), but recovered to 19.44?±?1.58 on day 7 (P?=?0.131). Total corneal thickness was 549.1?±?32.7??m before surgery and increased to 582.7?±?46.3??m on day 1 (P?=?0.001), but recovered to 566.4?±?29.7??m on day 3 (P?=?0.097). Densitometry reading correlated positively with corneal thickness (correlation coefficient?=?0.13, P?=?0.003). CONCLUSIONS:Densitometry is useful to detect corneal edema that is not detectable by slit-lamp examination.
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Project description:A 16-year-old female presented with poor vision in both eyes. On clinical examination, she had bilateral cataracts and optic disc edema bilaterally on ultrasound examination. Extensive intracranial calcification was evident on computerized tomography. Physical examination revealed short stature, rounded chubby face, dental abnormalities, brachydactyly, and obesity. Laboratory evidence of hypocalcemia, hyperphosphatemia, elevated parathyroid hormone level (indicative of pseudohypoparathyroidism) along with the constellation of phenotypical characteristics lead to a diagnosis of Albright's hereditary osteodystrophy. This case is being presented to increase awareness regarding presence of coexisting and previously undiagnosed hypocalcemic syndromes in pediatric cataracts. The role of an ophthalmologist may be pivotal in diagnosing such an entity as documented in the present case.
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Project description:The cornea, transparent and outermost structure of camera-type eyes, is prone to environmental challenges, but has remarkable wound healing capabilities which enables to preserve vision. The manner in which cell plasticity impacts wound healing remains to be determined. In this study, we report rapid wound closure after zebrafish corneal epithelium abrasion. Furthermore, by investigating the cellular and molecular events taking place during corneal epithelial closure, we show the induction of a bilateral response to a unilateral wound. Our transcriptomic results, together with our TGF-beta receptor inhibition experiments, demonstrate conclusively the crucial role of TGF-beta signaling in corneal wound healing. Finally, our results on Pax6 expression and bilateral wound healing, demonstrate the decisive impact of epithelial cell plasticity on the pace of healing. Altogether, our study describes terminally differentiated cell competencies in the healing of an injured cornea. These findings will enhance the translation of research on cell plasticity to organ regeneration.
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Project description:PurposeTo describe the presentation, clinical course and management of a patient with bilateral maculopathy associated with sertraline.ObservationsWe report a rare case of bilateral cystoid macular edema and subretinal fluid in a 78-year-old Asian Indian female who was on chronic sertraline therapy. The patient was initially misdiagnosed as intermediate uveitis and started on oral corticosteroids. However, multimodal imaging with fluorescein angiography and optical coherence tomography ruled out ocular inflammation. There was symmetrical bilateral macular involvement and changes on macular electroretinography, which provided clues to the diagnosis of toxic maculopathy. After cessation of sertraline therapy, the retinal pathology reversed with improvement in visual acuity.Conclusions and importanceDevelopment of cystoid macular edema due to sertraline is a very rare adverse event and must be considered by psychiatrists and ophthalmologists. Our case demonstrates this rare toxicity along with its imaging features, and reversal on cessation of sertraline therapy.
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Project description:Purpose:To describe the outcome of microscope integrated optical coherence tomography (MiOCT) guided removal of lenticulo-corneal adhesion and intralenticular lens aspiration (ILLA) in cases with anterior dislocation of the crystalline lens and corneal edema. Methods:MiOCT-guided ILLA was performed in three eyes of two cases of homocystinuria with spontaneous anterior dislocation of lens and corneal edema. Lenticulo-corneal adhesion was noted intraoperatively, which was not apparent pre-operatively. The lenticulo-corneal adhesion could be successfully peeled using intravitreal forceps and viscodissection with visco-dispersive viscoelastic under the guidance of MiOCT. Results:In all cases, the lenticulo-corneal adhesion could be successfully removed without any complication such as Descemet tear or worsening in corneal edema. Improvement in visual acuity was noted in all cases with resolution in corneal edema by 1 week. Conclusion:MiOCT-guided ILLA can be extremely useful in cases of lenticulo-corneal adhesion especially in cases with corneal edema.
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Project description:The osmosensitive transcription factor nuclear factor of activated T cells 5 (NFAT5; or tonicity-responsive enhancer binding protein; TonEBP) plays a key role in macrophage-driven regulation of cutaneous salt and water balance. In the immune-privileged and transparent cornea, disturbances in fluid balance and pathological edema result in corneal transparency loss, which is one of the main causes of blindness worldwide. The role of NFAT5 in the cornea has not yet been investigated. We analyzed the expression and function of NFAT5 in naive corneas and in an established mouse model of perforating corneal injury (PCI), which causes acute corneal edema and transparency loss. In uninjured corneas, NFAT5 was mainly expressed in corneal fibroblasts. In contrast, after PCI, NFAT5 expression was highly upregulated in recruited corneal macrophages. NFAT5 deficiency did not alter corneal thickness in steady state; however, loss of NFAT5 led to accelerated resorption of corneal edema after PCI. Mechanistically, we found that myeloid cell-derived NFAT5 is crucial for controlling corneal edema, as edema resorption after PCI was significantly enhanced in mice with conditional loss of NFAT5 in the myeloid cell lineage, presumably due to increased pinocytosis of corneal macrophages. Collectively, we uncovered a suppressive role for NFAT5 in corneal edema resorption, thereby identifying a novel therapeutic target to combat edema-induced corneal blindness.
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Project description:BackgroundCohen syndrome (Q87.8;ORPHA:193; OMIM#216550) is an autosomal recessive inherited genetic disorder caused by mutation in the VPS13B/COH1 gene. It is characterized by variable clinical symptoms such as deformity of the head, face, hands and feet, eye abnormalities, abdominal obesity, neutropenia and nonprogressive intellectual disability. The typical lesions in the eyeball in Cohen syndrome include high myopia, retinal dystrophy, strabismus, maculopathy and lens subluxation. The present study describes the coexistence of bilateral macular edema with pale optic disc in a patient with a homozygous deletion in the VPS13B/COH1 gene.Material and methodsA 6-year-old Caucasian girl with facial dysmorphism, microcephaly, prominent upper incisors, narrow hands with slender fingers, congenital heart defect and ophthalmic symptoms was subjected to genetic testing. The genetic evaluation revealed a homozygous deletion on the long arm of chromosome 8 encompassing 20-25 exons of the VPS13 gene, as confirmed by Cohen syndrome. She underwent a full ophthalmological examination with the assessment of slit lamp examination of anterior segment and fundoscopy, refraction error, biometry, central corneal thickness and additionally electroretinography, optical coherence tomography and fundus photography.ResultsIn the ophthalmologic examination, the girl had bilateral astigmatism accompanied by myopia and a marked reduction in central corneal thickness. Fundus examination showed pale optic nerve discs and "salt and pepper" retinopathy. Bilateral cystic macular edema was revealed in handheld optical coherence tomography. Electroretinography showed a reduced response amplitude of cones and rods.ConclusionIn a patient with high myopia, macular edema, pale optic disc and facial dysmorphism, Cohen syndrome should be considered in the differential diagnosis. The severity of individual clinical features in patients with Cohen syndrome varies. It can be assumed that the type of mutation affects the occurrence and severity of individual symptoms.
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