Coats'-like response in pars planitis.
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Adult↗
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Results for “Neovascularization, Pathologic”
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[Aging changes in conjunctival blood vessels].
The relation of the changes in the conjunctival blood vessels to the age were studied in a group of 217 persons aged 20 to 79 years. All persons suffering from arterial hypertension, diabetes, systemic diseases and manifested forms of arteriosclerosis were excluded. It has been proved that examination of the conjunctival blood vessels by means of the slot-lamp facilitates the study of the changes in the microscopic blood vessels in relation to the age. Most conspicuous was the increase of the meander course of the blood vessels, also the increasing number of blood vessels is more frequent in the group of older persons. Clusters of vessels and a narrowing of the diameter of the arterioles was seen only in persons over fifty years of age. The "upright" course of the arterioles was found only in individual cases and without any special dependence to age. Sacculations on the small veins and microaneurysms on the arterioles were not observed in any of the examined group of healthy persons.
Adult↗
Indocyanine green video angiography in patients with age-related maculopathy-related retinal pigment epithelial detachments.
Previous studies have stressed the benefit of laser photocoagulation for patients with age-related macular degeneration (AMD) and well-defined subretinal neovascularization (SRN). However, such lesions account for only 30% of cases with exudative age-related maculopathy. Especially in patients with retinal pigment epithelial detachment (PED), SRN is usually occult. This study was performed to reveal the role of digital indocyanine green (ICG) video angiography in the diagnosis of SRN in patients with PED. A total of 34 patients with AMD-associated retinal PED participated in the current study and underwent fluorescein and ICG angiography using scanning laser ophthalmoscopy. In these patients fluorescein angiography revealed no distinct SRN, whereas in 21 eyes (62%) ICG angiography showed well-demarcated choroidal neovascularization. The present study demonstrates that SRN can be detected in more than 50% of patients with PED by means of ICG video angiography. Therefore, ICG video angiography improves the detection of SRN in patients with AMD-associated PED.
Aged↗
Anechoic halo in solid liver tumors: sonographic, microangiographic, and histologic correlation.
The origin of the sonographic halo sign in liver metastases was studied after autopsy in 33 livers with macroscopic tumoral involvement. For 20 lesions a detailed comparison of findings from high-resolution 7.5- and 10-MHz sonography, microangiography, and histology was carried out. Histologic study focused on the tumor periphery and its relationship to the adjacent liver parenchyma. In particular, the type of tumor infiltration, the presence or absence of peritumoral fibrosis, and the degree of liver cell compression were assessed. In all but two cases the halo was extratumoral and was caused by peritumoral liver cell compression. In the remaining two cases the halo was tumoral and was caused by irregular fibrosis or vascularization.
Angiography↗
What is the role of radiation in the treatment of subfoveal membranes: review of radiobiologic, pathologic, and other considerations to initiate a multimodality discussion.
BACKGROUND: Single-dose-fraction conformal proton beam and multiple-fraction X ray dose schedules have been used to treat subfoveal neovascular membranes. All schedules successfully controlled membrane progression, stabilized vision in most patients, and increased visual acuity in some. Conformal protons also decreased the radiation dose to healthy tissues outside the designated volume (16 mm in diameter). It appears that radiation therapy could be useful and cost-effective, but neither the optimal time-dose schedule single or multiple dose fractions nor the type of radiation proton conformal beam or x-ray therapy are defined. METHODS: By means of an extensive literature survey, we reviewed the rationale for using radiation to treat subfoveal neovascularization, examined a paradigm of radiation interaction with tissue, reviewed the histopathology of neovascular membranes, and documented the role of growth factors in the pathophysiology of the disease. Accepting that the eye is an extracranial brain extension, and that its microvasculature has properties similar to brain microvessels, we reviewed the radiobiologic response of brain microvessels. We also revisited the controversy concerning the efficacy of single-dose-fraction vs. multifraction schedules. RESULTS: This paper outlines parameters within which radiation therapy's role might be defined, and proposes a clinical radiation-biology scoring program to evaluate radiation effects, based on the SOMA concept. CONCLUSION: A prospective, controlled clinical trial is feasible and is indicated to determine radiation therapy's role in managing the proliferative component of age-related macular degeneration.
Aged↗
Different determinants of neovascularization on the optic disc and on the retina in patients with severe nonproliferative diabetic retinopathy.
