scholarly journals An Iconic Case of Pigmentary Glaucoma: Brief Review of the Literature

2020 ◽  
Vol 11 (2) ◽  
pp. 377-384
Author(s):  
Mariachiara Di Pippo ◽  
Chiara Ciancimino ◽  
Luca Scuderi ◽  
Andrea Perdicchi

Pigment dispersion syndrome and pigmentary glaucoma are two conditions characterized by pigment dispersion originating from the posterior part of the iris and its accumulation on the trabecular meshwork, corneal endothelium, and anterior surface of the lens. The pigment on the trabecular meshwork can cause chronic inflammation with a secondary reduction of its function and an increase in intraocular pressure. The case presented represents a typical example of pigmentary glaucoma in a myopic patient in which all the signs, symptoms, and complications typical of these pathologies were present. We report and describe an 8-year-long follow-up period with clinical and instrumental examinations.

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 174 ◽  
Author(s):  
Yalong Dang ◽  
Susannah Waxman ◽  
Chao Wang ◽  
Priyal Shah ◽  
Ralitsa T. Loewen ◽  
...  

Background: Outflow regulation and phagocytosis are key functions of the trabecular meshwork (TM), but it is not clear how the two are related in secondary open angle glaucomas characterized by an increased particle load. We hypothesized that diminished TM phagocytosis is not the primary cause of early ocular hypertension and recreated pigment dispersion in a porcine ex vivo model. Methods: Sixteen porcine anterior chamber cultures received a continuous infusion of pigment granules (Pg), while 16 additional anterior chambers served as controls (C). Pressure transducers recorded the intraocular pressure (IOP). The phagocytic capacity of the trabecular meshwork was determined by fluorescent microspheres. Results: The baseline IOPs in Pg and C were similar (P=0.82). A significant IOP elevation occurred in Pg at 48, 120, and 180 hours (all P<0.01, compared to baseline). The pigment did not cause a reduction in TM phagocytosis at 48 hours, when the earliest IOP elevation occurred, but at 120 hours onward (P=0.001 compared to C). This reduction did not result in an additional IOP increase at 120 or 180 hours compared to the first IOP elevation at 48 hours (P>0.05). Conclusions: In this porcine model of pigmentary glaucoma, an IOP elevation occurs much earlier than when phagocytosis fails, suggesting that two separate mechanisms might be at work.


F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 174
Author(s):  
Yalong Dang ◽  
Susannah Waxman ◽  
Chao Wang ◽  
Priyal Shah ◽  
Ralitsa T. Loewen ◽  
...  

Background: Outflow regulation and phagocytosis are key functions of the trabecular meshwork (TM), but it is not clear how the two are related in secondary open angle glaucomas characterized by an increased particle load. We hypothesized that diminished TM phagocytosis is not the primary cause of early ocular hypertension and recreated pigment dispersion in a porcine ex vivo model. Methods: Sixteen porcine anterior chamber cultures received a continuous infusion of pigment granules (Pg), while 16 additional anterior chambers served as controls (C). Pressure transducers recorded the intraocular pressure (IOP). The phagocytic capacity of the trabecular meshwork was determined by fluorescent microspheres. Results: The baseline IOPs in Pg and C were similar (P=0.82). A significant IOP elevation occurred in Pg at 48, 120, and 180 hours (all P<0.01, compared to baseline). The pigment did not cause a reduction in TM phagocytosis at 48 hours when the earliest IOP elevation occurred, but at 120 hours onward (P=0.001 compared to C). This reduction did not result in an additional IOP increase at 120 or 180 hours compared to the first IOP elevation at 48 hours (P>0.05). Conclusions: In this porcine model of pigmentary glaucoma, an IOP elevation occurs much earlier than when phagocytosis fails, suggesting that two separate mechanisms might be at work.


2017 ◽  
Author(s):  
Yalong Dang ◽  
Susannah Waxman ◽  
Chao Wang ◽  
Ralista T. Loewen ◽  
Ming Sun ◽  
...  

AbstractPigment dispersion syndrome can lead to pigmentary glaucoma (PG), a poorly understood condition of younger, myopic eyes with fluctuating, high intraocular pressure (IOP). The absence of a model similar in size and behavior to human eyes has made it difficult to investigate its pathogenesis. Here, we present a porcine ex vivo model that recreates the features of PG including intraocular hypertension, pigment accumulation in the trabecular meshwork and relative failure of phagocytosis. Inin vitromonolayer cultures as well as inex vivoeye perfusion cultures, we found that the trabecular meshwork (TM) cells that regulate outflow, form actin stress fibers and have a decreased phagocytosis. Gene expression microarray and pathway analysis indicated key roles of RhoA in regulating the TM cytoskeleton, motility, and phagocytosis thereby providing new targets for PG therapy.


