scholarly journals The Effect of Intraocular Pressure-Lowering Medication on Metastatic Uveal Melanomas

Cancers ◽  
2021 ◽  
Vol 13 (22) ◽  
pp. 5657
Author(s):  
Jan Pals ◽  
Hanneke W. Mensink ◽  
Erwin Brosens ◽  
Robert M. Verdijk ◽  
Nicole C. Naus ◽  
...  
Keyword(s):  
Intraocular Pressure ◽  
Aqueous Humor ◽  
Medical Records ◽  
Ciliary Body ◽  
Retrospective Cohort ◽  
Survival Analyses ◽  
Aqueous Humor Outflow ◽  
Pressure Lowering ◽  
Secondary Analyses ◽  
Ciliary Body Melanoma

Background: There has been speculation that IOP-lowering medication, which increases aqueous humor outflow, increases the risk of metastatic uveal melanoma (UM). This hypothesis has not been studied previously but is relevant for UM patients who use IOP-lowering medication. The aim of the current study is to assess the association between the use of intraocular pressure (IOP)-lowering medication and the risk of metastatic UM, and mortality. Methods: A retrospective cohort study, in which patients from the Rotterdam Ocular Melanoma Study were included from 1986 onwards. Medical records were evaluated for use of IOP-lowering medication at baseline (i.e., before diagnosis). For each IOP-lowering medication, we divided patients into two groups for comparison (e.g., patients with alpha2-agonist use and patients without alpha2-agonist use). All patients underwent regular ophthalmic examinations and routine screening for metastasis. Survival analyses were initiated to compare groups in each IOP-lowering medication group. In addition, secondary analyses were performed to examine the association between IOP and the development of metastatic UM, and mortality. Results: A total of 707 patients were included of whom 13 patients used prostaglandin or pilocarpine at baseline. For alpha2-agonist, beta-blocker, carbonic anhydrase inhibitor, and oral IOP-lowering medication these were 4, 14, 11, and 12 patients, respectively. The risk of metastatic UM (choroid and ciliary body melanoma) among the prostaglandin/pilocarpine users was significantly higher than controls (HR [95% CI]: 4.840 [1.452–16.133]). Mortality did not differ significantly among the IOP-lowering medications groups, except for the prostaglandin or pilocarpine group (HR [95% CI]: 7.528 [1.836–30.867]). If we combined all IOP-lowering medication that increase aqueous humor outflow, the risk (HR [95% CI]) of metastatic UM and mortality was 6.344 (1.615–24.918) and 9.743 (2.475–38.353), respectively. There was an association between IOP and mortality, but not for the onset of metastatic UM. Conclusion: The use of topical prostaglandin or pilocarpine may increase the risk of metastatic UM and mortality compared to patients without prostaglandin or pilocarpine use. Therefore, use of IOP-lowering medication which increases aqueous humor outflow, should be avoided in patients with (presumed) UM.

scholarly journals Progressive spectacle correction in patients with ametropia and primary open-angle glaucoma

The Eye ◽  
2019 ◽  
Vol 125 (2019-1) ◽  
pp. 6-12
Author(s):  
Irina Gndoyan ◽  
Natalya Kuznetsova ◽  
Alexander Derevyanchenko
Keyword(s):  
Intraocular Pressure ◽  
Aqueous Humor ◽  
Primary Open Angle Glaucoma ◽  
Open Angle Glaucoma ◽  
Main Group ◽  
Control Group ◽  
Open Angle ◽  
Aqueous Humor Outflow ◽  
Vision Correction ◽  
Spectacle Correction

