Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the clinical observation of a 16-year-old male, with no particular medical or ocular history, who presented with loss of vision in the right eye on the first post-operative day after uncomplicated extraction of the four third molar roots under general anesthesia. Loss of vision, due to optic disc ischemia, persisted after 2 months. The clinical and pathogenic features of this rare optic nerve ischemia complication are discussed.
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PMID:[Optic nerve ischemia as a complication of dental extraction: a case report]. 1554 75

Acute retinal vascular occlusive disorders collectively constitute one of the major causes of blindness or seriously impaired vision, and yet there is marked controversy on their pathogeneses, clinical features and particularly their management. This is because the subject is plagued by multiple misconceptions. These include that: (i) various acute retinal vascular occlusions represent a single disease; (ii) estimation of visual acuity alone provides all the information necessary to evaluate visual function; (iii) retinal venous occlusions are a single clinical entity; (iv) retinal vein occlusion is essentially a disease of the elderly and is not seen in the young; (v) central retinal vein occlusion (CRVO) is one disease; (vi) fluorescein fundus angiography is the best test to differentiate ischemic from nonischemic CRVO; (vii) the site of occlusion in CRVO is invariably at the lamina cribrosa; (viii) clinical picture of CRVO is often due to compression or strangulation of the central retinal vein (CRV) in the lamina cribrosa and not its occlusion; (ix) an eye can develop both CRVO and central retinal artery occlusion (CRAO) simultaneously; (x) every eye with CRVO is at risk of developing neovascular glaucoma; (xi) lowering intraocular pressure (IOP) helps to improve retinal circulation in an eye with CRVO; (xii) every patient with retinal vein occlusion should have complete hematologic and coagulation evaluation; (xiii) the natural history of CRVO does not usually involve spontaneous visual improvement; (xiv) management of CRVO is similar to that of venous thrombosis anywhere else in the body, i.e. with aspirin and/or anti-coagulants; (xv) fibrinolytic agents can dissolve an organized thrombus in the CRV; (xvi) it is beneficial to lower blood pressure in patients with CRVO; (xvii) panretinal photocoagulation used in ischemic retinal venous occlusive disorders has no deleterious side-effects; (xviii) glaucoma or ocular hypertension can cause branch retinal vein occlusion; (xix) branch retinal vein occlusion can cause neovascular glaucoma; (xx) in eyes with CRAO, the artery is usually not completely occluded; (xxi) CRAO is always either embolic or thrombotic in origin; (xxii) amaurosis fugax is always due to retinal ischemia secondary to transient retinal arterial embolism; (xxiii) asymptomatic plaque(s) in retinal arteries do not require a detailed evaluation; (xxiv) retinal function can improve even when acute retinal ischemia due to CRAO has lasted for 20h or more; (xxv) CRAO, like ischemic CRVO, can result in development of ocular neovascularization; (xxvi) panretinal photocoagulation is needed for "disc neovascularization" in CRAO; (xxvii) fibrinolytic agents are the treatment of choice in CRAO; (xxviii) there is no chance of an eye with retinal arterial occlusion having spontaneous visual improvement; (xxix) absence of any abnormality on Doppler evaluation of the carotid artery or echography of the heart always rules out those sites as the source of embolism; and (xxx) absence of an embolus in the retinal artery means the occlusion was not caused by an embolus. The major cause of all these misconceptions is the lack of a proper understanding of basic scientific facts related to the various diseases. The objective of this paper is to discuss these misconceptions, based on these scientific facts, to clarify the understanding of these blinding disorders, and to place their management on a rational, scientific basis.
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PMID:Prevalent misconceptions about acute retinal vascular occlusive disorders. 1584 46

We report a patient having transient blindness due to severe stenosis of the internal carotid artery (ICA) with persistent primitive hypoglossal artery (PPHA). This 73 year-old man was admitted because of the transient visual impairment. At first, he had bilateral blindness for a several minutes and after that the right amaurosis continued for an hour. MRI showed an old lacunar infarction of the right caudate nucleus. Carotid duplex ultrasonography and conventional angiography demonstrated severe stenosis of the origin of the right ICA, and PPHA was arising from the right ICA at the level of 2nd cervical spine. The left ICA was normal. Because of the aplasia of the right vertebral artery and hypoplasia of the left vertebral artery, almost all blood flow of the basilar artery was supplied from the right ICA via PPHA. We considered that transient ischemia of both the bilateral posterior cerebral arteries and the right ocular artery occurred due to stenosis of the right ICA which branching PPHA. When ischemic neurological symptoms of multiple vascular territories occurr at the same time, we often think that ischemic mechanism was cardiogenic embolism. But we should recognize that stenosis of the ICA with PPHA cause the complex neurological deficits.
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PMID:[A case of transient blindness due to severe stenosis of the internal carotid artery with persistent primitive hypoglossal artery (PPHA)]. 1618 Jul 6

