Is primary open-angle glaucoma an ocular manifestation of systemic disease?

Wey, Stephanie; Amanullah, Sarah; Spaeth, George L.; Ustaoglu, Melih; Rahmatnejad, Kamran; Katz, L. Jay

doi:10.1007/s00417-019-04239-9

Cited by 30 publications

(18 citation statements)

References 98 publications

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“…While high intraocular pressure (IOP) is a well-known treatable risk factor, discussion remains regarding the exact mechanism of both primary open-angle glaucoma (POAG) and primary angle-closure glaucoma (PACG) (3)(4)(5). Notably, vascular dysfunction, autoimmune processes, impaired systemic oxidation/anti-oxidation balance and infl ammatory pathways are blamed as underlying molecular mechanisms (6)(7)(8)(9)(10)(11). Therefore, there could be a role of systemic infl ammation in the etiopathogenesis of glaucoma.…”

Section: Introductionmentioning

confidence: 99%

Systemic inflammation in both open-angle and angle-closure glaucoma: role of platelet-to-lymphocyte ratio

Karahan¹,

Kılıç²,

Güven³

2021

BLL

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AIM: To analyse the effect of systemic infl ammatory status in patients with primary open-angle glaucoma (POAG) and primary angle-closure glaucoma (PACG) by calculating platelet-to-lymphocyte ratio (PLR) and neutrophil-to-lymphocyte ratio (NLR). METHODS: This retrospective case-control study included 200 patients with POAG, 22 patients with PACG and 100 healthy subjects. The participants' white-blood-cell, lymphocyte, neutrophil, and platelet counts were recorded from previous blood assays. NLR and PLR were calculated manually. Results were compared among the groups. RESULTS: Both the POAG and PACG groups had higher platelet counts and PLR values than the control group (p=0.001 and p=0.001; respectively). The difference in NLR between POAG, PACG and control groups was not statistically signifi cant (p=0.076). The POAG group had higher NLR values than the control (p=0.035). CONCLUSION: Both the POAG and the PACG groups exhibited higher platelet and PLR levels than the control. These results indicate a potential role of systemic infl ammation in the pathogenesis of POAG and

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Section: Introductionmentioning

confidence: 99%

Systemic inflammation in both open-angle and angle-closure glaucoma: role of platelet-to-lymphocyte ratio

Karahan¹,

Kılıç²,

Güven³

2021

BLL

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“…Previous studies that examined the role of vascular function in glaucoma pathophysiology suggested that vasospasm, systemic hypotension, angiographic vascular perfusion defects, and alterations in blood flow parameters may result in or be a result of reduced vascular perfusion in the optic nerve head and/or retina consequently leading or at least contributing to glaucoma onset and progression [4,[28][29][30][31]. Some authors even regard normal tension glaucoma as an ocular manifestation of a systemic vascular dysfunction, as reflected in the so called Flammer syndrome [32,33]. Other research groups found retinal vascular abnormalities in normal-tension and high-tension glaucoma patients, which include narrowing of retinal blood vessels, optic disc hemorrhage, and reduction of blood vessel density [12,34,35].…”

Section: Discussionmentioning

confidence: 99%

Elevated Intraocular Pressure Causes Abnormal Reactivity of Mouse Retinal Arterioles

Gericke

Mann

Zadeh

et al. 2019

Oxidative Medicine and Cellular Longevity

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Objective. Glaucoma is a leading cause of severe visual impairment and blindness. Although high intraocular pressure (IOP) is an established risk factor for the disease, the role of abnormal ocular vessel function in the pathophysiology of glaucoma gains more and more attention. We tested the hypothesis that elevated intraocular pressure (IOP) causes vascular dysfunction in the retina. Methods. High IOP was induced in one group of mice by unilateral cauterization of three episcleral veins. The other group received sham surgery only. Two weeks later, retinal vascular preparations were studied by video microscopy in vitro. Reactive oxygen species (ROS) levels and expression of hypoxia markers and of prooxidant and antioxidant redox genes as well as of inflammatory cytokines were determined. Results. Strikingly, responses of retinal arterioles to stepwise elevation of perfusion pressure were impaired in the high-IOP group. Moreover, vasodilation responses to the endothelium-dependent vasodilator, acetylcholine, were markedly reduced in mice with elevated IOP, while no differences were seen in response to the endothelium-independent nitric oxide donor, sodium nitroprusside. Remarkably, ROS levels were increased in the retinal ganglion cell layer including blood vessels. Expression of the NADPH oxidase isoform, NOX2, and of the inflammatory cytokine, TNF-α, was increased at the mRNA level in retinal explants. Expression of NOX2, but not of the hypoxic markers, HIF-1α and VEGF-A, was increased in the retinal ganglion cell layer and in retinal blood vessels at the protein level. Conclusion. Our data provide first-time evidence that IOP elevation impairs autoregulation and induces endothelial dysfunction in mouse retinal arterioles. Oxidative stress and inflammation, but not hypoxia, appear to be involved in this process.

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“…Pathophysiologisch wird das POWG derzeit als eine neurodegenerative Erkrankung und die glaukomatöse Optikusneuropathie als ein Teil dieses Systemprozesses angesehen [5]. Neben einer Beteiligung des visuellen Kortex und dem Corpus geniculatum laterale ist auch das gesamte Zentralnervensystem (ZNS) betroffen [6 -9].…”

Section: Sekundäre Neuroprotektion Beim Glaukom Durch Ergänzende Mediunclassified

Sekundäre Neuroprotektion beim Glaukom durch ergänzende medikamentöse Therapiekonzepte

Erb

2020

Klin Monatsbl Augenheilkd

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ZusammenfassungDas primäre Offenwinkelglaukom (POWG) wird derzeit als eine neurodegenerative Systemerkrankung angesehen. Die alleinige individualisierte Augeninnendrucksenkung wird dabei dem komplexen Geschehen im chronischen Verlauf der Erkrankung nicht gerecht werden, sodass begleitende medikamentöse Therapiekonzepte sinnvoll sind. Anhand von 4 Therapiestrategien, wie die Verbesserung der mitochondrialen Atmungskette mit Coenzym Q10, die Stabilisierung der mitochondrialen und zellulären Plasmamembranen mit Citicolin, die Verminderung des oxidativen Stresses am Auge und im Körper mit Curcumin und die Verbesserung des Fettstoffwechsels, speziell des LDL-Cholesterins, mit der Anwendung der Statine, soll ein Einblick in mögliche additive Therapieansätze gegeben werden. Da neuroprotektive Therapien als Monotherapien wenig erfolgversprechend sein dürften, werden sie eher in der Kombination aus verschiedenen Therapieansätzen bestehen.

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Is primary open-angle glaucoma an ocular manifestation of systemic disease?

Cited by 30 publications

References 98 publications

Systemic inflammation in both open-angle and angle-closure glaucoma: role of platelet-to-lymphocyte ratio

Systemic inflammation in both open-angle and angle-closure glaucoma: role of platelet-to-lymphocyte ratio

Elevated Intraocular Pressure Causes Abnormal Reactivity of Mouse Retinal Arterioles

Sekundäre Neuroprotektion beim Glaukom durch ergänzende medikamentöse Therapiekonzepte

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