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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is important to establish the diagnosis of temporal arteritis because the disease is treatable; treatment may prevent blindness and even death. Temporal arteritis usually occurs in people older than 51 years of age, although very rarely, histologically documented disease occurs in younger people. The onset may be occult, so that there are few findings. A multitude of signs and symptoms may occur such as fever, headaches, malaise, weight loss, anemia, stroke, cranial nerve palsies, polymyalgia rheumatica, aortitis and other large vessel involvement. The eye may suffer from ischemic optic neuropathy (anterior or posterior), central or cilio-retinal arterial occlusion, ophthalmic artery ischemia, or extraocular muscle palsies. An arterial biopsy showing giant cell arteritis establishes the diagnosis. However, a negative biopsy does not rule out the disease because of the occasional presence of skip areas. Arteriography has only rarely yielded a positive temporal artery biopsy when the initial biopsy done elsewhere was negative. As a diagnostic parameter, the erythrocyte sedimentation rate is nonspecific, being elevated in diseases other than temporal arteritis and sometimes being falsely lowered by technical factors. Furthermore, the temporal artery biopsy is occasionally positive despite a normal erythrocyte sedimentation rate. Treatment is aimed at relieving the patient's symptoms and normalizing the erythrocyte sedimentation rate. Because of the wide spectrum of clinical and laboratory finding in temporal arteritis, no one specific treatment regimen with systemic corticosteroids works for all patients. Temporal arteritis is a well known disease of the elderly which ir rarely fatal but results in significant visual morbidity (Hinzpeter & Naumann, 1976; Spencer & Hoyt, 1960). Since Hutchinson's (1890) description, more than a thousand articles have been written on the subject (Cohen & Smith, 1974). Despite this, many unanswered questions and controversies remain concerning the diagnosis, prognosis and treatment of temporal arteritis. My goal is to review these questions and areas of controversy.
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PMID:Controversies regarding giant cell (temporal, cranial) arteritis. 39 20

Giant cell (temporal) arteritis G.C.(T) A. is common disorder and affects medium sized and large arteries in people over the age of fifty. Many series show that up to 50% of people with the clinical syndrome of polymyalgia rheumatica (PMR) go on to develop manifestations of G.C.(T) A. within a year; others may do so later. A critical review is offered of aspects of the subject which despite much study and research remain controversial or neglected. This includes epidemiology: statistics from routine autopsy suggests that the disease affects more people than are diagnosed clinically. The need to resolve uncertainty whether intracerebral vessels are involved or not, is now urgent, particularly in view of the wide spread use of short courses of Dexamethasone in the treatment of stroke. All clinicians should recognise the implications of the fact that they are dealing with a disease which may be active and yet symptomatically silent.
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PMID:Giant cell (temporal) arteritis-polymyalgia rheumatica: a critical review. 219 30

We have reviewed the clinical records and histology of 135 patients who underwent temporal artery biopsy between 1973 and 1978. Biopsies were classified histologically as giant-cell arteritis (17%), atypical arteritis (6%), healed arteritis (2%), arteriosclerosis (67%), atherosclerosis (5%), or normal (3%). Most of the histological diagnoses made at the time of biopsy were confirmed but eight cases which had originally been reported as atypical or healed arteritis were classified as arteriosclerosis when reviewed. All 33 patients with histological evidence of arteritis were accepted as clinical cases of temporal arteritis (31) or polymyalgia rheumatica (2) and treated with steroids. A further 24 patients had negative biopsies (arteriosclerosis or atherosclerosis) but were considered on clinical grounds to have cranial arteritis. They too were treated and made a full recovery. In 43 cases, all of whom had negative biopsies, a final diagnosis was reached which was thought to account for the clinical symptoms (e.g., cerebrovascular accident, rheumatoid disease, migraine, etc.). As less than 60% of patients with clinical temporal arteritis had positive biopsies, we suggest that this procedure could be omitted and replaced by a trial of steroid therapy. Biopsy should be reserved for patients with a strong medical contraindication to steroid therapy, or who fail to respond to treatment promptly.
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PMID:Temporal artery biopsy in giant-cell arteritis. A reappraisal. 727 Jul 80

