Giant Cell

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Bridget Zimmerman - One of the best experts on this subject based on the ideXlab platform.

  • ocular manifestations of Giant Cell arteritis
    American Journal of Ophthalmology, 1998
    Co-Authors: Sohan Singh Hayreh, Patricia Podhajsky, Bridget Zimmerman
    Abstract:

    Purpose To report the ocular manifestations of Giant Cell arteritis using the strict criterion of a positive temporal artery biopsy for diagnosis of Giant Cell arteritis. Methods In a prospective study from 1973 to 1995, we investigated 170 patients whose diagnosis of Giant Cell arteritis was confirmed on temporal artery biopsy. At the initial visit, all patients were questioned regarding systemic and ocular signs and symptoms of Giant Cell arteritis and underwent ophthalmic, erythrocyte sedimentation rate (Westergren), and C-reactive protein evaluations. Any patient with a high index of suspicion of Giant Cell arteritis was immediately started on systemic corticosteroid therapy and had temporal artery biopsy performed as soon as possible. Results Eighty-five (50.0%) of the 170 patients with Giant Cell arteritis proven by temporal artery biopsy presented with ocular involvement. Ocular symptoms in patients with ocular involvement were visual loss of varying severity in 83 (97.7%), amaurosis fugax in 26 (30.6%), diplopia in five (5.9%), and eye pain in seven (8.2%); ocular ischemic lesions consisted of arteritic anterior ischemic optic neuropathy in 69 (81.2%), central retinal artery occlusion in 12 (14.1%), cilioretinal artery occlusion in 12 (of 55 patients with satisfactory fluorescein angiography [21.8%]), posterior ischemic optic neuropathy in six (7.1%), and ocular ischemia in one (1.2%). In almost every patient with Giant Cell arteritis, fluorescein fundus angiography disclosed occlusive disease of the posterior ciliary arteries. Conclusion Because Giant Cell arteritis is a potentially blinding disease and its early diagnosis is the key to preventing blindness, it is important to recognize its various ocular manifestations.

Jorg J Goronzy - One of the best experts on this subject based on the ideXlab platform.

  • Giant Cell arteritis and polymyalgia rheumatica
    Annals of Internal Medicine, 2003
    Co-Authors: Cornelia M Weyand, Jorg J Goronzy
    Abstract:

    Both Giant-Cell arteritis and polymyalgia rheumatica are immune-mediated diseases that are treated with glucocorticoids, with higher doses used for Giant-Cell arteritis. Prompt initiation of high doses and a biopsy are recommended when ischemic optic neuropathy is suspected.

  • Giant Cell arteritis and polymyalgia rheumatica
    Annals of Internal Medicine, 2003
    Co-Authors: Cornelia M Weyand, Jorg J Goronzy
    Abstract:

    Giant-Cell arteritis is an immune-mediated disease characterized by granulomatous infiltrates in the wall of medium-size and large arteries. The immunopathology consists of 2 components. Excessive cytokine production (for example, of interleukin-1 and interleukin-6) induces systemic inflammation with an exuberant acute-phase response. In parallel, interferon-gamma, which is released by T Cells captured in the arterial wall, activates tissue-injurious macrophages. In response to the immune injury, the artery generates hyperplasia of the intima that leads to luminal occlusion and subsequent tissue ischemia. Despite the systemic character of the disease, distinct vascular territories are preferentially affected. On the basis of the predominant involvement, clinical subtypes can be distinguished: cranial Giant-Cell arteritis with ischemic complications in the eye, the face, and the central nervous system; large-vessel Giant-Cell arteritis with occlusions in the subclavian or axillary vessels; aortic Giant-Cell arteritis; Giant-Cell arteritis presenting as an intense systemic inflammatory syndrome with nonstenosing vasculitis; and "isolated" polymyalgia rheumatica with myalgias, systemic inflammation, and subclinical vasculitis. Temporal artery biopsy remains the diagnostic procedure of choice to detect arteritis in cranial vessels. In other vascular territories, Giant-Cell arteritis is most commonly diagnosed by vascular imaging. Laboratory studies characteristically document the marked elevations of nonspecific acute-phase reactants, such as C-reactive protein and erythrocyte sedimentation rate. Cytokines, such as interleukin-6, that induce the acute-phase reaction are currently being explored as more sensitive biological markers of disease activity. Corticosteroids are highly effective in suppressing systemic inflammation, but they do not eliminate the immune responses in the vessel wall. In general, the clinical outcome of Giant-Cell arteritis is exCellent, and efforts must now concentrate on tailoring therapies to the needs of the individual patient.

Gene G Hunder - One of the best experts on this subject based on the ideXlab platform.