2017 ◽  
Author(s):  
Yalong Dang ◽  
Susannah Waxman ◽  
Chao Wang ◽  
Ralitsa T. Loewen ◽  
Nils A. Loewen

AbstractPurposeOutflow regulation and phagocytosis are key functions of the trabecular meshwork (TM), but it is not clear how the two are related in secondary open angle glaucomas characterized by an increased particle load. We hypothesized that diminished TM phagocytosis is not the primary cause of early ocular hypertension and recreated pigment dispersion in a porcine ex vivo model.Materials and MethodsSixteen porcine anterior chamber cultures received a continuous infusion of pigment granules (P), while 16 additional anterior chambers served as controls (C). Pressure transducers recorded the intraocular pressure (IOP). The phagocytic capacity of the trabecular meshwork was determined by fluorescent microspheres.ResultsThe baseline IOPs in P and C were similar (P=0.82). A significant IOP elevation occurred in P at 48, 120, and 180 hours (all P<0.01, compared to baseline). The pigment did not cause a reduction in TM phagocytosis at 48 hours, when the earliest IOP elevation occurred, but at 120 hours onward (P=0.001 compared to C). This reduction did not result in an additional IOP increase at 120 or 180 hours compared to the first IOP elevation at 48 hours (P>0.05).ConclusionIn this porcine model of pigmentary glaucoma, an IOP elevation occurs much earlier than when phagocytosis fails, suggesting that two separate mechanisms might be at work.


2012 ◽  
Vol 93 (6) ◽  
pp. 969-972 ◽  
Author(s):  
R F Akhmetshin ◽  
E A Abdulaeva ◽  
S N Bulgar

Aim. To assess the pigment dispersion syndrome and pigmentary glaucoma treatment results. Methods. 22 patients (44 eyes) aged 16 to 38 years (male - 12, female - 10) were observed. Pigmentary glaucoma was diagnosed in 12 eyes, pigment dispersion syndrome - in 32 eyes. Visual acuity testing, visual field testing, biomicroscopy, ocular tonometry and tonography, ophthalmoscopy, gonioscopy, scanning laser ophtalmoscopy, computed perimetry were performed. The follow-up period ranged from 6 months to 10 years. All patients underwent laser iridotomy. All patients were treated with anti-glaucoma medications and antioxidants unless intraocular pressure was compensated. Results. Intraocular pressure was lowered to normal in 26 out of 44 eyes. Intraocular pressure was compensated on the rest of 18 eyes using treatment with local pressure-lowering medications and antioxidants. Laser iridotomy allowed to remove the anatomical predisposition (the main pathogenetic link) leading to additional pigment deposition and intraocular pressure increase. Prolonged use of antioxidants has resulted in tear outflow drainage and normalization level of intraocular pressure. Conclusion. Early diagnosis of the pigment dispersion syndrome and proper treatment tactics allows to prevent the pigmentary glaucoma development and to preserve the vision.


2010 ◽  
Vol 3 (1) ◽  
pp. 8-14
Author(s):  
Ellen Svarverud

Pigment dispersion syndrome (PDS) is a condition of the anterior segment of the eye characterised by pigment deposition on a number of ocular structures. The condition is usually bilateral but most commonly asymmetric. In PDS, pigment is released from the posterior surface of the iris due to friction between the zonules and the iris. In itself, the condition does not represent any problems for the patient, but pigment deposition in the trabecular meshwork may interfere with drainage of the anterior chamber fluid and cause pigmentary glaucoma (PG). This case report presents a young myopic female with many of the classic signs of PDS; Krukenberg’s spindle, transillumination of mid-peripheral iris, deep anterior chambers, concave iris profile and increased pigmentation in the trabecular meshwork. Various diagnostic methods were applied to reveal clinical signs and to establish the patient’s visual function. Optic nerve heads and intraocular pressure were normal, but visual fields were suspect. The patient was advised to make an appointment with an ophthalmologist. Risk factors for development of PG and management of patients with PDS will be discussed.


BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Carly van der Heide ◽  
Wes Goar ◽  
Kacie J. Meyer ◽  
Wallace L. M. Alward ◽  
Erin A. Boese ◽  
...  

Abstract Background Glaucoma is a leading cause of visual disability and blindness. Release of iris pigment within the eye, pigment dispersion syndrome (PDS), can lead to one type of glaucoma known as pigmentary glaucoma. PDS has a genetic component, however, the genes involved with this condition are largely unknown. We sought to discover genes that cause PDS by testing cohorts of patients and controls for mutations using a tiered analysis of exome data. Results Our primary analysis evaluated melanosome-related genes that cause dispersion of iris pigment in mice (TYRP1, GPNMB, LYST, DCT, and MITF). We identified rare mutations, but they were not statistically enriched in PDS patients. Our secondary analyses examined PMEL (previously linked with PDS), MRAP, and 19 other genes. Four MRAP mutations were identified in PDS cases but not in controls (p = 0.016). Immunohistochemical analysis of human donor eyes revealed abundant MRAP protein in the iris, the source of pigment in PDS. However, analysis of MRAP in additional cohorts (415 cases and 1645 controls) did not support an association with PDS. We also did not confirm a link between PMEL and PDS in our cohorts due to lack of reported mutations and similar frequency of the variants in PDS patients as in control subjects. Conclusions We did not detect a statistical enrichment of mutations in melanosome-related genes in human PDS patients and we found conflicting data about the likely pathogenicity of MRAP mutations. PDS may have a complex genetic basis that is not easily unraveled with exome analyses.


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