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)

Giant cell arteritis is characterized primarily by inflammation in certain large and medium-sized arteries. The major risk factors are age, female gender and Northern European descent. In this report we describe two cases of acute vision loss due to giant cell arteritis. In both cases the erythrocyte sedimentation rate (ESR) was below 50 mm/hr and the presenting complaint was foggy vision followed by acute blindness. The cases are to some extent different, for example in the former case the patient reported jaw claudication and ophthalmologic evaluation was consistent with anterior ischemic optic neuropathy. In the latter case there was narrowing and box-carring of blood cells in retinal arterioles, consistent with occlusion of the central retinal artery. This patient had recently finished a 2-year long treatment with glucocorticosteroids for polymyalgia rheumatica. The retina and the optic nerve do not survive for long without perfusion. If giant cell arteritis causes blindness in one eye there is significant risk for the other eye to go blind if no treatment is given. Corticosteroids can spare the other eye and suppress the underlying inflammatory disease process as well. It is vital to confirm the diagnosis of giant cell arteritis with a biopsy and start corticosteroid treatment as soon as possible, even before the biopsy is taken.
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PMID:[Giant cell arteritis - two cases with acute blindness]. 2019 97

Giant cell arteritis (GCA) is a chronic granulomatous vasculitis of large and medium size vessels in the elderly. A new-onset headache is the most frequent symptom. An anterior ischemic optic neuropathy (AION) is one of the most common causes of permanent visual loss. There are four cases with unusual presentation of giant cell arteritis, scalp abscess, prolonged transient monocular visual loss (TMVL), bilateral central retinal artery occlusion (CRAO), and chronic ear pain. All patients had pathologically proven giant cell arteritis, and three of them progressed to blindness in the end. Scalp abscess is a rare sign in GCA. Delay in diagnosis because confusion of the abscess after scalp ischemia with other cutaneous lesions may result in death. TMVL is the forewarning symptom of AION or CRAO in GCA. Early recognition of TMVL is important to make early diagnosis of GCA to prevent blindness. Spontaneous ear pain is extremely rare, and reports have documented delay in diagnosis of GCA resulting in irreversible blindness.
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PMID:A variety of atypical manifestations in giant cell arteritis. 2052 53

Giant cell arteritis with arteritic anterior ischemic optic neuropathy has rarely been diagnosed in Taiwan. Recently, we encountered a 76-year-old Taiwanese patient who presented with right visual impairment and marked pale swelling of his right disc. He also suffered body weight loss, general malaise and many typical manifestations of giant cell arteritis, such as jaw claudication, a tender, non-pulsating engorgement of his temporal arteries, and a highly elevated erythrocyte sedimentation rate and C-reactive protein level. Biopsy of his right superficial temporal artery revealed a granulomatous inflammation with multinucleated giant cell infiltration. This was a biopsy-proven case of giant cell arteritis with arteritic anterior ischemic optic neuropathy and indicated that although rare, this disease could occur in patients in Taiwan.
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PMID:Giant cell (Temporal) arteritis with anterior ischemic optic neuropathy: a biopsy-proven case in Taiwan. 2065 95

A 63-year-old woman developed consecutive visual loss in the presence of chronic renal failure on hemodyalisis, arterial hypertension, and pulmonary hypertension treated with sildenafil. Temporal artery biopsy was negative for giant cell arteritis. Bilateral, consecutive non-arteritic ischemic optic neuropathy was diagnosed. The implications and potential risk of sildenafil use in women are discussed.
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PMID:Not just for men. 2103 28

Ischemic optic neuropathies (IONs) consist primarily of two types: anterior ischemic optic neuropathy (AION) and posterior ischemic optic neuropathy (PION). AION comprises arteritic AION (A-AION: due to giant cell arteritis) and non-arteritic AION (NA-AION: due to other causes). PION consists of arteritic PION (A-PION: due to giant cell arteritis), non-arteritic PION (NA-PION: due to other causes), and surgical PION (a complication of several systemic surgical procedures). These five types of ION are distinct clinical entities etiologically, pathogenetically, clinically and from the management point of view. In the management of AION, the first crucial step with patients aged 50 and over is to identify immediately whether it is arteritic or not because A-AION is an ophthalmic emergency and requires urgent treatment with high-dose steroid therapy to prevent any further visual loss in one or both eyes. Patients with NA-AION, when treated with systemic corticosteroid therapy within first 2 weeks of onset, had significantly better visual outcome than untreated ones. Systemic risk factors, particularly nocturnal arterial hypotension, play major roles in the development of NA-AION; management of them is essential in its prevention and management. NA-PION patients, when treated with high-dose systemic steroid therapy during the very early stages of the disease, showed significant improvement in visual acuity and visual fields, compared to untreated eyes. A-PION, like A-AION, requires urgent treatment with high-dose steroid therapy to prevent any further visual loss in one or both eyes. There is no satisfactory treatment for surgical PION, except to take prophylactic measures to prevent its development.
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PMID:Management of ischemic optic neuropathies. 2135 Feb 82

