Neovascular lesion

Anonymous. Subfoveal neovascular lesions in age-related macular degeneration. Guidelines for evaluation and treatment in the macular photocoagulation study. Macular Photocoagulation Study Group. Arch Ophthalmol 1991 109 1242. 

The neovascular lesions of talc retinopathy are thought to be associated with peripheral arteriolar nonperfusion, which leads to retinal ischemia and secondary neovascularization. Such a pathogenesis is quite similar to that seen in sickle cell retinopathy and is confirmed by the predominantly supertemporal location of the neovascular proliferation. Macular fibrosis with significant visual loss has also been associated with talc retinopathy. 

CNV secondary to age-related macular degeneration CNV under the geometric center of the foveal avascular zone Evidence of classic CNV on fluorescein angiography Area of CNV at least 50% of the area of the total neovascular lesion Greatest linear dimension of lesion <5400 pm (not including any area of prior laser photocoagulation)... 

Macular Photocoagulation Study Group. Persistent and recurrent neovascularization after krypton laser photocoagulation for neovascular lesions of age-related macular degeneration. Arch Ophthalmol 1990 108(6) 825-831. 

El, T., Li, X.Y., and Paciotti, N.M., Fluorescein angiographic characteristics of subfoveal choroidal neovascular lesions secondary to age related maculopathy in pivotal Phase 111 trial for SnET2 PDT, Abstract, Association for Research in Vision and Opthamology, 2352, 2001. 

In many chronic inflammatory diseases, angiogenesis can be identified in the inflamed lesions. For example, in rheumatoid arthritis extensive neovascularization is present in the inflamed synovium where it is one of the earliest histopathological findings [36]. Since in RA synoviocytes exhibit characteristics of tumour cells, including somatic mutations in key regulatory genes such as H-ras and the p53 tumour suppressor, RA can be viewed as a multicentric tumour-like mass that invades and destroys its local environment [37]. Concurrent increased endothelial cell turnover may contribute to microvascular dysfunction and thereby facilitate persistent synovitis. 

Neovascularization in artherosclerotic lesions may be regulated by VEGF, as this factor is over-expressed by different cells in the plaque tissue [40-42]. The increased serum levels of VEGF that correlate with disease activity in patients with Crohn s disease and ulcerative colitis, indicate a role for this cytokine in promoting inflammation. Most likely, increased vascn-lar permeability and/or wound healing via its pro-angiogenic activity are the basis for this effect [43]. 

No exposure-related clinical signs or lesions of systemic toxicity and no oncogenic responses were observed in rats exposed by inhalation at concentrations of 0, 15, 45, or 135ppm 6 hours/day, 5 days/week, for 24 consecutive months." Dose-related changes occurred in the anterior portion of the olfactory epithelium and consisted of atrophy of the neurogenic epithelial cells followed by progressive hyperplasia of the reserve cells and ultimately loss of the upper epithelial cell layer. Opacity and neovascularization of the cornea were also observed in methyl acrylate-exposed animals. 

In addition to the work presented here, several alternative viral-vectored approaches have been reported recently. An adeno-associated viral vector (AAV) encoding the soluble VEGF receptor 1, sFlt-1, shows promise for long-term inhibition of two types of ocular neovascularization (Lai et al., 2002). This vector, when injected into the anterior chamber, resulted in expression in both the corneal endothelium and iris pigment epithelium and reduced corneal NV by 36%. Subretinal injection of the same vector reduced choroidal NV subsequent to laser lesions around the optic nerve. These results suggest that a secretable factor expressed in one or more transduced cell populations can be elfective in the control of ocular NV occurring in a disparate cell population. 

Although it has not been compared directly with verteporfin, rostaporfin appears to have the same potential for management of choroidal neovascularization. Fifteen minutes after intravenous infusion, a red nonthermal diode laser source (664 nm) is used to activate the drug. The phase III trial compared rostaporfin with placebo in over 900 patients with vision between 20/500 and 20/40 and determined that patients treated with rostaporfin 0.5 mg/kg had stable vision compared with placebo recipients (65.6% vs. 39.3%). Patients with vision better than 20/200 and study-compliant lesion size likewise had significantly higher rates of stable vision compared with placebo (63.2% vs. 25%). A smaller subset of patients with predominantly occult CNV detrived a treatment benefit relative to placebo for patients losing less than 15 letters of acuity (63.6% vs. 29.4%). 

Verteporfin in Photodynamic Therapy Smdy Group. Verteporfin therapy of subfoveal choroidal neovascularization in age-related macular degeneration two-year results of a randomized clinical trial including lesions with occult with no classic choroidal neovascularization—Verteporfin in Photodynamic Therapy Report 2. Am J Ophthalmol 2001 131 541. 

Thomas EL, Danis RP, SnET2 Smdy Group. Lesion progression and visual acuity outcomes for occult choroidal neovascularization treated with rostaporfin (SnET2) photodynamic therapy.ARVO abstract 2005 3571. 

Weigand SJ, Zimmer E, NorkTM, et al.VEGF trap both prevents experimental choroidal neovascularization and causes regression of established lesions in non-human primates. ARVO abstract 2005 1411/B180. 

Noninfectious indolent epithelial ulcers also can occur in HSK.These ulcers, formerly referred to as metaherpetic lesions, tend to be ovoid, 2 to 8 mm in size, with smooth rolled edges. They may be caused by damage to the epithelial basement membrane due to inflammation, tear film abnormalities, neurotropic cornea, or toxicity from antiviral medications. These ulcers may be recalcitrant, resulting in neovascularization and scarring. 

Bressler NM, Arnold J, Benchaboune M, et al. Verteporfin therapy of subfoveal choroidal neovascularization in patients with age-related macular degeneration additional information regarding baseline lesion composition s impact on vision outcomes— TAP Report No. 3. Arch Ophthalmol 2002 120 1443. 

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