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)

In 1970 a 62-year-old physician with hypertensive vascular disease suffered a small infarction in the left optic disc, which left him with a subtle paracentral temporal visual field defect in that eye. In 1973 he had another separate and distinct episode in the same eye, which produced a dense lower nasal field defect. Careful Hruby lens examination of the disc under high magnification revealed focal arteriolar disease in the optic nerve head corresponding to the field defects, and fluorescein angiography confirmed these findings. The importance of differentiating ischemic optic neuropathy, hypertensive optic neuropathy, and temporal arteritis with optic nerve involvement is emphasized, and the therapy of each is discussed.
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PMID:Hypertensive optic neuropathy. 108 Mar 8

We present a 63-year-old lady who had atrial myxoma. The diagnostic difficulties distinguishing this from giant cell arteritis are highlighted. In particular, both conditions caused choroidal and retinal infarcts, anterior ischaemic optic neuropathy, with raised acute phase reactants. The authors stress the importance of continued ophthalmoscopy as the fundal changes become more apparent.
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PMID:Myxoma mix-up. A case report. 140 Nov 69

Colour Doppler ultrasound allows simultaneous B scan and Doppler imaging and can be employed to determine the velocity of blood flow in the vasculature of the eye and orbit. We describe a case of cranial arteritis (giant cell arteritis) in which serial velocimetry recordings were obtained. At one stage in the disease process no blood flow was detectable in the orbit despite previously reliable recordings. This coincided with a deterioration of the clinical state of the patient as signified by recurrent anterior ischaemic optic neuropathy despite controlled symptomatology and erythrocyte sedimentation rate by prednisolone therapy. Subsequent increase in the immunosuppressive therapy was accompanied by a return of blood flow in the orbit. Colour Doppler ultrasound may prove to be a useful examination technique in the diagnosis and management of cranial arteritis.
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PMID:Colour Doppler ultrasound in the management of a case of cranial arteritis. 147 49

The haemorheological parameters haematocrit (Hct), plasma viscosity (PV), red cell aggregation (RCA), red cell filterability (RCF), apparent whole blood viscosity (WBV), and fibrinogen were measured in 31 patients with retinal artery occlusion (RAO), 25 patients with anterior ischaemic optic neuropathy (AION), and 19 patients with giant cell arteritis (GCA). The patient groups were compared with controls of same age and similar prevalence of cardiovascular risk factors. Patients with RAO and AION have a significantly decreased RCF in comparison with controls. All other parameters showed no differences. Patients with GCA had significantly decreased Hct and RCF and increased PV and fibrinogen. After 2 weeks of systemic treatment with high dose steroids in patients with GCA the plasma viscosity had returned to normal and was even lower than in controls, and the Hct and fibrinogen had reached normal levels.
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PMID:Haemorheological parameters in patients with retinal artery occlusion and anterior ischaemic optic neuropathy. 154 May 56

A 62-year-old lady with hypertension and diabetes developed bilateral, sequential ischemic optic neuropathy, progressive in the right eye. Because of a reported association between amiodarone and optic neuropathy with disc edema, the patient discontinued taking this medication; however, her visual loss continued. The differential diagnoses of bilateral ischemic optic neuropathy--including infiltrative optic neuropathy and temporal arteritis--were exhaustively investigated in this patient.
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PMID:Getting to the heart of visual loss: when cardiac medication may be dangerous to the optic nerves. 156 39

Giant cell arteritis (GCA) is an ophthalmic emergency because, if undetected or managed inadequately, there is a high risk of developing a painless, permanent blindness in one or both eyes; however, if it is quickly identified and treated urgently and aggressively, blindness is almost entirely preventable. The ocular manifestations of GCA are essentially ischaemic in nature, with blindness as the most dreaded complication. Blindness is usually due to anterior ischaemic optic neuropathy (AION) and occasionally to other causes, e.g. posterior ischaemic optic neuropathy or central retinal or cilioretinal artery occlusion, although extremely rarely it may be cortical in origin. Diplopia and other types of ophthalmoplegias are seen in some cases but are usually transient in nature. Ischaemic lesions of the anterior segment of the eye are also seen in a few cases. Diagnosis of arteritic AION is discussed at length. Finally, management of GCA from the point of view of visual loss is discussed in detail.
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PMID:Ophthalmic features of giant cell arteritis. 180 20

Temporal arteritis is a common cause of blindness. Prompt steroid treatment limits unilateral visual loss while protecting the contralateral eye. Established blindness is irreversible. We report a case of temporal arteritis in which an eye with no light perception secondary to an arteritic anterior ischaemic optic neuropathy regained 6/6 vision.
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PMID:Treatable blindness in temporal arteritis. 173 1

The involvement of antiphospholipid antibodies in the mediation of acute anterior ischaemic optic neuropathy (AION) was studied, in the light of recent associations between these autoantibodies and other vascular events. A strong association between IgG anticardiolipin antibodies and AION secondary to biopsy proven giant cell arteritis was identified, which did not exist with the 'non-arteritic', biopsy negative form of AION. The possible implications of this finding on the aetiology, diagnosis, and treatment of giant cell arteritis are discussed.
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PMID:Antiphospholipid antibodies in the aetiology of ischaemic optic neuropathy. 206 Jun 76

A 73-year-old women presented with a recurrent form of sporadic brachial plexus neuropathy, the so-called Parsonage and Turner syndrome. This diagnosis is based on clinical and electromyographic findings. Interestingly a biopsy of the temporal artery demonstrated a giant cell arteritis. The clinical picture started 2 weeks after an upper respiratory tract illness. The possible viral etiology of giant cell arteritis is considered. We think an immunological rather than ischemic disturbance may have caused the recurrent brachial plexus neuropathy. This case report suggests that giant cell arteritis be considered in the investigation of the Parsonage and Turner syndrome.
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PMID:Recurrent brachial plexus neuropathy and giant cell arteritis. 215 59

Ocular complications occurring in temporal arteritis are of different severities. These manifestations of the disease occurred in a population of 57 patients with diagnosis of temporal arteritis, in 16 of them (28%). The diagnosis was suggested by finding an inflammatory syndrome (high erythrocyte sedimentation rate) and confirmed by temporal artery biopsy. In making this diagnosis, it was helpful to find a history of characteristic temporal headaches, neckache, jaw claudication, fever and malaise or weight loss in addition to polymyalgia and polyarthralgia. 6 patients presented with diplopia and different ocular muscle or nerve palsies. The 10 others came for sudden loss of vision due to ischemic anterior or posterior neuropathy and in one case, central artery obliteration. Prompt treatment with steroids gave good results on oculomotor troubles and in preventing the risk of involvement of the fellow eye. But loss of vision did not regress with this treatment. That means the importance in making this diagnosis and starting very promptly this treatment.
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PMID:[Eye manifestations of Horton's disease]. 259 Sep 88


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