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Malignant Tumors and the Microcirculation
Published in John H. Barker, Gary L. Anderson, Michael D. Menger, Clinically Applied Microcirculation Research, 2019
Bernhard Endrich, Peter Vaupel
(1) Steroid-heparin combinations were found to dissolve the basement membrane of growing capillaries.41 One application presently under discussion among clinicians is the treatment of corneal neovascularization, which is refractory to conventional therapy. It also seems possible to suppress neovascularization in mast cell-rich inflammatory lesions or hemangiomas by corticosteroids alone, because of the high levels of endogenous heparin.
Mucous membrane pemphigoid
Published in Biju Vasudevan, Rajesh Verma, Dermatological Emergencies, 2019
Dipankar De, Sheetanshu Kumar, Sanjeev Handa
Corneal involvement can result in corneal scarring, corneal neovascularization, opacification, and ulceration, all of which result in compromised vision [29]. Eyelid involvement results in entropion, lagophthalmos, notching of lid margin, and trichiasis. These can cause further corneal damage, scarring, and secondary infectious keratitis [27]. Glaucoma is also known to occur in MMP patients, and is yet another cause of blindness [30].
Special Senses
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Kenneth A. Schafer, Oliver C. Turner, Richard A. Altschuler
Neovascularization (Figure 23.2a) is the formation of blood vessels in a normally avascular corneal stroma and may be associated with stromal edema and inflammation (Klintworth and Burger 1983). New blood vessels are often more permeable, leak fluid, and may enhance stromal migration of inflammatory cells. Occasionally in rabbits, individual limbal blood vessels may spontaneously extend a short distance into the peripheral cornea. Neovascularization may also occur after topical administration of compounds (e.g., EP4-prostaglandin E2 agonists) (Aguirre et al. 2009). Once vessels are present, they often persist as nonperfused ghost vessels. Vascular endothelial growth factor (VEGF) inhibitors have been investigated as treatment for corneal neovascularization (Chen et al. 2009).
Monolith/Hydrogel composites as triamcinolone acetonide carriers for curing corneal neovascularization in mice by inhibiting the fibrinolytic system
Published in Drug Delivery, 2022
Cixin Huang, Xia Qi, Huilin Chen, Chao Wei, Xiaolin Qi, Hongwei Wang, Hua Gao
Corneal neovascularization is a category of pathological angiogenesis that threatens the vision and even causes blindness (Ueta et al., 2019; Cho et al., 2020). Pro-angiogenic factors and anti-angiogenic factors are two counterbalancing systems that determine the formation of new blood vessels (Senturk et al., 2016; Wang et al., 2019). Inflammation and other causes can break the balance of the two systems, consequently resulting in corneal neovascularization (Senturk et al., 2016). Cornea transplantation, laser therapy, steroids, anti-vascular endothelial growth factor (VEGF) agents, insulin receptor substrate-1 proteins, matrix metalloproteinase inhibitors, fine needle diathermy and gene therapy targeting VEGF have been widely used in the management of corneal neovascularization (Sharif and Sharif, 2019). Among them, steroids and anti-VEGF agents are currently the mainstay initial treatment approaches. Owing to their low cost and ease of manufacture, steroids (injections and topical treatments) have become an important alternative in the prevention and treatment of corneal neovascular diseases.
Comparison of the effect of topical bevacizumab and sorafenib in experimental corneal neovascularization
Published in Cutaneous and Ocular Toxicology, 2020
Hakan Yildirim, Orhan Aydemir, Mehmet Balbaba, İbrahim Hanifi Özercan, Nevin İlhan
Growth factors play an important role in corneal neovascularization. Of these, VEGF is of great importance as it is directly effective on the vascular endothelium. In previous studies have shown that angiogenic factors increase and anti-angiogenic factors decrease during neovascularization23. VEGF is secreted from macrophages, T cells, retinal pigment epithelial cells, smooth muscle cells and tumour cells by stimulation of various environmental factors and particularly following hypoxia24. VEGF release has been shown to increase in many eye-related clinical conditions such as inflammatory diseases of the cornea, contact lens wear, hypoxia, chemical traumas, and keratitis25. In cases with neovascularization of human corneas, both VEGF and VEGF receptor levels have been found to be higher than normal26.
Protective Effect of TLR4 Ablation against Corneal Neovascularization following Chemical Burn in a Mouse Model
Published in Current Eye Research, 2019
Moran Friedman, Tamar Azrad-Lebovitz, Dana Morzaev, Alon Zahavi, Neelan J. Marianayagam, James D. Nicholson, Myles Brookman, Shalom Michowiz, Edith Hochhauser, Nitza Goldenberg-Cohen
Physiological angiogenesis is the growth of new blood vessels from preexisting ones. Aberrant angiogenesis is a significant pathologic factor in diseases of the ocular surface (corneal inflammation, traumatic corneal disease) and retina (choroidal neovascularization in age-related macular degeneration or diabetic retinopathy) and various cancers.1 In the normally avascular cornea, an imbalance between angiogenic and anti-angiogenic factors may lead to the formation of new vasculature.2 Corneal neovascularization may be induced by inflammatory, infectious, degenerative, or traumatic eye disorders. It plays a pathologic role in most corneal diseases3,4 and is a high risk factor for rejection after corneal transplantation.5 It is also a major cause of blindness due to lack of adequate anti-angiogenic treatment options to prevent its progression. Neovascularization in the retina is currently treated by drugs that act against vascular endothelial growth factor (VEGF), such as ranibizumab (Lucentis) and bevacizumab (Avastin).6 However, although VEGF is also an essential factor in corneal angiogenesis and is found at increased levels in vascularized corneas in both animal models and humans,7 the long-term effectiveness of anti-VEGF drugs in the cornea has not been proven. Steroids may also downregulate VEGF levels, thereby reducing neovascularization, but they are associated with multiple complications, including glaucoma and cataract, as well as a delay in corneal epithelial regrowth.4