Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glaucoma is a leading cause of irreversible blindness in the world. Currently, glaucoma is diagnosed as a progressive optic neuropathy with characteristic optic disc and nerve fiber layer damage, usually associated with loss of visual function. The intraocular pressure (IOP) is the most important risk factor for the disease, although a significant proportion of patients do not have elevated IOP. Other risk factors include older age, African descent, myopia and family history of the disease. The ophthalmoscopic examination of the optic disc is essential to identify the signs of glaucomatous optic neuropathy, such as increased cupping, neuroretinal rim thinning or optic disc hemorrhages. Glaucomatous visual field loss usually starts in the periphery, and loss of central vision does not occur until late in the course of the disease. Visual function is most commonly assessed by standard automated perimetry; however, as many as 50% of nerve fibers can be lost before the appearance of visual field defects in this test. Newer technologies have been developed to find more sensitive ways to detect early glaucoma using both functional (short-wavelength automated perimetry and frequency-doubling perimetry) and structural (scanning laser topography, optical coherence tomography and scanning laser polarimetry) measurements. The management of glaucoma is based on lowering the intraocular pressure to prevent further optic nerve damage. Currently, there are five major classes of medications that are used to lower the intraocular pressure: Beta-adrenergic antagonists, adrenergic agonists, parasympathomimetics, prostaglandin-like analogues and carbonic anhydrase inhibitors. The goal of therapy is to maintain adequate vision for patients during their lifetime, keeping in mind the possible adverse effects of the drugs. If additional lowering of IOP is indicated or if medication fails to sufficiently lower the IOP, laser trabeculoplasty is usually the next step. If IOP is still not adequately controlled, incisional glaucoma surgery is indicated. Neuroprotective agents, which directly protect the optic nerve in glaucoma, are being evaluated in clinical trials.
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PMID:Medical backgrounders: glaucoma. 1258 21

Current best practice for primary open-angle glaucoma case-finding comprises history-taking, disc examination, intraocular pressure measurement and suprathreshold visual field analysis (SVFA). An alternative case-finding technique was formulated replacing SVFA with computerised quantitative disc assessment, using the Heidelberg retinal tomograph II (HRT II). Each approach was adopted by four optometrists who screened 29 POAG and 37 normal patients. Average sensitivities and specificities were similar in the two groups [sensitivity 71% (SVFA) vs 69% (HRT II); specificity 94% both groups]. Our inclusion of pre-perimetric glaucoma cases limited the sensitivity of the optometrists in this study. There was evidence to suggest that the optometrists tended to miss early changes at the optic disc such as disc haemorrhage, nerve fibre layer defects and subtle neuroretinal thinning.
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PMID:Sensitivity and specificity of two glaucoma case-finding strategies for optometrists. 1282 24

DBA/2J (D2) mice develop a form of progressive pigmentary glaucoma with increasing age. We have compared retinal cell populations of D2 mice with those in control C57BL/6J mice to provide information on retinal histopathology in the D2 mouse. The D2 mouse retina is characterized by a reduction in retinal thickness caused mainly by a thinning of the inner retinal layers. Immunocytochemical staining for specific inner retinal neuronal markers, viz., calbindin for horizontal cells; protein kinase C (PKC) and recoverin for bipolar cells, glycine, gamma-aminobutyric acid (GABA), choline acetyltransferase (ChAT), and nitric oxide synthase (NOS) for amacrine cells, and osteopontin (OPN) for ganglion cells, was performed to detect preferentially affected neurons in the D2 mouse retina. Calbindin, PKC, and recoverin immunoreactivities were not significantly altered. Amacrine cells immunoreactive for GABA, ChAT, and OPN were markedly decreased in number, whereas NOS-immunoreactive amacrine cells increased in number. However, no changes were observed in the population of glycine-immunoreactive amacrine cells. These findings indicate a significant loss of retinal ganglion and some amacrine cells, whereas glycinergic amacrine cells, horizontal, and bipolar cells are almost unaffected in the D2 mouse. The reduction in amacrine cells appears to be attributable to a loss of GABAergic and particularly cholinergic amacrine cells. The increase in nitrergic neurons with the consequent increase in NOS and NO may be important in the changes in the retinal organization that lead to glaucomain D2 mice. Thus, the D2 mouse retina represents a useful model for studying the pathogenesis of glaucoma and mechanisms of retinal neuronal death and for evaluating neuroprotection strategies.
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PMID:Changes in retinal neuronal populations in the DBA/2J mouse. 1571 80

Inhaled corticosteroids continue to be hallmark players in asthma control. In time, they induced fear, hope, and created numerous discussions in specialty literature. Usually, the studies focus more on their beneficial effects and less on adverse effects. Surprisingly, lately more was written about systemic effects. A detailed review of some recent studies demonstrates that the most feared systemic effects (risk for osteoporosis due to calcium and phosphate metabolic changes, adrenal suppression, skin thinning, cataract, growth problems in children and teenagers, glaucoma) are very rare. The local effects, if properly addressed by the physician and patient, can be largely diminished. The conclusion of this article is that there is a non-due fear for this class of medication with certain virtues in asthma and COPD therapy.
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PMID:[Inhaled corticosteroids and the local effects--a justified fear?]. 1619 32

We report a case of unilateral glaucoma with falsely low intraocular pressure reading as a result of scleral thinning from anterior scleritis.
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PMID:Anterior scleritis, scleral thinning, and intraocular pressure measurement. 1632 90

