Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pars plana vitrectomy (PPV) with silicone oil implantation (SOI) was performed for advanced proliferative diabetic retinopathy (PDR) in 110 eyes of 98 diabetic patients. In 77 eyes (70%) it was a primary SOI as part of the initial operation; in 33 eyes (30%) it was a secondary SOI in reoperations. Indications for SOI were traction retinal detachment of the posterior pole, combined traction and rhegmatogenous detachment, vitreous haemorrhage with florid vascularised fibrous proliferations, and recurrent vitreous haemorrhage after PPV. The patients were followed up for 24 to 72 months, with a mean of 53 months. At the end of follow-up, anatomical success was achieved in 63 eyes (57%), and functional success with visual acuity 0.01 and better in 35 eyes (32%). Functional failures were caused by retinal redetachment in 47 eyes (43%), by secondary glaucoma in 10 eyes (9%), retinal ischemia in 15 eyes (13%) and keratopathy in three eyes (3%). The functional success rate decreased with follow-up from 67% after six months to 50% by 60 months after SOI. Silicone oil bubble in the anterior chamber, rubeosis iridis, cataract, and glaucoma were the most frequent postoperative complications. PPV with SOI was highly effective in many serious complications of advanced PDR. Functional success was mostly lasting and markedly improved the quality of life of these patients.
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PMID:Long-term results of pars plana vitrectomy and silicone oil for complications of diabetic retinopathy. 801 22

Eighty cases Diabetic Cystoid Macular Edema, with or without central spaces underwent photocoagulation from 1978 to 1989 using a horseshoe or ring pattern. Initial visual acuity ranged from 20/25 for far vision and 20/20 for near vision to a central scotoma, with an average of 20/60 for far vision and 20/50 for near vision. As initial treatment, we performed 63 horseshoe pattern and 13 ring pattern photocoagulation around the macula; an additional photocoagulation was carried out in 29 cases, one month to seven years later (average of 18.3 months), either on medial to the previous treatment (18), or closing the initial horseshoe pattern (10) or resulting in focal treatment (13), or associating any of these three. The cystoid macular edema disappeared in 47 cases, decreased in 15 cases, and remained in 14 cases, with a follow up ranging from 6 months to 10.5 years (average of 41.6 months). The post laser visual acuity range from 20/25 for far vision and 20/20 for near vision, to a central scotoma again, with an average of 20/60 for far and near visions. During the follow up various reasons of visual impairment were observed: cataract, intravitreal hemorrhage, epiretinal membrane, macular pucker and macular ischemia. Our results compared with the published ones concerning a grid pattern photocoagulation are encouraging. It is very important to stress that this photocoagulation is only aimed toward the macular edema itself: if necessary it should be associated with a grid pattern or a focal photocoagulation aimed toward extramacular edema.
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PMID:[Treatment by horseshoe pattern photocoagulation of diabetic cystoid macular edema]. 817 74

A 67-year-old woman experienced a severe headache and vomiting. A computed tomographic (CT) scan showed a mild subarachnoid hemorrhage. Cerebral angiography revealed a saccular aneurysm at the apex of the basilar artery. Several days later, she noticed mild hemiparesis of the left extremities. She underwent a clipping operation on the aneurysm by approaching from the right temporal love. Postoperatively, she developed diplopia and dilatation of the left pupil. Cerebral angiography revealed an occlusion of the left posterior cerebral artery. She was admitted to another hospital in order to continue rehabilitation. General physical examination was normal. Neurological examination revealed paralysis of the left medial and left inferior rectus muscles and palsy of the left inferior oblique muscle. The pupil of the left eye was dilated, measuring 5 mm in diameter, and it did not constrict to any stimuli. The left superior rectus and levator palpebrae superioris functioned normally. Visual acuity and visual fields were normal except for the influence of a senile cataract. She had a mild left hemiparesis, slight left ataxia and slurred speech. She had numbness of the left half of the body. A CT scan showed small low density areas in the right thalamus and left cerebellar hemisphere. Her ophthalmologic findings were compatible with the inferior branch palsy of the oculomotor nerve. The ophthalmoplegia of this case seems to be due to partial damage of the oculomotor nerve induced by ischemia of vascular supply. It is supposed to be caused by a vasospasm of the left posterior cerebral artery following a clipping operation of the basilar apex aneurysm.
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PMID:[Inferior branch palsy of the oculomotor nerve following clipping of basilar apex aneurysm]. 831 94

