Cases reported "Glaucoma, Open-Angle"

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1/136. ciliary body melanocytoma with anterior segment pigment dispersion and elevated intraocular pressure.

    PURPOSE: To discuss a case in which melanocytoma of the ciliary body presented with widespread pigment dispersion and elevated intraocular pressure (IOP). methods: A 64-year old woman presented with increased IOP and persistent anterior segment inflammation in her right eye. She had undergone a trabeculectomy for uncontrolled IOP before presentation. Slit-lamp examination, gonioscopy, and ultrasound biomicroscopy revealed a ciliary body mass with extension into the subconjunctiva in addition to widespread pigmentary dispersion in the anterior segment. Enucleation of the right eye was performed for histopathologic evaluation, as a diagnosis of ciliary body melanoma was made on clinical examination. RESULTS: Histopathologic findings were diagnostic of a melanocytoma of the ciliary body with necrosis and focal malignant transformation with extension of melanocytoma cells and melanophages into the subconjunctival space, trabecular meshwork, and anterior chamber angle. CONCLUSION: Melanocytoma of the ciliary body is a rare intraocular tumor that may present with pigment dispersion and secondary elevated IOP. Careful examination of the anterior segment is imperative in such cases.
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2/136. A GLC1A gene Gln368Stop mutation in a patient with normal-tension open-angle glaucoma.

    PURPOSE: To present a case involving a patient with normal-tension glaucoma with a Gln368Stop mutation of the myocilin/trabecular meshwork inducible glucocorticoid response protein (MYOC/TIGR) gene. methods: Slit-lamp biomicroscopic and gonioscopic examination, morphometry of the optic disc, 24-hour intraocular pressure (IOP) profile, and perimetry were performed to determine the phenotype of the patient. neurologic examination and a computed tomographic (CT) scan of the brain were performed to rule out a neurologic disorder. Single-strand confirmation polymorphism (SSCP) analysis and subsequent sequence analysis of blood was performed for genotyping of the GLC1A gene. RESULTS: A nonsense codon, namely a Gln368Stop mutation in the third exon of the GLC1A gene, was found in this patient with normal-tension glaucoma. CONCLUSION: In contrast to previous reports, a Gln368Stop mutation of the GLC1A gene need not be confined to patients with glaucomatous optic atrophy due to high IOP. The pathogenesis of glaucoma associated with GLC1A gene mutations might be more complex than expected, and (unknown) suppressor mechanisms have to be considered.
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3/136. A false-positive Seidel test after Ahmed valve insertion.

    An 80-year-old monocular man with long-standing primary open angle glaucoma underwent successful filtering surgery in his sighted right eye in 1980. He subsequently developed a cataract and had an uncomplicated clear cornea phacoemulsification with posterior chamber intraocular lens in 1996. Post-operatively, the filtration bleb remained very avascular but shallowed; the intraocular pressure increased and remained uncontrolled despite maximally tolerated medical therapy. His vision improved to 6/7.5 and automated perimetry revealed a less than 5 degrees small central island of vision. His left eye was phthisical with no light perception.
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4/136. Cystoid macular edema associated with latanoprost therapy in a case series of patients with glaucoma and ocular hypertension.

    OBJECTIVE: To identify coexisting ocular diagnoses in a case series of eyes that developed cystoid macular edema (CME) associated with latanoprost therapy. DESIGN: Retrospective observational case series. PARTICIPANTS: Seven eyes of seven patients who developed CME possibly associated with latanoprost treatment were studied. INTERVENTION: When these patients, all of whom were treated with latanoprost in addition to other glaucoma medications, described blurred vision or eye irritation, ocular examination revealed CME, which was confirmed by fluorescein angiography. Latanoprost was discontinued, and in three cases topical corticosteroids and nonsteroidal anti-inflammatory agents were used to treat the CME. MAIN OUTCOME MEASURES: visual acuity and intraocular pressure were determined before latanoprost use began, during therapy, and after latanoprost use ceased. In these cases, resolution of CME was documented clinically after discontinuing latanoprost. RESULTS: Clinically significant CME developed after 1 to 11 months of latanoprost treatment, with an average decrease of 3 lines in Snellen visual acuity. intraocular pressure decreased an average of 27.9% during treatment. Cystoid macular edema was confirmed in all cases by fluorescein angiography. In these seven patients, the following coexisting ocular conditions may have placed these eyes at risk for prostaglandin-mediated blood-retinal barrier vascular insufficiency: history of dipivefrin-associated CME, epiretinal membrane, complicated cataract surgery, history of macular edema associated with branch retinal vein occlusion, history of anterior uveitis, and diabetes mellitus. In all cases, the macular edema resolved following discontinuation of latanoprost, in some instances with concomitant use of steroidal and nonsteroidal anti-inflammatory agents. CONCLUSIONS: In this case series of pseudophakic, aphakic, or phakic eyes, the temporal relationships between the use of latanoprost and developing CME, and the resolution of CME following cessation of the drug, suggest an association between latanoprost and CME. In all cases, coexisting ocular conditions associated with an altered blood-retinal barrier were present.
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5/136. Endocapsular hematoma: report of a case following glaucoma surgery in a pseudophakic eye.