A 22-year-old woman underwent 360 degrees trans-scleral contact diode laser cyclophotocoagulation for refractory glaucoma. Conjunctival burns and scleral thinning were noticed inferonasally at the last laser application. Intraocular pressure in the first week was normal. Six months later the patient presented with encysted filtering bleb and high intraocular pressure. Ultrasound biomicroscopy revealed a full thickness sclerostomy. This report suggests that inadvertent sclerostomy may present with encysted bleb months after trans-scleral contact diode laser cyclophotocoagulation.
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PMID:Inadvertent sclerostomy with encysted bleb following trans-scleral contact diode laser cyclophotocoagulation. 1645 Dec 68

Aerosolized medications maximize clinical benefit by targeting the airways and minimize side effects by reducing (though not eliminating) systemic exposure. Aerosolized drugs delivered with a facemask may inadvertently deposit on the face and in the eyes, raising concerns about cutaneous and ocular side effects with these drugs. Cases of anisocoria have been reported from exposure of the eyes to aerosol bronchodilators. Whether inhaled corticosteroids (ICS) can cause skin and eye problems like those seen with systemic or topical steroids is more difficult to answer. Patients who take ICS may have other corticosteroid exposures, or have other conditions that predispose them to side effects, making the analysis of the ICS risk challenging. Also, many studies were not designed to search for cutaneous or ocular effects, or may have been too short to detect these effects. Nevertheless, ICS have been associated with an increased risk of skin thinning, bruising, cataracts and possibly glaucoma in adults, but not in children. The risks increase with advanced age, higher doses, and longer duration of use. In children, the risks of cataracts and glaucoma were negligible with ICS, whether a mouthpiece or a mask interface was used. Side effects like skin rash and conjunctivitis occurred at low frequencies similar to placebo or comparator drugs. We do not know whether exposed children will have increased risks from ICS later in life. Therefore, it is wise to avoid face and eye deposition when possible, and to use the minimally effective dose.
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PMID:Clinical side effects during aerosol therapy: cutaneous and ocular effects. 1741 1

A 9.5-year-old, male castrated European Short-haired (ESH) cat was presented with bilateral glaucoma associated with pectinate ligament dysplasia and an open iridocorneal angle (ICA) upon gonioscopy. The right eye (OD) was avisual and slightly enlarged; the left eye (OS) was still visual. Intraocular pressure (IOP) had been controlled with medical therapy over a 1.5 year-period in both eyes (OU). Eventually IOP could not be adequately controlled medically and the painful and blind right eye was enucleated and transscleral diode laser cyclophotocoagulation was performed twice in the left eye with less than optimal results and progressive loss of vision. Histopathology of the right eye showed goniodysgenesis characterized by failure of differentiation of the pectinate ligament, which existed as a solid sheet of uveal tissue at the entrance of a hypoplastic ciliary cleft, which contained loose mucoid mesenchymal tissue. The trabecular meshwork was hypoplastic and the scleral venous plexus could not be identified. Other findings of chronic glaucoma were inner retinal atrophy, optic nerve atrophy with disc cupping, scleral thinning, peripheral corneal vascularization and pigmentation, and mild focal iridal mononuclear inflammatory cell infiltrate.
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PMID:Goniodysgenesis associated with primary glaucoma in an adult European Short-haired cat. 1797 28

Ocular defects and age-related lesions in mutant (GUB strain) Japanese quail (Coturnix coturnix japonica), phenotypically characterised by silver plumage, are described. Grossly, a circular area of hypopigmentation in the posterior retina with thinning of the subjacent sciera was observed in all GUB quails. As the birds matured, the thinned sciera progressed to scierai ectasia. Histologically, the sciera at the ectatic area consisted of an outer fibrous layer and was devoid of the inner cartilaginous shell. Atypical differentiation and duplication of the retina with absence of the choroid was common at the ectatic area. The retina, choroid, ciliary body and iris were all poorly pigmented. With increasing age, the ectatic area became cystic, and the duplicated retina degenerated and atrophied. In addition, there were mononuclear cell infiltration in the stroma of the iris and ciliary body, anterior and posterior synechiae, cataract and/or glaucoma in aged GUB quails. These findings suggest that posterior scierai ectasia in the GUB strain of Japanese quails may have developed secondarily to a congenital structural defect of the posterior portion of sciera associating with general ocular defects.
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PMID:Scierai ectasia associated with hereditary retinal dysplasia in a mutant strain of Japanese quail (Coturnix coturnix japonica). 1848 90

The glaucomas are a group of potentially blinding optic neuropathies that are characterized by progressive pathological losses of the retinal ganglion cells (RGCs) and their axons that form the optic nerve. The causes are unknown and, therefore, the diagnosis and assessment of progression of disease depends on ophthalmic testing to identify and quantify clinical characteristics of glaucomatous neuropathy, such as the pattern of visual field defects and/or thinning of the retinal nerve fiber layer. To relate these clinical measurements to the basic pathology of glaucoma, a neuron doctrine for glaucoma has been proposed to correlate data from standard tests (standard automated perimetry and optical coherence tomography) to the loss of RGCs. The doctrine was derived through initial laboratory studies of experimental glaucoma in macaque monkeys and, then, modified and refined though patient-based clinical investigations. The final formulation of the doctrine produced concordance between subjective and objective measurements when the results were translated to their common parameter of RGCs, for both normal vision and defective vision from glaucoma. Thus, it was concluded that for individual patients, alterations in structure-function relationships usually should be in agreement for the degree and location of visual field defects caused by glaucoma.
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PMID:Charles F. Prentice Award Lecture 2006: a neuron doctrine for glaucoma. 1852 Oct 13


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