  • polymyalgia rheumatica and Giant Cell arteritis
    The Lancet, 2008
    Co-Authors: Carlo Salvarani, Fabrizio Cantini, Gene G Hunder
    Abstract:

    Polymyalgia rheumatica and Giant-Cell arteritis are closely related disorders that affect people of middle age and older. They frequently occur together. Both are syndromes of unknown cause, but genetic and environmental factors might have a role in their pathogenesis. The symptoms of polymyalgia rheumatica seem to be related to synovitis of proximal joints and extra-articular synovial structures. Giant-Cell arteritis primarily affects the aorta and its extracranial branches. The clinical findings in Giant-Cell arteritis are broad, but commonly include visual loss, headache, scalp tenderness, jaw claudication, cerebrovascular accidents, aortic arch syndrome, thoracic aorta aneurysm, and dissection. Glucocorticosteroids are the cornerstone of treatment of both polymyalgia rheumatica and Giant-Cell arteritis. Some patients have a chronic course and might need glucocorticosteroids for several years. Adverse events of glucocorticosteroids affect more than 50% of patients. Trials of steroid-sparing drugs have yielded conflicting results. A greater understanding of the molecular mechanisms involved in the pathogenesis should provide new targets for therapy.

Sohan Singh Hayreh - One of the best experts on this subject based on the ideXlab platform.

  • ocular manifestations of Giant Cell arteritis
    American Journal of Ophthalmology, 1998
    Co-Authors: Sohan Singh Hayreh, Patricia Podhajsky, Bridget Zimmerman
    Abstract:

    Purpose To report the ocular manifestations of Giant Cell arteritis using the strict criterion of a positive temporal artery biopsy for diagnosis of Giant Cell arteritis. Methods In a prospective study from 1973 to 1995, we investigated 170 patients whose diagnosis of Giant Cell arteritis was confirmed on temporal artery biopsy. At the initial visit, all patients were questioned regarding systemic and ocular signs and symptoms of Giant Cell arteritis and underwent ophthalmic, erythrocyte sedimentation rate (Westergren), and C-reactive protein evaluations. Any patient with a high index of suspicion of Giant Cell arteritis was immediately started on systemic corticosteroid therapy and had temporal artery biopsy performed as soon as possible. Results Eighty-five (50.0%) of the 170 patients with Giant Cell arteritis proven by temporal artery biopsy presented with ocular involvement. Ocular symptoms in patients with ocular involvement were visual loss of varying severity in 83 (97.7%), amaurosis fugax in 26 (30.6%), diplopia in five (5.9%), and eye pain in seven (8.2%); ocular ischemic lesions consisted of arteritic anterior ischemic optic neuropathy in 69 (81.2%), central retinal artery occlusion in 12 (14.1%), cilioretinal artery occlusion in 12 (of 55 patients with satisfactory fluorescein angiography [21.8%]), posterior ischemic optic neuropathy in six (7.1%), and ocular ischemia in one (1.2%). In almost every patient with Giant Cell arteritis, fluorescein fundus angiography disclosed occlusive disease of the posterior ciliary arteries. Conclusion Because Giant Cell arteritis is a potentially blinding disease and its early diagnosis is the key to preventing blindness, it is important to recognize its various ocular manifestations.

Cornelia M Weyand - One of the best experts on this subject based on the ideXlab platform.

  • Giant Cell arteritis and polymyalgia rheumatica
    Annals of Internal Medicine, 2003
    Co-Authors: Cornelia M Weyand, Jorg J Goronzy
    Abstract:

    Both Giant-Cell arteritis and polymyalgia rheumatica are immune-mediated diseases that are treated with glucocorticoids, with higher doses used for Giant-Cell arteritis. Prompt initiation of high doses and a biopsy are recommended when ischemic optic neuropathy is suspected.

  • Giant Cell arteritis and polymyalgia rheumatica
    Annals of Internal Medicine, 2003
    Co-Authors: Cornelia M Weyand, Jorg J Goronzy
    Abstract:

    Giant-Cell arteritis is an immune-mediated disease characterized by granulomatous infiltrates in the wall of medium-size and large arteries. The immunopathology consists of 2 components. Excessive cytokine production (for example, of interleukin-1 and interleukin-6) induces systemic inflammation with an exuberant acute-phase response. In parallel, interferon-gamma, which is released by T Cells captured in the arterial wall, activates tissue-injurious macrophages. In response to the immune injury, the artery generates hyperplasia of the intima that leads to luminal occlusion and subsequent tissue ischemia. Despite the systemic character of the disease, distinct vascular territories are preferentially affected. On the basis of the predominant involvement, clinical subtypes can be distinguished: cranial Giant-Cell arteritis with ischemic complications in the eye, the face, and the central nervous system; large-vessel Giant-Cell arteritis with occlusions in the subclavian or axillary vessels; aortic Giant-Cell arteritis; Giant-Cell arteritis presenting as an intense systemic inflammatory syndrome with nonstenosing vasculitis; and "isolated" polymyalgia rheumatica with myalgias, systemic inflammation, and subclinical vasculitis. Temporal artery biopsy remains the diagnostic procedure of choice to detect arteritis in cranial vessels. In other vascular territories, Giant-Cell arteritis is most commonly diagnosed by vascular imaging. Laboratory studies characteristically document the marked elevations of nonspecific acute-phase reactants, such as C-reactive protein and erythrocyte sedimentation rate. Cytokines, such as interleukin-6, that induce the acute-phase reaction are currently being explored as more sensitive biological markers of disease activity. Corticosteroids are highly effective in suppressing systemic inflammation, but they do not eliminate the immune responses in the vessel wall. In general, the clinical outcome of Giant-Cell arteritis is exCellent, and efforts must now concentrate on tailoring therapies to the needs of the individual patient.