Almost all patients with type I and many with type II diabetes develop proliferative retinopathy. This entity consists of two components: new blood vessels on the optic disc (NVD), which frequently lead to visual loss, and new blood vessels elsewhere on the retina (NVE), which do not pose such a serious threat to vision. This study examined determinants of neovascularization specifically on the optic disc in eyes with severe nonproliferative retinopathy. The study eyes were under surveillance as the untreated control eyes of participants in the Diabetic Retinopathy Study. During the 5-year follow-up period, NVE developed in almost all of the eyes, whereas the cumulative incidence of NVD in these same eyes was 64% and varied according to several factors. The risk of NVD in a study eye was increased if the contralateral treated eye had NVD rather than NVE or severe nonproliferative retinopathy (odds ratio [OR], 6.1; P < .0001). It was also increased if the study eye had, at the baseline examination, soft exudates and intraretinal microvascular abnormalities (OR, 5.7; P = .002) or soft exudates alone (OR, 4.0; P = .04). Nephropathy and poor glycemic control were each associated with a two-fold increase in risk but neither was statistically significant. Eyes of individuals over 40 years of age were protected from the development of NVD (OR, 0.5; P < .05). The findings of this study support the hypothesis that, in patients with diabetes, the development of NVD is determined by different factors than the development of NVE.
Adolescent↗
Profound central visual loss and ocular neovascularization in idiopathic recurrent branch retinal arterial occlusion.
The authors report a 65-year-old healthy, white man who experienced a dramatic loss of central vision. Iris neovascularization, rubeotic glaucoma, disc neovascularization and subhyaloid hemorrhage developed after multiple, recurrent, idiopathic branch retinal arterial occlusions. Vitreous and perivascular inflammation were prominent associated clinical features. Systemic steroids were useful in suppressing intraocular and perivascular inflammation, yet neither steroid nor anticoagulant therapy effectively prevented recurrent occlusive episodes. Retinal neovascularization and rubeotic glaucoma were successfully managed with scatter panretinal photocoagulation. Episodic intraocular inflammation and ocular neovascularization have been noted in one-third of patients sustaining recurrent idiopathic branch retinal arterial occlusions.
Aged↗
Pathogenesis of laser-induced choroidal subretinal neovascularization.
The early stages (1 day to 3 weeks) in the development of laser-induced choroidal subretinal neovascularization were studied in the monkey eye. Histopathology revealed that the intense laser beam disrupted the choroid/Bruch's membrane/retinal pigment epithelium (RPE) complex and initiated a repair process. Although all lesions received the same energy density, the initial choroidal wound varied among the lesions: in some, the necrotic choroid was surrounded by hemorrhagic retinal detachment with RPE denudation; in others, the necrotic choroid was surrounded only by minimal damage to the RPE monolayer. Formation of the choroidal wound was followed by an inflammatory response. Later, newly formed choroidal tissue filled the wound and continued to proliferate towards the subretinal space. RPE cells from the edges of the wound proliferated over the newly formed subretinal tissue and closed the wound. In lesions with a large area of damaged RPE, coverage of the wound was slow; fluid accumulated in the subretinal space, and the lesions demonstrated pooling of fluorescein on angiography (leaky lesions). In lesions with minimal damage to RPE monolayer, closure of the wound was rapid, and the proliferating choroidal tissue did not reach the subretinal space. There was no subretinal fluid accumulation and no pooling of fluorescein on angiography (nonleaky lesions). Our results indicate that both the amount of damage of the choroid/Bruch's membrane/RPE complex and the ability of RPE cells around the damaged area to proliferate and restore the continuity of the RPE layer determine the evolution of newly formed choroidal fibrovascular tissue into a subretinal membrane with or without pooling.
Animals↗
[A role of the retinal pigment epithelium in the involution of subretinal neovascularization].
We clarified a role of the retinal pigment epithelium (RPE) in the regression of experimentally induced subretinal neovascularization (SRN) in monkey. Eight eyes of 5 rhesus monkeys were used in this study. Two weeks after intense krypton laser photocoagulation to the posterior pole of the fundus, 0.5M l-ornithine hydrochloride solution 0.03 ml was injected intravitreously for the purpose of selective RPE damage. After ornithine injection, SRN continued without any evidence of spontaneous regression over 8 weeks following photocoagulation. Histopathologically, SRN developed with wide lumen in the subretinal space accompanied with serous detachment of the sensory retina, and new vessels were not enveloped completely by the proliferating RPE cells. We already showed that experimentally induced subretinal neovascularizations naturally regress spontaneously by envelopment of RPE cells 5 to 8 weeks after photocoagulation. Our results suggested that SRN persist actively without regression due to incomplete enclosure by RPE by selective damage of RPE at the active stage of SRN. We have confirmed that the RPE cells played an important role at the involution stage of SRN.