Purpose: To determine the role that progressive spectacle lenses play in intraocular pressure compensation and stabilization of the glaucomatous process in patients with primary open-angle glaucoma (POAG) combined with presbyopia and refractive errors. Material and methods. 29 patients (53 eyes) aged 43 to 67 years with I-II stage POAG and a certain type of refractive error were enrolled into study. All patients had intraocular pressure (IOP) compensated to the target level on medication. Patients of the main group (17 people, 32 eyes) used universal progressive spectacle lenses with optimized surface. The patients of the control group (12 people, 21 eyes) used separate monofocal glasses for near and distance vision as a method of ametropia correction. Visual acuity test, refractometry, pneumotonometry, tonography, automated static perimetry were applied for monitoring the patients. The measurements were taken before spectacle correction and a year after its prescription. Results. A decrease of IOP (p=0.01) and an increase of the aqueous humor outflow coefficient (p<0.01) were determined after one year use of the recommended type of vision correction in the main group, whereas in the control group there was an increased level of IOP (p<0.05) and a reduced aqueous humor outflow coefficient (p<0.2). Conclusion. The use of progressive spectacle lenses as a method of permanent vision correction reliably reduces IOP and improves the aqueous humor outflow in patients with early-stage POAG. The absence of negative visual field dynamics indicates the stabilization of the glaucomatous process.

Anterior Chamber Angle and Iris-Lens Contact Alteration During Pupillary Dilation

2011 ◽  
Author(s):  
Sara Jouzdani ◽  
Rouzbeh Amini ◽  
Victor H. Barocas
Keyword(s):  
Intraocular Pressure ◽  
Anterior Chamber ◽  
Aqueous Humor ◽  
Ciliary Body ◽  
Ocular Tissue ◽  
Posterior Chamber ◽  
Pupillary Dilation ◽  
Anterior Chamber Angle ◽  
Aqueous Outflow ◽  
Chamber Angle

The aqueous humor (AH) provides oxygen and nutrients for the avascular ocular tissue specifically, the cornea and lens. AH is secreted by the ciliary body into the posterior chamber, passes through pupil, and drains into the anterior chamber (Fig. 1a). Resistance to the aqueous outflow generates the intraocular pressure (IOP), which is 15–20 mmHg in the normal eyes.

scholarly journals Systemic Hypertension Effects on the Ciliary Body and Iris. An Immunofluorescence Study with Aquaporin 1, Aquaporin 4, and Na+, K+ ATPase in Hypertensive Rats

Cells ◽  
2018 ◽  
Vol 7 (11) ◽  
pp. 210 ◽  
Author(s):  
Ibrahim González-Marrero ◽  
Luis Hernández-Abad ◽  
Emilia Carmona-Calero ◽  
Leandro Castañeyra-Ruiz ◽  
José Abreu-Reyes ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Intraocular Pressure ◽  
Aqueous Humor ◽  
Ciliary Body ◽  
Aquaporin 4 ◽  
Systemic Hypertension ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Aquaporin 1 ◽  
Wistar Kyoto

Aquaporin 1 (AQP1) and aquaporin 4 (AQP4) have been identified in the eye as playing an essential role in the formation of the aqueous humor along with the Na+/K+ ATPase pump. Different authors have described the relationship between blood pressure, aqueous humor production, and intraocular pressure with different conclusions, with some authors supporting a positive correlation between blood pressure and intraocular pressure while others disagree. The aim of this work was to study the effect of high blood pressure on the proteins involved in the production of aqueous humor in the ciliary body (CB) and iris. For this purpose, we used the eyes of spontaneously hypertensive rats (SHR) and their control Wistar-Kyoto rats (WKY). Immunofluorescence was performed in different eye structures to analyze the effects of hypertension in the expression of AQP1, AQP4, and the Na+/K+ ATPase α1 and α2 subunits. The results showed an increase in AQP1 and Na+/K+ ATPase α1 and a decrease in AQP4 and Na+/K+ ATPase α2 in the CB of SHR, while an increase in AQP4 and no significant differences in AQP1 were found in the iris. Therefore, systemic hypertension produced changes in the proteins implicated in the movement of water in the CB and iris that could influence the production rate of aqueous humor, which would be affected depending on the duration of systemic hypertension.

scholarly journals The Effects of Prostaglandin Analogs on Intraocular Pressure in Human Eye for Open Angle Glaucoma

2020 ◽  
Vol 10 (2) ◽  
pp. 176-180
Author(s):  
Shabab Akbar ◽  
Sapna Ratan Shah
Keyword(s):  
Fluid Flow ◽  
Intraocular Pressure ◽  
Aqueous Humor ◽  
Trabecular Meshwork ◽  
Ciliary Body ◽  
Open Angle Glaucoma ◽  
Posterior Chamber ◽  
Open Angle ◽  
Permeable Channel ◽  
Aqueous Outflow