Diabetic retinopathy is a frequently observed complication in both type 1 and type 2 diabetes, specially in patients with long term disease and poor glicemic control. Irreversible visual loss appears at the final stages of diabetic retinopathy and it is considered one of the most tragic of diabetic complications. It is also considered an important factor of morbidity and has a high economical impact once it is the leading cause of blindness. The pathophysiology of the retinal microvascular alterations is related to the chronic hyperglycemia that leads to the following circulatory disturbances: loss of vascular tonus, increase in vascular permeability, edema and exudation, with vascular obstruction and ischemia that stimulates neovascularization, which may lead to fibrous retraction and vitreous hemorrhages with retinal detachment. Recent studies have indicated that the strict glicemic and blood pressure controls are effective in reducing or blocking the progression of retinopathy. Up to now no pharmacological agents have shown to be effective in preventing or reducing neovascularization and visual loss. Presently, the most effective available treatment for proliferative retinopathy is laser photocoagulation. Further studies are needed to obtain new products and technologies that could effectively prevent or block retinopathy progression.
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PMID:[Diabetic retinopathy]. 1618 49

Diabetic eye disease affects quality of life for patients with diabetes by decreasing visual acuity and increasing the risk of blindness. In the course of diabetic retinopathy (DR) the loss of capillary integrity, microaneurysm formation, and ischemia is observed, which in turn drives the progression of DR. The macular edema is the result of fluid accumulation in the retina secondary to capillary leakage and/or microaneurysms. This contributes to loss of vision in DR. There is substantial evidence that control over metabolic factors can effectively prevent the development and progression of DR. For many patients who fail to achieve the optimal level of metabolic control the standard care should include the early detection and timely treatment of DR. Laser photocoagulation therapy, and vitrectomy are invasive methods, recommended to treat only the late stages of disease. A number of pharmacological agents that could slow the progression of DR in earlier stages are now being tested. It is likely that at least one of these agents, will be effective in reducing the progression of DR and the associated vision loss. With the introduction of these drugs in the coming years, there will be a need for improved screening and monitoring of patients with DR. New technologies are giving patients more access to optimal screening and may make this a more achievable goal.
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PMID:[Diabetic retinopathy. Current opinion on pathophysiology, diagnostics and therapy]. 1622 43

Recently, type 2 diabetes seems to be increasing annually in all developed countries. The outcome of type 2 diabetes is often tragic due to succession of complications including renal disorders requiring hemodialysis, blindness, and limb amputation. The expenses for the care of diabetic patients are also a large burden on the society. These circumstances strongly indicate the necessity of prevention. For satisfactory prevention, the clarification of the etiology related to lifestyle is important, but it remains insufficient to date. In this paper, we present a hypothesis of the etiology of type 2 diabetes from the viewpoint of microcirculation. As mentioned later, an unhealthy lifestyle first causes disturbance of the microcirculation, and a portion of the blood is considered to bypass the capillaries via arteriovenous shunts. This prevents the delivery of glucose and insulin to cells of peripheral tissues, causing hyperglycemia unrelated to the cell insulin sensitivity or the endocrine state, i.e., apparent reduction of insulin sensitivity. Disturbance of the microcirculation also causes oxidative stress in peripheral tissues by inducing ischemia and hypoxia. This oxidative stress is considered to further exacerbate reduction of insulin sensitivity. This hypothesis is supported by the well-known fact that insulin sensitivity recovers with improvement in lifestyle including moderate exercise.
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PMID:Disturbance of microcirculation due to unhealthy lifestyle: Cause of type 2 diabetes. 1624 54

Bilateral vision loss during hemodialysis is a rare but devastating entity, with grim prognosis for sight. The etiologies are diverse but share ischemia as a common mechanism. This is a report of a patient with bilateral sight loss during hemodialysis, with early hyperbaric treatment and return of visual acuity to baseline. Hyperbaric treatment should be considered, where early administration is possible, for bilateral blindness during hemodialysis.
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PMID:Hyperbaric therapy for bilateral visual loss during hemodialysis. 1654 83