A 67-year-old diabetic man suffered from right neovascular glaucoma following the ipsilateral cataract surgery. Three years later, he underwent left cataract surgery and again developed left neovascular glaucoma after the operation. Fluorescein angiogram showed a marked delay in retinal circulation. Moreover, severe stenosis of bilateral carotid origins and reflux of bilateral ophthalmic arteries were ascertained by neurosonographical examination such as duplex cervical echography and transcranial Doppler, as well as an angiogram. Brain imaging demonstrated asymptomatic watershed infarction in the left parieto-occipital cortex. Chronic ocular ischemia caused by carotid stenosis is one of the decisive risk factors for secondary glaucoma after cataract surgery. Preoperative neurosonographical screening tests are required to decrease ocular surgery complications, especially in the aged, and diabetic patients.
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PMID:[A diabetic patient with bilateral carotid stenosis who developed neovascular glaucoma following cataract surgery]. 856 40

It is thought that dystrophic changes in the human aging anterior eye are due to lipid peroxidation in both the cortical and nuclear structures of the lens under the conditions of ischemia. These changes are often accompanied by only lens opacification (senile cataract-SC) or by formation of amorphous or fibrillar deposits in anterior eye, disturbances of eye hydrodynamics and lens opacification (pseudoexfoliation syndrome-PES). Our results suggest that the main reason of dystrophic changes in the tissues of the aging anterior eye is the disturbance of the haemato-ophthalmic barrier and that the plasma kallikrein-kinin system takes part in this disturbance. Penetration of plasma proteins, such as C-reactive protein, complement components, immunoglobulins and coagulation factors, from plasma into the aqueous humor is responsible for damaging epithelial structures of anterior eye and formation of pseudoexfoliative material. Using ELISA, the C-reactive protein, IgG and IgM antigens have been shown to localize on the surface of the opaque lenses. Presence of these complement binding proteins in the superficial lens structures as well as the high C3a concentration in the aqueous humor substantiates the pathogenic role of complement activation in the lenticular epithelium upon cataract and PES formation.
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PMID:Hageman factor and kallikrein in pathogenesis of senile cataracts and the pseudoexfoliation syndrome. 879 92

Apoptosis is a form of genetically programmed cell death that can be induced by a variety of different stimuli. It is often referred to as a form of cellular suicide. Typically, apoptosis is characterized by the condensation and shrinkage of the cellular nucleus and cytoplasm, followed by the complete fragmentation of the cell and subsequent phagocytosis of the debris by surrounding cells. Although important during development, and also for maintaining homeostasis in some adult tissues, apoptosis can also be associated with disease processes. Recent laboratory studies indicate that apoptosis is a mechanism of cell death in several important ocular diseases including glaucoma, retinitis pigmentosa, cataract formation, retinoblastoma, retinal ischemia, and diabetic retinopathy. This review summarizes the results of these studies and provides a brief description of some of the key molecules that are involved in the genetic regulation of apoptosis. It is possible that a complete understanding of how these molecules function may someday lead to new treatment options aimed at blocking the death of cells in a variety of ocular diseases.
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PMID:Apoptosis in ocular disease: a molecular overview. 901 Aug 66

A 19-year-old female manifested severe bilateral panuveitis with neovascularization in the iris, optic disc, and retina. Fluorescein fundus angiography showed dye leakage from the optic disc and retinal blood vessels, and a large non-perfused area was present in the peripheral retina of the right eye. Sarcoidosis was diagnosed histologically by conjunctival and skin biopsy. Although the patient was given a large dose of a corticosteroid systemically and received panretinal photocoagulation, a dense vitreous hemorrhage and cataract were apparent in the right eye. The right visual acuity decreased to hand motions. A pars plana lensectomy and vitrectomy were performed. After vitrectomy, inflammation and neovascularization regressed and the visual acuity improved to 20/100. Proliferative membrane obtained during vitrectomy was histopathologically studied by light and electron microscopy. Many new vessels containing neutrophils were observed. A direct effect of inflammation as well as ischemia in the retina may have been the stimulus for the proliferative changes.
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PMID:[A case of sarcoidosis with proliferative retinopathy]. 920 43