Giant cell arteritis (GCA) is closely identified with the temporal arteritis-polymyalgia rheumatica syndrome of the elderly. It is also a systemic disease that can cripple and kill. Up to 15% of patients with temporal arteritis may have angiographic evidence of extracranial GCA, and aortic insufficiency, ruptured aortic aneurysm, aortic dissection, stroke, or myocardial infarction may be the initial manifestation of systemic GCA. A review of 72 cases of aortic and extracranial GCA, all with histopathologic verification of the disease, revealed that 25% of patients with aortic and extracranial large-vessel GCA had asymptomatic temporal arteritis; the ascending aorta and aortic arch were most frequently involved (39%), followed by the subclavian and axillary arteries (26%), and the femoropopliteal arteries (18%). Nine patients (12.5%) underwent an upper or lower limb amputation. Of the 18 patients whose death was directly attributable to extracranial GCA the causes were ruptured aortic aneurysm (6), aortic dissection (6), stroke (3), and myocardial infarction (3). The findings of these 72 cases caution against attributing all aortic and large-vessel arterial disease in the elderly to atherosclerosis and emphasize that timely surgical intervention may be necessary for life-saving and limb-salvage in patients with aortic and extracranial GCA.
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PMID:Aortic and extracranial large vessel giant cell arteritis: a review of 72 cases with histopathologic documentation. 766 46

IgG antibodies to cardiolipin and beta 2-glycoprotein I were looked for using an enzyme-linked immunosorbent assay (ELISA) in 19 patients with giant cell arteritis (meeting 1990 American College of Rheumatology criteria), including 16 with concomitant polymyalgia rheumatica (meeting Bird's criteria) and in three patients with isolated polymyalgia rheumatica. IgG anti-cardiolipin antibodies were demonstrated in eight patients (36%) and IgG anti-beta 2-glycoprotein I antibodies in two patients (9%) including one without anti-cardiolipin antibodies. Titers of anti-cardiolipin antibodies ranged from 27 to 190 units of IgG antiphospholipid antibodies (UGPL) (mean 71 UGPL). Of the eight patients with anti-cardiolipin antibodies, two had giant cell arteritis without polymyalgia rheumatica and six had polymyalgia rheumatica with clinical (n = 2) or histologic (n = 4) evidence of giant cell arteritis. None of the three patients with polymyalgia rheumatica but no giant cell arteritis had anti-cardiolipin or anti-beta 2 glycoprotein I antibodies. The VDRL was negative in the 14 patients who had this test. Tests for lupus anticoagulant were performed routinely, always with negative results. Among giant cell arteritis patients, those who tested positive for anticardiolipin antibody had significantly higher values for the erythrocyte sedimentation rate (p < 0.006) and for serum C-reactive protein (p < 0.03) and fibrinogen values (p = 0.05), and a trend toward higher platelet counts, as compared to those who tested negative for anticardiolipin antibody. The mean daily prednisone dose at the time of sampling was significantly lower in giant cell arteritis patients with anti-cardiolipin antibodies (p < 0.05); this difference may account for the apparent correlation between anti-cardiolipin antibodies and laboratory markers for inflammation. These data, as well as findings from serial measurements, suggest that anti-cardiolipin antibodies are present early in the course of giant cell arteritis and disappear within a few weeks of initiation of corticosteroid therapy in a dose of more than 25 mg prednisone per day. In this study, only one patient without anticardiolipin antibodies developed a cerebrovascular accident. Positive tests for anti-cardiolipin antibody or anti-beta 2 glycoprotein I antibody in a patient with polymyalgia rheumatica suggest a diagnosis of concomitant giant cell arteritis, which is usually symptomatic.
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PMID:Antibodies to cardiolipin and beta 2 glycoprotein I in patients with polymyalgia rheumatica and giant cell arteritis. 873 42

Temporal cell arteritis is a systemic vasculitis occurring mainly in the elderly. Classic symptoms such as headache, jaw claudication, visual changes, and polymyalgia rheumatica make the diagnosis relatively easy. Occult or asymptomatic presentations, however, are often missed or attributed to another cause. It is important for clinicians to be aware of the diverse presentations of this disease to avoid unnecessary investigations and prevent complications such as visual loss, myocardial ischemia, cerebrovascular accident, and death. This report presents the case of a patient who was referred with anemia and an elevated erythrocyte sedimentation rate, and who developed a headache during the hospital admission.
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PMID:Temporal arteritis: a review and case history. 879 58

Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are closely related disorders found predominantly in older patients. These disorders, which are being recognized more frequently, are more common in women, in Caucasians, and in various geographic locations. Early recognition and treatment may prevent possible catastrophic consequences of GCA, such as blindness, stroke, or dissection of the aorta. Although diagnosis is fairly easy with the classic presentation, it may be missed when the patient presents with nonspecific constitutional symptoms. An increased awareness among primary care physicians will aid in the prevention of much of the morbidity and mortality related to these diseases.
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PMID:Giant cell arteritis and polymyalgia rheumatica: clues to early diagnosis. 919 89

