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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 a vasculitis of large and medium size arteries, especially those of the aortic arch with an extracranial distribution, but also the aorta and some of its larger branches. It is characterised by the presence of mononuclear inflammatory infiltrates close to the internal elastic lamina formed by lymphocytes and macrophages, which in slightly more than 50% of the cases contain multinucleate giant cells. The morbidity associated with this disease is related to phenomena of distal ischemia to the luminal stenosis of the inflamed arteries, and to a lesser extent to the formation of aneurisms due to the weakening of the arterial wall. With an unknown aetiology, its pathogenesis is immune through the migration and location of gamma-INF -producing T cells in the adventitia of the inflamed arteries, it being assumed that this is the place of immune stimulation by a still unidentified antigen. The recruitment and activation of macrophages by this cytokine is one of the most important points of its pathogenesis. The destruction by these of the arterial elastic tissue is a relevant phenomenon, as is the production of other factors promoting neoangiogenesis and a proliferation of neointime, responsible through obliterating light for the ischemic manifestations of the disease. The process is accompanied by an important systemic repercussion characterised by a strong reaction of acute phase and general but barely specific symptoms of disease. On the other hand, an important percentage of patients show a clinical picture of polymyalgia rheumatica, an entity that has a historical and controversial relationship to this arteritis. In recent years important contributions have been made to the understanding of the immune mechanisms involved in its pathogenesis.
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PMID:[Etiopathogenesis of giant cell arteritis]. 1275 11

Giant cell arteritis (GCA), a vasculitis that targets medium- and large-size arteries, is ranked as a medical emergency because of its potential to cause blindness and stroke. The typical lesions, granulomas in the vessel wall, are formed by IFN-gamma-producing CD4+ T cells and macrophages. CD4+ T cells undergo in situ activation in the adventitia, where they interact with indigenous dendritic cells. Tissue injury is mediated by several distinct sets of macrophages that are committed to diverse effector functions. The dominant tissue injury in the media results from oxidative stress and leads to smooth muscle cell apoptosis and nitration of endothelial cells. Macrophage-derived growth factors are instrumental in driving the response-to-injury program of the artery that causes intimal hyperplasia and vessel occlusion. Clinical manifestations are those of tissue ischemia or a syndrome of exuberant systemic inflammation. The vascular and the systemic components of GCA contribute differentially to the disease, leading to distinct clinical phenotypes of this arteritis. Immunologically most interesting is polymyalgia rheumatica, in which the systemic component is combined with aborted vasculitis, suggesting a role for artery-specific tolerance mechanisms.
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PMID:Immunopathways in giant cell arteritis and polymyalgia rheumatica. 1487 49

Ischemia-induced biliary tract lesions, called ischemic cholangitis, often lead to strictures of biliary ducts and cholestasis. Causes of ischemic changes of the biliary tract can be found in the arterial blood supply or in the peribiliary capillary plexus. Known examples are thrombosis after transplantation, intraoperative ligation, or the application of chemotherapeutic drugs. Rarely, such changes are due to inflammation of the blood vessels, such as occurs in polyarteritis nodosa or giant cell arteritis. We present a report of a 49-year old man with leucocytoclastic vasculitis after viral infection, influenza vaccination, and antibiotic treatment, leading to florid ischemic cholangitis. We conclude that hypersensitivity vasculitis must be included in the differential diagnosis of cholestasis and cholangitis.
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PMID:Florid ischemic cholangitis due to leucocytoclastic vasculitis. 1506 28

Giant cell arteritis, a primary vasculitis of medium-sized and large arteries, causes vessel occlusion through fast and concentric intimal hyperplasia. Contextual parameters, especially the topography of the arterial wall, have emerged as critical pathogenic elements. Experimental data support the concept that the disease is initiated in the most outer layer of the arterial wall, the adventitia. CD4 T cells are recruited to the adventitia, undergo local activation and subsequently orchestrate macrophage differentiation. T cells and macrophages infiltrate into all wall layers and acquire different effector functions dependent on cues in their immediate microenvironment. The end result is myofibroblastic proliferation, luminal stenosis, and tissue ischemia. Adaptive immune responses in the adventitia are triggered by a population of indigenous dendritic cells (DC) placed at the adventitia-media junction. These arterial DCs have a unique surface receptor profile, including a series of Toll-like receptors (TLR). Responsiveness of such arterial DCs to blood-borne stimuli has been studied in human arteries engrafted into immunodeficient mice. Ligands of TLR4 are able to start maturation of adventitial DCs which fail to leave the peripheral tissue site. Instead, these adventitial DCs produce chemokines, recruit T cells, and support their local activation. These data identify tissue-residing DCs as gatekeepers in vasculitis and support the model that TLR ligands function as instigators of vessel wall inflammation.
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PMID:Toll-like receptors in giant cell arteritis. 1587 19

