“…ET-1-induced glaucomatous optic neuropathy has been reported in the eyes of a variety of model animals: rabbits, primates, mice and rats [23]. Intraocular ET-1 injections induce chronic ischemia of the optic nerve that causes retinal ganglion cell-specific death and glaucomatous cupping of the optic nerve head (ONH).…”
Endothelin-1 (ET-1) is a potent vasoconstrictor and is considered to have a key role in the regulation of ocular perfusion and glaucoma pathogenesis. High ET-1 and ET A -receptor levels are reported in patients with primary open-angle glaucoma (POAG). We compared the mean plasma ET-1 and ET Areceptor concentration of controls and patients with early and advanced POAG stage, and assessed the correlation with the retinal nerve fibre layer (RNFL) thickness. The study included a total of 75 participants, aged 45-83 years: 25 (controls), 22 (early glaucoma) and 28 (advanced glaucoma). The plasma concentration of ET-1 and ET A -receptor was determined by enzyme-linked immunosorbent assay. The RNFL thickness was evaluated with spectral-domain optical coherence tomography. The mean ET-1 concentration was lower in the control group (4.88 § 1.75 pg/mL) than in the early and advanced POAG group (6.33 § 2.38 and 6.34 § 1.56 pg/mL). Statistically significant difference was found between the mean ET-1 concentrations in controls and glaucoma patients (p = 0.029 -early glaucoma, p = 0.018 -advanced glaucoma), and no significant difference was observed between the two POAG groups (p = 0.998). The mean ET A -receptor concentration was highest in the control group (1209.28 § 314.48 pg/mL) and the differences between the three groups were significant. Significant relationship was found only between ET-1 and RNFL. This study demonstrated the role of ET-1 in glaucoma pathogenesis based on the observed significant high ET-1 and ET A -receptor plasma levels in POAG patients. A new therapeutical approach needs to be considered in some patients.
“…ET-1-induced glaucomatous optic neuropathy has been reported in the eyes of a variety of model animals: rabbits, primates, mice and rats [23]. Intraocular ET-1 injections induce chronic ischemia of the optic nerve that causes retinal ganglion cell-specific death and glaucomatous cupping of the optic nerve head (ONH).…”
Endothelin-1 (ET-1) is a potent vasoconstrictor and is considered to have a key role in the regulation of ocular perfusion and glaucoma pathogenesis. High ET-1 and ET A -receptor levels are reported in patients with primary open-angle glaucoma (POAG). We compared the mean plasma ET-1 and ET Areceptor concentration of controls and patients with early and advanced POAG stage, and assessed the correlation with the retinal nerve fibre layer (RNFL) thickness. The study included a total of 75 participants, aged 45-83 years: 25 (controls), 22 (early glaucoma) and 28 (advanced glaucoma). The plasma concentration of ET-1 and ET A -receptor was determined by enzyme-linked immunosorbent assay. The RNFL thickness was evaluated with spectral-domain optical coherence tomography. The mean ET-1 concentration was lower in the control group (4.88 § 1.75 pg/mL) than in the early and advanced POAG group (6.33 § 2.38 and 6.34 § 1.56 pg/mL). Statistically significant difference was found between the mean ET-1 concentrations in controls and glaucoma patients (p = 0.029 -early glaucoma, p = 0.018 -advanced glaucoma), and no significant difference was observed between the two POAG groups (p = 0.998). The mean ET A -receptor concentration was highest in the control group (1209.28 § 314.48 pg/mL) and the differences between the three groups were significant. Significant relationship was found only between ET-1 and RNFL. This study demonstrated the role of ET-1 in glaucoma pathogenesis based on the observed significant high ET-1 and ET A -receptor plasma levels in POAG patients. A new therapeutical approach needs to be considered in some patients.
“…Endothelin-1 (ET-1) is a potential participant in the local regulation of intraocular pressure, ocular blood vessel tone, and iris smooth muscle tone, suggesting that it may be an important mediator in the development of ocular pathologic conditions. [13]. Lower ET-1 plasma levels were found in the optic neuropathy.…”
Introduction. ANCA-associated vasculitis (AAV) and polyarteritis nodosa (PAN) are systemic vasculitis with inflammation and necrosis of small and medium vessels in multiple organs. [1]. The clinical manifestations vary from local form with single-organ involvement to multisystem life-threatening patterns. The two types of ANCA are generally distinguished, antibodies against proteinase-3 (PR3), which are typical for granulomatosis with polyangiitis (GPA), and antibodies against myeloperoxidase (MPO), which are predominantly detected in patients with microscopic polyangiitis (MPA) and some patients with eosinophilic granulomatosis with polyangiitis (EGPA).[2]. Negative PR3-ANCA and MPO-ANCA do not exclude the diagnosis of ANCA-associated vasculitis. The limited form of vasculitis is often ANCA-negative. Different clinical manifestations of vasculitis are associated with a certain frequency of detection of ANCA. According to Lionaki S. et al., the majority of patients with isolated renal disease were positive for MPO-ANCA (81%), while almost all patients with bone destruction or saddle-shaped deformity of the nose showed PR3-ANCA (94%). [3].Ophthalmological manifestations, including ocular or orbital involvement, are common clinical signs of systemic vasculitis that occur in 16-52% of patients with AAV and in 10-20% of patients with PAN. [4][5][6]. Eye involvement is an initial presenting finding in 8% to 16% of patients. [6][7][8]. Ocular involvement is frequently seen in GPA, but rarely in EGPA and MPA. [9]. Gender predominance of ophthalmological manifestation is still discussed. Some studies have reported a male predominance of 57-63% [4, 10], the others have shown a female predominance of 51 -72%. [5,11]. All parts of the eye and orbit can be affected; however, scleritis and orbital mass are the most common presenting manifestation. Conjunctivitis, peripheral ulcerative keratitis, uveitis, choroidal disease, and retinal vasculitis can be also the clinical features of systemic vasculitis. The orbital mass formation is a clinical indication for ANCA testing. [12]. Eye damage can lead to blindness and significant socio-economic consequences. The mortality rate of patients with ocular manifestations in AAV is 2.75-fold higher than patients with other inflammatory eye disorders [10]. That's why the early recognitions of ocular disease and evaluation of other signs of systemic process are the corner stone in diagnosis of AAV and PAN.Most of the previous studies of ophthalmological manifestations of AAV were limited to case reports, case series or retrospective studies. There are no specific laboratory markers for ocular involvement in systemic vasculitis. Endothelin-1 (ET-1) is a potential participant in the local regulation of intraocular pressure, ocular blood vessel tone, and iris smooth muscle tone, suggesting that it may be an important mediator in the development of ocular pathologic conditions. [13]. Lower ET-1 plasma levels were found in the optic neuropathy. [14].
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.