PurposeThe aim of this report is to present a case of a patient, metal foundry worker, who had been exposed to industrial silver salts for over 20 years. It is well established that chronic exposure to silver compounds can cause accumulation of silver deposits in various tissues. This condition is referred to as argyrosis or argyria, whereas changes related to eye tissues are defined as ocular argyrosis.MethodsA complete eye examination, corneal confocal microscopy, kinetic and static visual field test, posterior segment optical coherent tomography, pattern visual evoked potentials (PVEP), flash visual evoked potentials, multifocal electroretinogram, pattern electroretinogram (PERG), full-field electroretinography (FERG) and electrooculogram were all performed.ResultsEye examination revealed decreased visual acuity, corneal deposits and drusenoid changes within the macula. Although electrophysiology tests did not show changes in the function of retinal pigment epithelium, they revealed abnormal function of photoreceptors in the central and peripheral retina. PERG abnormalities and delayed latency of P100 wave in PVEP confirmed impaired function of the inner layers of the retina in the macular region.ConclusionsCorneal confocal microscopy and electrophysiological tests may help confirm the diagnosis of ocular argyrosis.
BackgroundThe aim of this article was to describe the role of ceruloplasmin and to report preliminary results of ceruloplasmin concentrations in patients with primary open-angle glaucoma (POAG) with cataract and in patients with only cataract.Glaucoma, a neurodegenerative disease, is a heterogeneous group of conditions characterized by loss of retinal ganglion cells (RGC), their axons, progressive optic nerve damage, and visual field deterioration.Material/MethodsThe POAG group included 30 patients and the cataract group included 25 patients.ResultsCeruloplasmin plays an essential role in iron metabolism and inactivating free radicals. In the presented pilot study, serum ceruloplasmin level was lower in the POAG group in comparison to the group with only cataract.ConclusionsIn treating persistent inflammation in the course of glaucoma, antiglaucoma drugs may increase the permeability of the blood-ocular barrier, which may be connected with the lower concentration of serum ceruloplasmin in the glaucoma patients group.
ObjectiveManagement of Graves’ orbitopathy remains a challenge. Our previous case report has shown promising results for rabbit antithymocyte globulin (rATG) in the treatment of Graves’ orbitopathy.DesignWe present the response of 7 individuals with active moderate-to-severe steroid-resistant Graves’ orbitopathy to rATG, representing preliminary results from a prospective single-center study.MethodsrATG was administered intravenously at a dose of 0.8–1.0 mg/kg daily (cumulative dose of 150–200 mg). The primary outcome measures at weeks 24 and 48 were ≥2-point reduction in Clinical Activity Score from baseline, a proptosis response, a diplopia response, and improvement of distant best-corrected visual acuity and mean retinal sensitivity. Key secondary outcomes included stabilization of ganglion cell complex thickness, a decrease of retinal nerve fiber layer in OCT, and a reduction in CD4/CD8 ratio and TRAb at 48 weeks.ResultsAn improvement in clinical activity score was observed in all patients, with disease inactivation in 3 cases. Proptosis reduction equal to or greater than 2 mm was noted for 8 of 10 eyes. Diplopia improved in three of 6 patients. There was an improvement in best-corrected visual acuity (from 0.69 to 0.78) and mean retinal sensitivity (from 20.8 to 23.5 dB). In addition, there was a long-lasting improvement in CD4/CD8 ratio in 6 patients. Two patients experienced adverse events (influenza and serum sickness).ConclusionrATG therapy offers a long-lasting improvement in moderate-to-severe steroid-resistant Graves’ orbitopathy with improvement in functional vision (reduction of diplopia, improvement of visual acuity, retinal sensitivity, and VEP pattern). The therapy is well-tolerated.Clinical Trial RegistrationClinicalTrials.gov, identifier NCT05199103.
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