Animals↗
[Peripheral vascular bed of neoplasms--an unknown area in cancer pathology].
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Angiogenesis Inducing Agents↗
Argon laser scatter photocoagulation in treatment of branch retinal vein occlusion. A prospective clinical trial.
The objective of this prospective study was to ascertain whether scatter argon laser photocoagulation to the involved sector in major branch retinal vein occlusion and ischemic hemicentral retinal vein occlusion (a) prevents development of retinal and/or optic disk neovascularization and vitreous hemorrhage, and (b) affects visual acuity, visual fields and macular retinal lesions. The study was done in 271 eyes allocated to either treated (n = 61 eyes) or untreated (n = 210) groups. In this study, on an average follow-up of 3.6 years, the laser treatment (1) significantly reduced the risk of development of retinal neovascularization and vitreous hemorrhage, (2) did not affect the visual acuity and macular retinal lesions, and (3) produced a significant worsening in the peripheral visual fields compared to the untreated eyes. In view of our findings, we recommend that argon laser photocoagulation treatment should be given only when neovascularization is seen and not otherwise, because in the latter case, its detrimental effects may outweigh its beneficial ones.
Aged↗
Recurrent subarachnoid bleeding in association with dural substitute. Report of three cases.
Three cases of recurrent subarachnoid bleeding are reported. The hemorrhages occurred at intervals of up to 10 years after posterior fossa craniotomy with closure using grafts of Silastic dural substitute. In one case, reexploration showed that the hemorrhage had arisen from a neomembrane formed at the site of the dural substitute; in the others, circumstantial evidence suggested a similar pathology.
Adolescent↗
Increased expression of placenta growth factor in proliferative diabetic retinopathy.
Proliferative diabetic retinopathy is thought to be mediated by the hypoxic regulation of angiogenic growth factors, in particular the vascular endothelial growth factor (VEGF) family. The aim of this study was to determine if placental growth factor (PIGF), a recently identified member of the VEGF family, was expressed in diabetic eyes undergoing preretinal neovascularization. Rabbit anti-PIGF antiserum was raised using a 20-amino acid N-terminal sequence to PIGF and did not cross react with VEGF165. Immunohistochemistry was performed on specimens of normal retina (n = 8), diabetic retina in the absence (n = 7) and presence (n = 4) of proliferative retinopathy, scatter laser-treated diabetic retina (n = 7), excised fibrovascular preretinal membranes (n = 12), and nondiabetic fibrocellular epiretinal (n = 7) membranes. PIGF levels were also determined in vitrectomy specimens from patients with either proliferative diabetic retinopathy or macular hole. PIGF immunoreactivity was intensely localized to the endothelial and perivascular regions of newly formed blood vessels of excised fibrovascular preretinal membranes. Intense localization of PIGF protein was also observed in superficial retinal vessels in diabetic retinae adjacent to neovascular preretinal membranes. Localization of PIGF was weak or absent in diabetic retinae that showed no evidence of neovascular proliferation. PIGF protein was also absent in normal retinae, in diabetic retinae that had received extensive treatment with scatter laser photocoagulation, and in nonvascularized epiretinal membranes. PIGF was present in all diabetic vitreous samples (mean 103 pg/ml) but nondetectable in control samples. These results strongly implicate a role for PIGF in the pathogenesis of proliferative diabetic retinopathy.
Adult↗
Site-directed neovessel formation in vivo.
Angiogenesis is an important component of organogenesis and wound repair and occurs during the pathology of oncogenesis, atherogenesis, and other disease processes. Thus, it is important to understand the physiological mechanisms that control neovascularization, especially with methods that permit the molecular dissection of the phenomenon in vivo. Heparin-binding growth factor-1 was shown to bind to collagen type I and type IV. When complexed with gelatin, heparin-binding growth factor-1 can induce neovascularization at polypeptide concentrations that are consistent with the biological activity of the mitogen in vitro. The adsorption strategy induces rapid blood vessel formation at and between organ- and tissue-specific sites and permits recovery of the site-specific implant for examination and manipulation by molecular methods.
Animals↗
[A pathological study on the change in tumor stroma in gastric cancer].
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Adenocarcinoma↗
Senile disciform macular degeneration complicated by massive hemorrhagic retinal detachment and angle closure glaucoma.