We report a case of giant cell arteritis in an 80-year-old woman who presented with chronic mesenteric ischemia to our vascular surgery service. Computed tomography, arteriography, and magnetic resonance angiography revealed long, smooth stenosis of the superior mesenteric artery and focal stenosis of the celiac artery. After the patient was found to have an elevated erythrocyte sedimentation rate and a positive temporal artery biopsy specimen, glucocorticoid therapy was initiated. Giant cell arteritis is a rare and easily overlooked cause of vascular insufficiency that can result in a devastating clinical outcome if not recognized before surgical therapy or other interventions are attempted.
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PMID:Giant cell arteritis manifesting as mesenteric ischemia. 1627 65

We describe a patient who, during tapering of corticosteroids prescribed for temporal arteritis (TA), developed nocardiosis that was mimicking a specific relapse. An isolated choroidal ischemia was thought to be a symptom of TA. Steroid therapy was intensified and, while on aggressive steroid therapy, the patient died of septic shock. Autopsy revealed occult disseminated nocardiosis with septic arteritis and apparently cured TA. Visual loss occurring during TA treatment should lead clinicians to consider a specific relapse as well as an opportunistic infection like nocardiosis.
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PMID:Visual loss mimicking a treated temporal arteritis relapse. 1686 19

Giant cell arteritis is a systemic vasculitis that affects large- and medium sized arteries. The most common ophthalmic manifestation of this disease is anterior ischemic optic neuropathy, leading to acute, painless visual loss in one or both eyes. It is caused by ischemia of the optic nerve head, which is mainly supplied by the short posterior ciliary arteries. Early diagnosis is the key to correct management and prevention of visual loss in the second eye. The treatment of choice for arteritic ischemic optic neuropathy is high dose of systemic corticosteroids. Only such treatment may prevent blindness. The authors presented a case of a 62 years man with anterior ischemic neuropathy in one eye, which was diagnosed as arteritic form caused by giant cell arteritis. The correct diagnosis was based on typical clinical signs of ischemic changes in the optic nerve head and diagnostic criteria for giant cell arteritis, advocated by American College of Rheumatologists.
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PMID:[Anterior ischemic optic neuropathy associated with giant cell arteritis. Case report]. 1688 58

Giant cell arteritis is a rare systemic vasculitis affecting large- and medium-sized arteries. Focal arteries lesions, include mononuclear cells infiltration of the vessel wall with giant cell formation. It is a disease of elderly persons and can result in a wide variety of systemic, neurological and ophthalmic complications, due to ischemia. The incidence of visual loss and ocular involvement varies between 14-88%, but one of the most common and severe complications is anterior ischemic optic neuropathy. The other ocular ischemic lesions include: central retinal artery occlusion, choroidal ischemia, diplopia, ocular motor paresis, anterior uveitis, cataract, ocular hypotony, corneal oedema and ulcerations, episcleritis and anterior scleritis, orbital cellulitis and pseudotumor. Because giant cell arteritis is potentially blinding disease, early diagnosis and immediate treatment with high dose corticosteroids may prevent further damage to the affected eye and prevent visual loss in the opposite eye. The purpose of this review is to revise established knowledge and to highlight the recent developments in diagnosis and management of giant cell arteritis.
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PMID:[A new approach towards giant cell arteritis]. 1702 3

The giant cell arteritis and its symptoms are usually non-specific and accompanied with symptoms of polymyalgia rheumatica. As complications of the giant cell arteritis ischemia, infarction or rupture of the damaged vessel can occur. We report on a 56-year-old female patient, who suffered for one year about weight loss, tiredness and intolerance as well as symptoms of polymyalgia rheumatica. Gastroscopy and colonoscopy showed normal findings. In the context of the malignancy search we made a computer tomography and magnet resonance tomography. The data showed an enlargement and an enhancement of the aorta, which led us to the suspicion of a giant cell arteritis. We started immediately with a medical treatment. The biopsy of the arteries temporales supported histological the diagnosis.
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PMID:[MRI-based diagnosis of giant cell arteritis]. 1721 10

We reviewed the clinical manifestations of mesenteric vasculitis due to giant cell arteritis (GCA) and considered features of the mesenteric anatomy in relationship to disease expression. We compiled and reviewed a case series by systematic identification of patients previously reported in the English-language literature to have mesenteric involvement from known GCA. Included in the analysis was a detailed case review of a patient with GCA and small bowel infarction seen at our institution. Twelve patients were identified with mesenteric ischemia attributed to GCA. Concomitant cranial and abdominal symptoms were present in 7 of the 12 patients, and cranial symptoms were absent in 5 patients who presented with abdominal complaints. The abdominal symptoms fell within a spectrum ranging from chronic postprandial symptoms to acute abdominal pain. Survival was observed in only 6 of the 12 cases, 3 of whom required bowel resection and were treated with high-dose corticosteroids. Review of the anatomic features of the specialized splanchnic circulation reveals an extensive collateral network that may protect against early disease expression from ischemia, despite mesenteric arteritic involvement. Mesenteric vasculitis resulting in small bowel infarction has only rarely been described in GCA but represents a serious and potentially treatable complication. We propose an explanation, based on mesenteric vascular anatomy, for the infrequency of symptomatic expression of this entity and suggest that occult mesenteric GCA may be present far more often than recognized.
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PMID:Mesenteric involvement in giant cell arteritis. An underrecognized complication? Analysis of a case series with clinicoanatomic correlation. 1820 70


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