Cardiovascular complications are the leading cause of morbidity and mortality in patients with diabetes mellitus; up to 80% of deaths in patients with diabetes are closely associated with vascular disease. The ability of the organism to form a collateral network of blood vessels constitutes an important response to vascular occlusive disease and determines to a large part the clinical consequences and severity of tissue ischemia. The development of new vessels is significantly reduced in diabetic patients with coronary or peripheral artery disease. This probably contributes to the severe course of limb ischemia in diabetic patients, in which peripheral artery disease often results in foot ulceration and lower extremity amputation. Diabetic retinopathy remains one of the major causes of acquired blindness in developed nations. This is true despite the development of laser treatment, which can prevent blindness in the majority of those who develop macular edema or proliferative diabetic retinopathy. The hallmark of diabetic retinopathy is the lack of microvessels in the macula, leading to hypoxia, associated with peripheral retinal neovascularization that may ultimately cause severe vitreous cavity bleeding and/or retinal detachment. The factors that stimulate retinal blood vessel growth have not been fully defined, but there is accumulating evidence that the renin-angiotensin-bradykinin system may be involved in a number of retinal vascular disorders, including retinopathy of prematurity and proliferative diabetic retinopathy. Only a few studies have specifically evaluated the effect of diabetes on angiogenesis in ischemic vascular disease and in the retina. Moreover, the mechanisms by which diabetes could both limit the formation of new blood vessels in most organs and simultaneously induce proliferative diabetic retinopathy remain largely undefined. In the present review, we aimed to briefly describe the main molecular mechanisms involved in the ischemia-induced angiogenesis, and their alterations in diabetes. Possible therapeutic strategies to restore angiogenesis in diabetic patients are also listed.
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PMID:[Diabetes and peripheral arterial occlusive disease: therapeutic potential and pro-angiogenic strategies]. 1670 93

Giant cell arteritis is a systemic vasculitis that affects large- and medium sized arteries. The most common ophthalmic manifestation of this disease is anterior ischemic optic neuropathy, leading to acute, painless visual loss in one or both eyes. It is caused by ischemia of the optic nerve head, which is mainly supplied by the short posterior ciliary arteries. Early diagnosis is the key to correct management and prevention of visual loss in the second eye. The treatment of choice for arteritic ischemic optic neuropathy is high dose of systemic corticosteroids. Only such treatment may prevent blindness. The authors presented a case of a 62 years man with anterior ischemic neuropathy in one eye, which was diagnosed as arteritic form caused by giant cell arteritis. The correct diagnosis was based on typical clinical signs of ischemic changes in the optic nerve head and diagnostic criteria for giant cell arteritis, advocated by American College of Rheumatologists.
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PMID:[Anterior ischemic optic neuropathy associated with giant cell arteritis. Case report]. 1688 58

The process of building new blood vessels (angiogenesis) and controlling the propagation of blood vessels (anti-angiogenesis) are fundamental to human health, as they play key roles in wound healing and tissue growth. More than 500 million people may stand to benefit from anti- or pro-angiogenic treatments in the coming decades [National Cancer Institute (USA), Cancer Bulletin, volume 3, no. 9, 2006]. The use of animal models to assay angiogenesis is crucial to the search for therapeutic agents that inhibit angiogenesis in the clinical setting. Examples of persons that would benefit from these therapies are cancer patients, as cancer growth and spread is angiogenesis-dependent, and patients with aberrant angiogenesis in the eye, which may lead to blindness or defective sight. Recently, anti-angiogenesis therapies have been introduced successfully in the clinic, representing a turning point in tumor therapy and the treatment of macular degeneration and heralding a new era for the treatment of several commonly occurring angiogenesis-related diseases. On the other hand, pro-angiogenic therapies that promote compensatory angiogenesis in hypoxic tissues, such as those subjected to ischemia in myocardial or cerebral hypoxia due to occluding lesions in the coronary or cerebral arteries, respectively, and in cases of poor wound healing, are also being developed. In this review, the current major and newly introduced preclinical angiogenesis assays are described and discussed in terms of their specific advantages and disadvantages from the biological, technical, economical and ethical perspectives. These assays include the corneal micropocket, chick chorioallantoic membrane, rodent mesentery, subcutaneous (s.c.) sponge/matrix/alginate microbead, s.c. Matrigel plug, s.c. disc, and s.c. directed in vivo angiogenesis assays, as well as, the zebrafish system and several additional assays. A note on quantitative techniques for assessing angiogenesis in patients is also included. The currently utilized preclinical assays are not equivalent in terms of efficacy or relevance to human disease. Some of these assays have significance for screening, while others are used primarily in studies of dosage-effects, molecular structure activities, and the combined effects of two or more agents on angiogenesis. When invited to write this review, I was asked to describe in some detail the rodent mesenteric-window angiogenesis assay, which has not received extensive coverage in previous reviews.
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PMID:In vivo models of angiogenesis. 1698 23


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