Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Stereophotographs of the optic disc were reviewed in 78 patients with ischemic optic neuropathy (ION). Only 10% (6) of 61 nonarteritic (idiopathic) ION eyes developed optic disc cupping similar to that seen in glaucomatous eyes. Five of ten eyes with ION due to giant cell arteritis had cupping simulating glaucoma; however, two had elevated intraocular pressure, and the other three had large physiologic cups in the opposite eye. Optic disc pallor was proportionately more severe in ION eyes than in glaucomatous eyes of similar cup size. While there are similarities in the type of visual field loss in ION and glaucoma, the two disorders differ in the usual appearance of the disc after field loss has occurred and in the portion of the field most frequently affected. These observations suggest that if both disorders have an ischemic mechanism, there is a difference in the nature or distribution of the ischemia. There should be little difficulty under most circumstances in making the clinical differentiation between a disc that has suffered ION and a disc that has suffered pressure-induced damage, although occasional instances of ION may be classified as low-tension glaucoma on the basis of field loss and cupping without elevated intraocular pressure.
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PMID:Cupping of the optic disc in ischemic optic neuropathy. 92 94

An 80-year-old male patient with histologically confirmed temporal arteritis presented with two very rare complications: ocular hypotony and bilateral scalp necrosis. The intraocular pressure gradually normalized on high-dose cortisone therapy. Scalp necrosis was surgically removed and covered with a split-skin graft with good incorporation of the transplant. Scalp necrosis as well as ocular hypotony are serious complications of temporal arteritis, indicating a poor prognosis. To date three similar cases have been reported in the literature.
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PMID:[Temporal arteritis with hypotension syndrome and necrosis of the scalp]. 358 38

Acute ocular hypotony is a serious, but rare complication of temporal arteritis. It occurs equally often in men and women, and appears mostly in patients older than 70 years. This complication may occur in one or in both eyes. In the literature 7 cases of temporal arteritis accompanied by ocular hypotony have been reported. Hypotony probably results from a restricted production of aqueous humor caused by involvement of the arteries supplying the ciliary body. A high-dose corticoid therapy may normalize completely the intraocular pressure, and a timely treatment may preserve a satisfactory vision, since an insufficient perfusion of the optic disc does not necessarily occur. Scalp necrosis and diplopia may appear at the same time, and are a sign of multiple involvement of the arterial vessels.
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PMID:Acute ocular hypotony. A rare complication of temporal arteritis. 726 3

Circulatory disorders of the optic nerve may be classified into acute and chronic lesions as well as into anterior and posterior ones. In general, anterior lesions clinically prevail; they are located around the lamina cribrosa and are pathogenetically explained as a consequence of decreased blood flow in the posterior ciliary arteries as well as in the perilaminar capillaries. The symptoms of the acute anterior lesions are described. The nerve head infarction may be induced by various circulatory disorders such as arteriosclerosis, diabetes, elevated blood pressure, giant cell arteritis or other collagen diseases, but also by others. The particular importance of giant cell arteritis is stressed. The prognosis of acute anterior ischemic optic neuropathy is poor, possibilities of treatment are discussed. The chronic anterior lesion is considered to be caused by an imbalance between intraocular pressure and the perfusion pressure in the posterior ciliary arteries and consequently in the perilaminar capillaries. The clinical signs ('low tension glaucoma') are described, the therapeutic measures, although limited, are outlined. The ischemic lesions of the posterior part of the optic nerve are less well defined. However, theoretical considerations as well as clinical experience suggest that such lesions occasionally occur taking either an acute or a chronic course.
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PMID:Circulatory disorders of the optic nerve. 745 23

Patients with anterior ischemic optic neuropathy due to giant cell arteritis are thought to develop optic disc cupping, resembling that seen in glaucomatous eyes, while such cupping does not seem to occur in nonarteritic anterior ischemic optic neuropathy. However, this remains controversial. We describe a patient with arteritic anterior ischemic optic neuropathy (the clinical diagnosis was confirmed with a biopsy from the temporal artery) who developed disc cupping within 4 months after acute episode. This patient never had elevated intraocular pressure, and prior to the acute event the optic nerve heads had had a normal appearance with a physiologic cup.
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PMID:Optic disc cupping in arteritic anterior ischemic optic neuropathy. 784 52

An 84-year-old woman presented with bilateral visual loss that had appeared 3 days previously. Split lamp examination showed bilateral corneal edema with normal intraocular pressure. The patient complained of headache and vomiting, and finally collapsed. Elevated levels of inflammation markers led to the suspicion of an inflammatory disease. After investigation for internal or neurological diseases, a biopsy of the temporal artery was performed. Giant cell arteritis (Horton's disease) was found, and steroid therapy was begun. The patient's general condition then improved.
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PMID:[Acute visual loss with bilateral corneal edema]. 2038 45

Giant cell arteritis (GCA) is an ophthalmic emergency which requires early diagnosis and treatment with high dose systemic corticosteroids in order to prevent permanent visual loss. However, systemic corticosteroids have significant ocular side effects including cataract formation, raised intraocular pressure, and less commonly, central serous chorioretinopathy (CSCR). We report a case of visual loss secondary to CSCR complicating corticosteroid therapy in GCA. When assessing patients with systemic conditions such as GCA or other vasculitic process, who complain of visual loss which is getting worse on corticosteroid treatment, clinicians should consider other causes such as CSCR as part of the differential diagnosis. Extra caution should be exercised in such cases as increasing the dose of corticosteroids might aggravate CSCR resulting in further visual loss.
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PMID:Steroid induced central serous chorioretinopathy in giant cell arteritis. 2384 Sep 98