The effects of Prostaglandin Analogs on intraocular pressure and increased aqueous outflow via trabecular meshwork into the schlemm’s canal has been studied in this present research paper. Aqueous humor is an outflow, which flows at the back of the iris in the posterior chamber all the way through the pupil aperture, out into the anterior chamber, and drain from the eye via drainage slope. The eye keeps on making aqueous humor in the ciliary body and it passes through the trabecular meshwork into the scheme of the canal, the key drainage from the eye and it finally goes to the “collector channels” and due to the less amount of aqueous humor fluid flow from the drainage angle, the pressure in the eye starts to increase. For this study, the canal of Schlemm is assumed as a permeable channel. And it is connected by trabecular meshwork. The inner layer of the canal's wall has been assumed as permeable. And the aqueous humor drains into the canal through this porous tissue wall. The objective of this paper is to discuss the effect of prostaglandin analogs on intraocular pressure as the Prostaglandin Analogs work by increasing the outflow of aqueous from the eye.

scholarly journals New Insights Into Pathophysiological Mechanisms Regulating Conventional Aqueous Humor Outflow

Medicina ◽  
2013 ◽  
Vol 49 (4) ◽  
pp. 26 ◽  
Author(s):  
Daiva Paulavičiūtė-Baikštienė ◽  
Rūta Baršauskaitė ◽  
Ingrida Janulevičienė
Keyword(s):  
Intraocular Pressure ◽  
Aqueous Humor ◽  
Trabecular Meshwork ◽  
Kinase Inhibitors ◽  
Transforming Growth Factor ◽  
Protein Kinase Inhibitors ◽  
Pathophysiological Mechanisms ◽  
Aqueous Humor Outflow ◽  
Trabecular Meshwork Cells ◽  
Glaucoma Treatment

The aim of the article was to overview the pathophysiology of the conventional outflow pathway, trabecular meshwork, and intraocular pressure and to discuss the options of future glaucoma treatment directed to improvement in aqueous outflow. The literature search in the Medline, Embase, and Cochrane databases from April to May 2012 was performed; a total of 47 articles analyzed. The diminished conventional pathway may be altered by several pathophysiological mechanisms like TM obstruction caused by transforming growth factor-β2, clastic nondeformable cells, macrophages leaking from hypermature cataract, iris pigment, lens capsular fragments after YAG-laser posterior capsulotomy, proteins and their subfragments. It is known that trabecular meshwork contraction reduces outflow, and the actomyosin system is directly linked to this mechanism. New glaucoma drugs are still under investigation, but it is already proven that agents such as latranculin-B are effective in improving aqueous drainage. Selective Rho-associated coiled coilforming protein kinase inhibitors have been shown to cause a significant improvement in outflow facility and may become a new option for glaucoma treatment. Caldesmon negatively regulates actin-myosin interactions and thus increases outflow. Stem cells may replace missing or nonfunctional trabecular meshwork cells and hopefully will bring a new treatment solution. Pathophysiological mechanisms regulating conventional aqueous humor outflow are still not fully understood and require further investigations. Future treatment decisions should be directed to a specific mechanism regulating an elevation in intraocular pressure.

Development of a Two-Color Fluorescent Tracer Technique to Study Aqueous Outflow Patterns and Outflow Resistance in Human Eyes

2007 ◽  
Author(s):  
Steven J. Folz ◽  
Hiayan Gong ◽  
Darryl R. Overby
Keyword(s):  
Intraocular Pressure ◽  
Aqueous Humor ◽  
Tracer Technique ◽  
Outflow Resistance ◽  
Fluorescent Tracer ◽  
Aqueous Humor Outflow ◽  
Elevated Intraocular Pressure ◽  
Human Eyes ◽  
Outflow Pathway ◽  
Aqueous Outflow

Glaucoma is a leading cause of blindness, and elevated intraocular pressure (IOP) characteristic of glaucoma is caused by increased aqueous humor outflow resistance. Studies have localized the bulk of outflow resistance to particular regions along the outflow pathway — namely, the inner wall endothelium of Schlemm’s canal and its underlying juxtacanalicular tissue (JCT) [1] — but the hydrodynamic details of how aqueous humor flows through these tissues and how these tissues generate outflow resistance are not well understood.

