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Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nine patients with histologically confirmed Horton's diseases were explored by Doppler ultrasound examination, before and after corticotherapy, of the cervical arteries, temporal arteries (N = 9), and branches of the ophthalmic artery: internal nasal (N = 9), central retinal, and supraorbital (N = 6). Excellent correlations existed between histological findings and results of Doppler examination, concerning the severity of the lesions (80% correlation). Circulatory slowing was evident in the ophthalmic vessels studied, with alterations in the shape of peak velocities in 6 of the 9 cases. Major abnormalities were present in 3 patients; two of them presenting transient or permanent amaurosis. Doppler curves improved after corticotherapy, their shape and amplitude becoming equivalent to those of a control population of the same age. Doppler examinations appear to be of diagnostic value in Horton's disease, as well as being able to predict the risk of ophthalmological complications; more effective surveillance of corticotherapy is possible.
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PMID:[Doppler examination in temporal arteritis. Preliminary results (author's transl)]. 732 Jun 44

Three patients with atypical ocular involvement due to histologically verified giant cell arteritis are reported. Prior to diagnosis, the first patient had periods of amaurosis fugax. He presented with normal vision. In spite of high-dose systemic corticosteroid therapy, he became blind in the terminal stage of his disease due to bilateral occipital cortex infarctions, verified by CT-scan. Autopsy revealed involvement of several intracranial arteries. In case No. 2 there was severe unilateral visual loss and cotton-wool exudates in both eyes. Central vision recovered after corticosteroid therapy; in our experience this is unusual. In case No. 3 irreversible unilateral visual loss was typical for GCA, but the association with polyneuropathy unique. Neurological remission coincided with systemic corticosteroid therapy.
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PMID:Atypical visual loss in giant cell arteritis. 774 91

We report a prospective study of 42 patients with biopsy-proven giant cell arteritis (CGA) who recovered for more than one year (mean follow up of 71 months since withdrawal of steroid treatment). It was used the same regimen of prednisone and well closely monitored along the whole treatment. In 22 patients, dapsone was given concomitantly with prednisone. Mean duration of steroid therapy was 23.1 months (range: 6-57 months); it was significantly decreased with treatment by dapsone (12 months and 12 days). Age, sex, initial clinical and biological (acute phase reactants) findings did not provide useful information for predicting steroid treatment needed for recovery. Thirty-six relapses were observed in 22 patients (60%) during treatment or after its withdrawal. Incidence of relapses declined during steroid treatment and relapses were (only) observed over first 6 months after steroid withdrawal. Three amaurosis fugax occurred at the beginning of treatment and an axillar bilateral stenosis was also observed. Forty-eight side effects of corticosteroids were recorded in 26 patients (63%): myopathy (n = 12), bone complications (n = 11), metabolic complications (n = 9). Twelve patients (63%) had experienced side effects of dapsone. This study emphasized the difficulty in treating CGA. Close monitoring is required. A steroid regimen is recommended.
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PMID:[Clinical course of Horton disease. Apropos of 42 cured patients]. 809 45

We report two patients with giant cell arteritis and unusual neuro-ophthalmic findings. One patient developed a horizontal one and a half syndrome associated with upright posture. The responsible lesion was dorsal pontine infarction. The other patient had bright light-induced amaurosis fugax in the absence of extracranial carotid occlusive disease. Both patients continued to have symptoms despite the use of high-dose intravenous corticosteroids. The manifestations of both patients occurred early in the course of giant cell arteritis and were flow related.
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PMID:Giant cell arteritis with unusual flow-related neuro-ophthalmologic manifestations. 937 44

One of the most susceptible sites to vascular diseases is the optic nerve head. By innovative approaches using morphometry and in situ hybridization, vascular and extracellular characteristics of the human optic nerve head were examined. Nonarteritic ischemic optic neuropathy occurs due to vascular insufficiency within the optic nerve head. Various local and systemic risk factors have been proposed among which smoking and acute hypotension are now included. Anatomically abnormal discs such as the small optic disc, tilted disc, and optic nerve drusen are recognized as "disks at risk" and hyperopia may be an additional predisposing factor. Ocular, neurological, and vascular disorders due to giant cell arteritis were reviewed. Intravenous high-dose methylprednine should be administered in certain cases. Differentiating nonarteritic from arteritic ischemic optic neuropathy is sometimes difficult. Isolated choroidal ischemia or choroidal filling delay may be an indication of giant cell arteritis. Studies have been conducted on the vascular event, amaurosis fugax (transient monocular visual loss), and the results of some of these studies are discussed.
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PMID:Neuro-ophthalmic aspects of vascular disease. 1015 Aug 24

Ocular manifestations of giant cell arteritis, of which permanent amaurosis overshadows all others, occur still frequently. They are usually preceeded by the classical signs of temporal arteritis, which should allow an earlier diagnosis and prompt corticosteroid treatment. Indeed, corticosteroids have proved very effective in preventing ocular complications. Once permanent amauposis is present, the treatment is still urgent, in order to avoid the involvement of the other eye and to restore some vision of the affected eye. However, once the eye is damaged, there is little hope that corticosteroid treatment will improve the vision, depending essentially upon which delay it has been started. These fearsome ocular complications argue for a better knowledge of the suggestive signs of temporal arteritis and highlight the urgency of corticosteroid treatment.
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PMID:[Ocular complications of Horton's disease]. 1021 96