Giant cell arteritis (Horton's disease) is an inflammatory panarteritis occurring most frequently in the elderly. Its common ocular manifestations are anterior ischemic optic neuropathy, choroidal ischemia and central retinal artery occlusion. We describe a case of Horton's disease revealed by a retinal detachment, optic neuropathy and severe choroidal ischemia. Prompt treatment with corticosteroids led to preservation of vision and resolution of the retinal detachment. This observation of a retinal detachment revealing a giant cell arteritis had not been yet reported in the literature.
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PMID:[Exsudative retinal detachment indicative of a giant cell arteritis. A case report]. 2156 51

Giant cell arteritis (GCA) is a systemic vasculitis that affects the aorta and its major branches. Involvement of the ciliary artery can result in ischemic optic neuropathy and subsequent blindness, which is typically irreversible. If GCA is suspected, treatment with glucocorticoids should be initiated promptly to prevent further vision loss. However, given the need for prolonged therapy with glucocorticoids and the morbidity associated with their use, diagnosis should be confirmed. Clinical features and laboratory findings are neither sensitive nor specific for GCA. The mainstay of diagnosis remains histopathologic examination of a section of the superficial temporal artery. Several imaging studies have been used to evaluate the temporal artery but, at present, their utility as alternatives to a temporal artery biopsy is limited. Recent advances in imaging modalities have allowed detailed noninvasive imaging of the large arteries and are a useful adjunct for the diagnosis of GCA, particularly in patients with primarily large-vessel involvement in whom temporal artery biopsy is often negative.
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PMID:Recent advances in diagnostic strategies for giant cell arteritis. 2220 35

Giant cell arteritis (GCA) is an important cause of preventable blindness, most commonly due to anterior ischemic optic neuropathy. Ischemic tissue injury is the end result of a process that begins within the walls of susceptible arteries in which local dendritic cells (DCs) recruit and activate CD4 T cells that, in turn, direct the activity of effector macrophages. In response to the immune attack, the blood vessel forms lumen-stenosing intima. Multiple cascades of excessive T-cell reactivity contribute to the autoimmune features of giant cell arteritis with TH1 and TH17 immunity responsible for the early phase and TH1 immunity promoting chronic-smoldering inflammation. These cascades are only partially overlapping, supporting the concept that a multitude of instigators induce and sustain vascular inflammation. The artery actively participates in the abnormal immune response through endogenous immune sentinels, so-called vascular DCs embedded in the adventitia. Advancing age, the strongest of all risk factors for GCA, contributes to both, the dysfunction of the immune system and the vascular system. Expansion of the therapeutic armamentarium for GCA needs to focus on approaches that mitigate the impact of the aging artery and adapt to the needs of the immunosenescent host.
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PMID:The immunopathology of giant cell arteritis: diagnostic and therapeutic implications. 2425 17

Sectoral choroidal ischemia is a classic sign of giant cell arteritis, although the latter is more typically associated with anterior ischemic optic neuropathy or central retinal artery occlusion. We report the case of an acute choroidal ischemia in a 68-year-old, one-eyed patient, who presented with deterioration of visual acuity and metamorphopsia in his left eye (his right eye was counting fingers due to high myopia). Fundus examination revealed retinal pigment epithelium (RPE) alterations and slow choroidal perfusion on fluorescein angiography. Macular Optical Coherence Tomography (OCT) showed a total disruption of the photoreceptor layer. Although prompt corticosteroid therapy preserved some vision, secondary macular retinal pigment epithelial changes limited the visual outcome. No other ophthalmological signs were observed in follow-up.
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PMID:[Acute sectoral choroidal ischemia: a case report]. 2298 23

We describe a 54-year-old diabetic woman who developed ischemic optic neuropathy followed by acute retinal necrosis and multiple areas of focal venous beading. Vitreous fluid contained amplifiable VZV DNA but not HSV-1, CMV or toxoplasma DNA. The clinical presentation was remarkable for jaw claudication and intermittent scalp pain, prompting a temporal artery biopsy that was pathologically negative for giant cell arteritis, but notable for VZV antigen. The current case adds to the clinical spectrum of multifocal VZV vasculopathy. The development of acute VZV retinal necrosis after ischemic optic neuropathy supports the notion that vasculitis is an important additional mechanism in the development of VZV retinal injury.
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PMID:VZV multifocal vasculopathy with ischemic optic neuropathy, acute retinal necrosis and temporal artery infection in the absence of zoster rash. 2331 50


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