Tobacco smoke is composed of as many as 4,000 active compounds, most of them toxic on either acute or long-term exposure. Many of them are also poisonous to ocular tissues, affecting the eye mainly through ischemic or oxidative mechanisms. The list of ophthalmologic disorders associated with cigarette smoking continues to grow. Most chronic ocular diseases, with the possible exception of diabetic retinopathy and primary open-angle glaucoma, appear to be associated with smoking. Both cataract development and age-related macular degeneration, the leading causes of severe visual impairment and blindness, are directly accelerated by smoking. Other common ocular disorders, such as retinal ischemia, anterior ischemic optic neuropathy, and Graves ophthalmopathy, are also significantly linked to this harmful habit. Tobacco smoking is the direct cause of tobacco-alcohol amblyopia, a once common but now rare disease characterized by severe visual loss, which is probably a result of toxic optic nerve damage. Cigarette smoking is highly irritating to the conjunctival mucosa, also affecting the eyes of nonsmokers by passive exposure (secondhand smoking). The dangerous effects of smoking are transmitted through the placenta, and offspring of smoking mothers are prone to develop strabismus. Efforts should be directed toward augmenting the campaign against tobacco smoking by adding the increased risk of blindness to the better-known arguments against smoking. We should urge our patients to quit smoking, and we must make them keenly aware of the afflictions that can develop when smoke gets in our eyes.
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PMID:The association between cigarette smoking and ocular diseases. 963 2

It is apparent that there are many unanswered questions about the pathogenesis of CRS. For instance, the chance of embryonic infection decreases in the second semester only to increase again in the third trimester. This is presumably due to unspecified changes in the placenta. When the embryo is infected early in the first trimester it does not appear to have any conventional immunological response to prevent spread of the virus. Yet it has been suggested that only 1 in 10(3) to 10(5) of its cells become infected. If this is true, what controls the spread of the virus in the early embryo? Why does the virus not affect major morphogenetic processes? There is considerable evidence that the virus spreads through the vascular system of the infected fetus and the observed cardiovascular, CNS, and hearing defects may be primarily due to focal cytopathic damage to the walls of blood vessels and lining of the heart; subsequent organ infection and/or ischemia may lead to further damage. Damage to blood vessels is probably extensive throughout the fetus and may be the cause of the generalized growth retardation. The effects in the eye appear to be due to a direct cytopathic effect, particularly on the lens. The short susceptible period for cataract formation is consistent with the protective effect of the lens capsule. Deafness, cardiovascular and neurological damage, and retinopathy all occur when infection takes place in the first 16 weeks of gestation and are rare after this time, despite the absence of any obvious morphological or functional changes in the susceptible structures. This termination of susceptibility in the second trimester is consistent with development of the fetal immune response and increased transfer of maternal IgG. The effect on blood vessels in particular may be limited by antibody production, although existing endothelial infection and damage may be progressive. The fetus seems unable to rid itself of established intracellular virus. The causes of the well-established late manifestations remain unknown. If these serious late-appearing effects are due to prenatal damage, then it is possible that other human teratogens may also cause unexpected late symptoms. This should also be a concern in the area of animal reproductive toxicology testing.
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PMID:Teratogen update: congenital rubella. 969 40

A 75-year-old man suffered from right neovascular glaucoma following ipsilateral cataract surgery. Cerebral angiogram showed occlusion of the right internal carotid artery and the steal phenomenon of right ophthalmic artery. Chronic ocular ischemia caused by carotid occlusion and ophthalmic artery steal phenomenon is one of the decisive risk factors for secondary glaucoma after cataract surgery.
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PMID:[Neovascular glaucoma following cataract surgery--a case report]. 1058 30


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