scholarly journals Mechanotransduction and dynamic outflow regulation in trabecular meshwork requires Piezo1 channels

2020 ◽  
Author(s):  
Oleg Yarishkin ◽  
Tam T. T. Phuong ◽  
Jackson M. Baumann ◽  
Michael L. De Ieso ◽  
Felix Vazquez-Chona ◽  
...  
Keyword(s):  
Intraocular Pressure ◽  
Shear Flow ◽  
Aqueous Humor ◽  
Trabecular Meshwork ◽  
Molecular Mechanisms ◽  
Pressure Sensors ◽  
Focal Adhesions ◽  
Ruthenium Red ◽  
Pressure Transducers ◽  
Aqueous Humor Outflow

AbstractMechanosensitivity of the trabecular meshwork (TM) is a key determinant of intraocular pressure (IOP) yet our understanding of the molecular mechanisms that subserve it remains in its infancy. Here, we show that mechanosensitive Piezo1 channels modulate the TM pressure response via calcium signaling and dynamics of the conventional outflow pathway. Pressure steps evoked fast, inactivating cation currents and calcium signals that were inhibited by Ruthenium Red, GsMTx4 and Piezo1 shRNA. Piezo1 expression was confirmed by transcript and protein analysis, and by visualizing Yoda1-mediated currents and [Ca2+]i elevations in primary human TM cells. Piezo1 activation was obligatory for transduction of physiological shear stress and was coupled to reorganization of F-actin cytoskeleton and focal adhesions. The importance of Piezo1 channels as pressure sensors was shown by the GsMTx4 -dependence of the pressure-evoked current and conventional outflow function. We also demonstrate that Piezo1 collaborates with the stretch-activated TRPV4 channel, which mediated slow, delayed currents to pressure steps. Collectively, these results suggest that TM mechanosensitivity utilizes kinetically, regulatory and functionally distinct pressure transducers to inform the cells about force-sensing contexts. Piezo1-dependent control of shear flow sensing, calcium homeostasis, cytoskeletal dynamics and pressure-dependent outflow suggests a novel potential therapeutic target for treating glaucoma.Significance StatementTrabecular meshwork (TM) is a highly mechanosensitive tissue in the eye that regulates intraocular pressure through the control of aqueous humor drainage. Its dysfunction underlies the progression of glaucoma but neither the mechanisms through which TM cells sense pressure nor their role in aqueous humor outflow are understood at the molecular level. We identified the Piezo1 channel as a key TM transducer of tensile stretch, shear flow and pressure. Its activation resulted in intracellular signals that altered organization of the cytoskeleton and cell-extracellular matrix contacts, and modulated the trabecular component of aqueous outflow whereas another channel, TRPV4, mediated a delayed mechanoresponse. These findings provide a new mechanistic framework for trabecular mechanotransduction and its role in the regulation of fast fluctuations in ocular pressure, as well as chronic remodeling of TM architecture that epitomizes glaucoma.

scholarly journals Pharmacologic Trabeculectomy—Modulation of Aqueous Humor Outflow Through the Trabecular Meshwork

2015 ◽  
Vol 8 (1) ◽  
pp. 46
Author(s):  
Syed Shoeb Ahmad ◽  
Syed Zia-ur-Rahman ◽  
Norlina Ramli ◽  
Shuaibah Abdul Ghani ◽  
◽  
...  
Keyword(s):  
Aqueous Humor ◽  
Trabecular Meshwork ◽  
Ciliary Body ◽  
Aqueous Humor Outflow ◽  
Aqueous Humor Dynamics ◽  
Aqueous Outflow

“Pharmacologic trabeculectomy” is a term used to describe the modulation of aqueous outflow by the biochemical manipulation of the trabecular meshwork. Most of the medications currently in use either reduce aqueous production or increase its outflow through the ciliary body. However, there is a new group of agents being investigated, which can increase the facility of aqueous humor outflow through the trabecular meshwork. Thus, these agents will be able to provide a more physiologic means to control aqueous humor dynamics. This review sheds light on this concept of “medical trabeculectomy.”

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