    The authors describe a case of an endocapsular hematoma that occurred in a 69-year-old pseudophakic diabetic male following mitomycin C (MMC) augmented trabeculectomy for neovascular glaucoma (NVG). The clinical course of the patient is described, and the unique features of this case are presented and discussed. The endocapsular hematoma absorbed in 6 weeks with conservative management. The patient regained the preoperative visual acuity of 20/30, and his intraocular pressure was controlled without any glaucoma medication. The iris neovascularization regressed. This case is the first report of an endocapsular hematoma following glaucoma filtering surgery in a pseudophakic eye with neovascular glaucoma.
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6/136. Clinical phenotype of a Japanese family with primary open angle glaucoma caused by a Pro370Leu mutation in the MYOC/TIGR gene.

    PURPOSE: To present the phenotype of two patients with primary open angle glaucoma (POAG) caused by a mutation of the myocilin/trabecular meshwork-inducible glucocorticoid response (MYOC/TIGR) gene. methods: Complete ocular examinations were performed on the 13-year-old proband, her father, mother, and sister. dna analysis was performed to detect the mutant gene. RESULTS: The proband and her father were found to have a mutation of the MYOC/TIGR gene. Both patients carried a heterozygous mutation in the 1,109th nucleotide, which corresponds to the 370th amino acid residue of the MYOC/TIGR gene. The clinical characteristics of both patients were: (1) development of POAG at an early age, (2) high peaks of intraocular pressure. and (3) poor response to medical treatment. CONCLUSIONS: The phenotype of these patients with a mutation of the MYOC/TIGR gene agreed with reports of other patients with mutations at other loci in this gene. The discovery of the MYOC/TIGR gene not only makes early detection of glaucoma possible, but also presents a new direction for investigating the pathogenesis of glaucoma.
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7/136. Effects of methotrexate treatment on serum immunoreactivity of a patient with normal-pressure glaucoma.

    PURPOSE: Increased serum immunoreactivity to retinal proteins may have a role in the disease process of some glaucoma patients. We describe a patient with normal-pressure glaucoma whose serum immunoreactivity to retinal proteins regressed after methotrexate treatment for rheumatoid disease. METHOD: Case report. RESULTS: In a 66-year-old white female with normal-pressure glaucoma and rheumatoid disease, sequential Western blots using patient sera against retinal proteins demonstrated a decrease in the immunoreactive bands after treatment. During the treatment period of 3 years, her visual fields appeared to have improved. optic disk examination during the short periods without treatment, however, disclosed new, bilateral splinter hemorrhages on the optic disks. CONCLUSION: These observations suggest a potential role for immune-based intervention in similar patients.
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8/136. Change in optic disc topography associated with diurnal variation in intraocular pressure.

    PURPOSE: A case demonstrating significant changes in optic disc topography from variation in intraocular pressure (IOP) is demonstrated. methods: Within a single 24-hour period, confocal scanning laser ophthalmoscopic images were obtained in the left eye of a patient during an IOP peak (60 mmHg) and during an IOP trough (18 mmHg). RESULTS: During an IOP trough, paired t tests showed significant reduction in cup area, cup volume, mean cup depth, and maximum cup depth, and a significant increase in rim area and cup-to-disc (CD) ratio. CONCLUSION: Under certain conditions, optic disc topography may be affected by diurnal variations in IOP.
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9/136. Unilateral glaucomatous damage in a patient with hemifacial spasm.

    We report a patient with hemifacial spasm of the right hemiface and ipsilateral glaucomatous optic neuropathy. No risk factors were found to explain the unilateral glaucoma. Ocular pressure readings were always within normal range.
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10/136. Unilateral capsular glaucoma after long-standing bilateral pigmentary glaucoma.

    In 1964 we treated a 42-year-old woman diagnosed to have classical bilateral pigment dispersion syndrome combined with an intraocular pressure (IOP) of up to 28 mmHg in both eyes. The patient now has a daughter, also with pigment dispersion syndrome. Miotic treatment brought the IOPs to normal, and 8 years later when the disease was in the inactive phase all treatment could be discontinued. At the age of 67 years, exfoliation deposits became visible in the right eye only, but the IOPs were still below 21 mmHg. Four years later, the pressure of the right eye rose to 31 mmHg. During the next few years all available IOP-lowering medications and laser trabeculoplasty failed, and finally trabeculectomy had to be performed to keep the pressure of the right eye under control and to halt visual field changes, which had already appeared. This case illustrates that development of exfoliation syndrome may take place irrespective of pigment dispersion, and that their simultaneous occurrence may lead to an IOP rise that is resistant to medical therapy and laser trabeculoplasty. It additionally provides further clues to the pathogenesis of capsular glaucoma.
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