Six eyes developed angle-closure glaucoma secondary to total hemorrhagic retinal detachment that occurred as a rare complication of senile disciform macular degeneration. The patients were all elderly with known senile macular choroidal degeneration. They had no history of eye surgery and experienced sudden loss of vision followed by pain. Balloons of retinal detachment were pushed tightly against the lens in a characteristic "Y suture" appearance causing shallowing of the anterior chamber and glaucoma. Pathologic examination of three eyes revealed that the choroid was not detached but that a massive subretinal hemorrhage was present. Neovascular tissue in macular disciform lesions was found in every case and was the probable source of hemorrhage. Sheets of avulsed retinal outer segments were seen incarcerated in subretinal blood in two cases, and drainage of this subretinal blood in three cases did not restore useful vision.
Aged↗
Mast cell interactions with the nervous system: relationship to mechanisms of disease.
In summary, mast cell interactions in the nervous system are relevant to both physiological processes (i.e. reproduction) and pathologic states (i.e. inflammatory demyelination, painful disorders, toxic and metabolic disease, and tumor angiogenesis). Their physiologic roles may contribute to gender-related vulnerability to inflammatory disease and may modulate sensitivity to pain. Mast cells are universally involved in tissue repair and they release and respond to trophic factors such as NGF. These cells also produce and react to cytokines, and thus appear to play a role in tissue degeneration as well as repair. In certain neurological diseases, i.e. multiple sclerosis and Guillain-Barré syndrome, the ability of mast cell proteases to degrade specific myelin proteins suggests that these cells are agents, rather than bystanders, in the demyelinative process. Even more intriguing is their recently identified capacity to process bacterial antigen as efficiently as activated macrophages, suggesting that a more critical role than previously suspected might be considered for mast cells in CNS and PNS demyelination. In experimental metabolic disorders such as galactose intoxication and thiamine deficiency, mast cells appear to play a pathogenic role. Thus, in galactose intoxication, altered BNB vascular permeability occurs in conjunction with mast cell proliferation and degranulation, while in thiamine deficiency, increased histamine levels have been reported in the rat thalamus (79) and are associated with cell death and proliferation as well as mast cell degranulation (Powell and Langlais, unpublished observations). Structural interactions between mast cells and a variety of other cells have been observed, as well as close approximation of mast cells to nerve endings in tissues in which mast cells are especially active. Due to their paracrine nature, mast cells can modulate events in their microenvironment through explosive degranulation, piecemeal degranulation, or "transgranulation" as they insert granules into neighboring cells. Lastly, these cells play specific roles in reparative processes, e.g. angiogenesis, and are active in neoplastic states, including von Recklinghausen's disease (neurofibromatosis). Their involvement may have been underestimated in neuropathological studies, to date, by a reliance on staining techniques that are inadequate for identifying degranulated and therefore activated mast cells (4). More exacting histochemical and immunostaining procedures will help to fully realize the extent of their participation in physiological and pathological processes.
Animals↗
Subfoveal choroidal neovascularization in punctate inner choroidopathy. Surgical management and pathologic findings.
PURPOSES: To evaluate submacular surgery for the management of subfoveal choroidal neovascularization in punctate inner choroidopathy, to describe the histopathology and ultrastructure of the excised subretinal tissue, and to propose a staging system that characterizes the development of choroidal neovascularization with associated subretinal fibrosis. METHODS: The authors reviewed the records of five patients (6 eyes) with punctate inner choroidopathy who underwent submacular surgery for subfoveal choroidal neovascularization. Surgical specimens were examined using light and transmission electron microscopy. RESULTS: Visual improvement was noted postoperatively in all six eyes, with follow-up ranging from 8 to 36 months (median, 14 months). Recurrences (6 in 4 eyes) were common. Five of the six recurrences required additional procedures: three were managed surgically, two with laser photocoagulation, and one with observation. "Bridging" of separate foci of choroidal neovascularization resulted in stellate or "dumbbell-shaped" areas of subretinal fibrosis in four of six eyes. Histopathologic evaluation of the excised tissue showed endothelial-lined vascular channels, retinal pigment epithelium, lymphocytes, plasma cells, fibrocytes, collagen fragments, and rarely, outer retinal elements. CONCLUSIONS: Subfoveal choroidal neovascularization in punctate inner choroidopathy may be managed with submacular surgery. Recurrences are common and may result in substantial loss of vision. Choroidal neovascular membranes with an accompanying fibrotic reaction are responsible for the stellate or dumbbell-shaped areas of subretinal fibrosis. No beneficial effect was demonstrated using corticosteroid treatment of the choroidal neovascularization.
Adult↗