Neurological manifestations are common in giant cell arteritis. Both the central and peripheral nervous system can be involved. The most dreaded manifestations are visual loss and stroke. Both frequently have premonitory symptoms, such as amaurosis fugax, blurry vision, diplopia, transient ischemic attacks, and jaw claudication. Although most of these manifestations occur prior to steroid therapy, they may also develop during the early phase of therapy, or during tapering of the dose of steroids. Earlier diagnosis, close monitoring and improving the treatment protocols may prevent mortality and improve morbidity in these cases.
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PMID:Neurologic manifestations of giant cell arteritis. 1094 54

Giant cell (temporal) arteritis (GCA) is the most common systemic vasculitis in Western countries. It involves large and medium-sized vessels with predisposition to the cranial arteries in the elderly. Cranial ischemic complications, in particular permanent visual loss, constitute the most feared aspects of this vasculitis. Although the use of corticosteroids and a higher physician awareness may have contributed to a decrease in the frequency of severe ischemic complications, permanent visual loss is still present in 7%-14% of patients. To investigate further the incidence, trends, and clinical spectrum of visual manifestations in patients with GCA, we examined the features of patients with biopsy-proven GCA diagnosed at the single reference hospital for a defined population in northwestern Spain during an 18-year period. Predictive factors for the development of any visual manifestation, not only permanent visual loss, were also examined. Between 1981 and 1998, 161 patients were diagnosed with biopsy-proven GCA. Visual ischemic complications were observed in 42 (26.1%), and irreversible blindness, mainly due to anterior ischemic optic neuropathy and frequently preceded by amaurosis fugax, was found in 24 (14.9%). Despite a progressive increase in the number of new cases diagnosed, there was not a significant change in the proportion of patients with visual manifestations during the study period (p = 0.37). Patients with visual ischemic complications had lower clinical and laboratory biologic markers of inflammation. Indeed, during the last years of the study, anemia was associated with a very low risk of visual complications. Also, HLA-DRB1*04-positive patients had visual manifestations more commonly. Patients with other ischemic complications developed irreversible blindness more frequently. The best predictors of any visual complication were HLA-DRB1*04 phenotype (odds ratio [OR] 7.47) and the absence of anemia at the time of admission (OR for patients with anemia = 0.07). The best predictors of irreversible blindness (permanent visual loss) were amaurosis fugax (OR 12.63) and cerebrovascular accidents (OR 26.51). The present study supports the claim that ocular ischemic complications are still frequent in biopsy-proven GCA patients from southern Europe. The presence of other ischemic complications constitutes an alarm for the development of irreversible blindness. In contrast, a higher inflammatory response may be a protective factor against the development of cranial ischemic events.
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PMID:Visual manifestations of giant cell arteritis. Trends and clinical spectrum in 161 patients. 1103 76

Temporal arteritis (TA) is a vasculitis involving mainly cranial branches of the aorta that can lead to ischemic complications such as amaurosis or ischemic stroke. Increment in the platelet count has been described in the acute period of the disease. We studied retrospectively the platelet count in patients with TA, its association with ischemic complications and quantified its response to therapy. We found thrombocytosis in 44% of 34 patients with TA, with a mean reduction in the platelet count of 25.1% after therapy. We were also able to quantify the increment in the platelet count at the onset of the disease and its response to prednisone in a group of 5 patients. We did not find any relation between platelet count and ischemic complications of the disease or the result of the temporal artery biopsy. In conclusion TA is associated with an increase in the platelet count, with a 25% reduction after prednisone therapy. These two determinations are not related to ischemic complications of the disease.
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PMID:Increment of the platelet count in temporal arteritis: response to therapy and ischemic complications. 1115 Aug 40

Vasospasm can have many different causes and can occur in a variety of diseases, including infectious, autoimmune, and ophthalmic diseases, as well as in otherwise healthy subjects. We distinguish between the primary vasospastic syndrome and secondary vasospasm. The term "vasospastic syndrome" summarizes the symptoms of patients having such a diathesis as responding with spasm to stimuli like cold or emotional stress. Secondary vasospasm can occur in a number of autoimmune diseases, such as multiple sclerosis, lupus erythematosus, antiphospholipid syndrome, rheumatoid polyarthritis, giant cell arteritis, Behcet's disease, Buerger's disease and preeclampsia, and also in infectious diseases such as AIDS. Other potential causes for vasospasm are hemorrhages, homocysteinemia, head injury, acute intermittent porphyria, sickle cell disease, anorexia nervosa, Susac syndrome, mitochondriopathies, tumors, colitis ulcerosa, Crohn's disease, arteriosclerosis and drugs. Patients with primary vasospastic syndrome tend to suffer from cold hands, low blood pressure, and even migraine and silent myocardial ischemia. Valuable diagnostic tools for vasospastic diathesis are nailfold capillary microscopy and angiography, but probably the best indicator is an increased plasma level of endothelin-1. The eye is frequently involved in the vasospastic syndrome, and ocular manifestations of vasospasm include alteration of conjunctival vessels, corneal edema, retinal arterial and venous occlusions, choroidal ischemia, amaurosis fugax, AION, and glaucoma. Since the clinical impact of vascular dysregulation has only really been appreciated in the last few years, there has been little research in the according therapeutic field. The role of calcium channel blockers, magnesium, endothelin and glutamate antagonists, and gene therapy are discussed.
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PMID:Vasospasm, its role in the pathogenesis of diseases with particular reference to the eye. 1128 96


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