Molecular studies of giant cell arteritis indicate that T cells are recruited to the wall of medium-sized and large arteries, are activated locally, produce IL-2 and IFN-gamma, and regulate the activity of tissue-infiltrating macrophages. Downstream effects of T cell activation include the production of proinflammatory cytokines, metalloproteinases, and growth factors. Growth factors are instrumental in the process of intimal hyperplasia, leading to luminal occlusion and tissue ischemia. The amounts of IL-2, IFN-gamma, and the growth factor PDGF in the vascular lesions varies among patients and are correlated with differences in patterns of clinical manifestations. Giant cell arteritis complicated by cranial ischemia, such as anterior optic neuropathy or stroke, is characterized by high levels of IFN-gamma and PDGF. If the IFN-gamma-PDGF loop is less developed, fever and wasting can dominate the disease. Dominant production of IL-2 is associated with polymyalgia rheumatica. The finding of different inflammatory pathways translating into different clinical phenotypes may reflect differences in the contribution of the arterial wall. Alternative hypotheses include a role of multiple disease-inducing antigens with different tissue distributions or tropisms.
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PMID:Giant cell arteritis--a molecular approach to the multiple facets of the syndrome. 992 95

Pain associated with geant cell arteritis (GCA) is typically continuous, with exacerbations that often occur at night. Contact is painful and can precipitate an exacerbation of pain lasting several hours. The superficial temporal artery is the most common target of GCA but symptoms vary according to the predominant site of arterial inflammation. As a result, GCA can present in different ways with headaches being mild or absent in some patients. In nearly 40% of patients with biopsy-documented GCA, palpation of the branches of the external carotid artery fails to demonstrate any abnormalities. This arteritis affects the aortic arch and all its branches giving rise to a broad range of neurologic symptoms, for example, ocular disease, ischemic stroke, aortic dissection, etc. About 30% of patients also have symptoms of polymyalgia rheumatica. Demonstration of an inflammatory syndrome is important and temporal artery biopsy is the last element of the diagnostic. In some locations of the GCA angiography is useful. Treatment, commonly including corticosteroids, should be initiated as early as possible. Prevention of osteoporosis should be initiated especially in elderly subjects. In some cases other treatments are useful anticoagulants, immunosuppressive therapies, dapsone.
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PMID:[Headache due to temporal arteritis]. 1107 51

The purposes of this article are to report a case with temporal arteritis (TA) and to summarize and reanalyze the cases of temporal arteritis associated with fever in published articles for understanding better the clinical features of TA. A case with biopsy-proven TA is reported. The publications with TA and fever were searched by using MEDLINE in English from 1966 to 1999. Three hundred sixty cases of temporal arteritis associated with fever were reanalyzed. The results showed that a case of biopsy-proven TA with typically clinical manifestation was initially misdiagnosed and that the reanalysis of 360 cases revealed that the common clinical findings at presentation were abnormal temporal arteries, headache, low fever, loss of weight, polymyalgia rheumatica, jaw claudication, vision disorder, arthralgis or myalyias, and ear pain and that the uncommon clinical findings at presentation were high fever, malaise, anorexia, breast pain, transient ischemic attack/stroke, cough, mental disorder, diarrhea, and uterine prolapse, etc. Laboratory findings were the range of erythrocyte sedimentation rate (ESR) 14 to 149 with a mean of 97.0 mm/hr, white blood cells being normal or increased in the range of 10.9 to 22.9 x 10(9)/L, hemoglobin level 7 to 16 g/dL, the platelets count increased to 785 x 10(9)/L, and microscopic hematuria. The diagnosis was made by a combination of clinical features, an increased ESR, a response to steroids, and, most specifically, temporal artery biopsy. The initial diagnosis was misdiagnosed in 38.2% of patients. In conclusion, the features of TA associated with fever have not been widely appreciated yet. TA is a common cause of fever of unknown origin (FUO) in the elderly. TA should be considered when patients complain of common and uncommon manifestations. An elevated ESR will aid in the diagnosis of TA, and temporal artery biopsy will provide certainty.
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PMID:Temporal arteritis and fever: report of a case and a clinical reanalysis of 360 cases. 1110 64


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