The role of parvovirus B19 in the pathogenesis of giant cell arteritis: a preliminary evaluation. (9/363)

OBJECTIVE: To determine whether parvovirus B19 DNA is more likely to be present in the temporal arteries of patients with giant cell arteritis (GCA) than in the temporal arteries of control subjects. METHODS: We prospectively examined temporal artery biopsy (TAB) tissue from 50 consecutive patients presenting for TAB for the presence of B19 DNA using the polymerase chain reaction (PCR). Clinical and demographic information was obtained from the patients' medical records. A separate PCR analysis of 30 original tissue specimens was conducted at the Centers for Disease Control and Prevention (CDC) using primers directed toward another target sequence in the nonstructural coding area of B19. RESULTS: The 50 patients had an average age of 70.8 years; 27 (54%) were female. Amplicons for human beta-globulin, but not for cytomegalovirus, were produced for all tissue samples. The PCR results for B19 agreed in 29 of 30 samples tested by our institution and by the CDC (97% agreement; kappa = 0.9). A comparison of the B19 DNA analysis and the results of TAB indicated a statistically significant association between histologic evidence of GCA and the presence of B19 DNA in TAB tissue (chi2 = 10.38, P = 0.0013). CONCLUSION: These findings suggest that B19 may play a role in the pathogenesis of GCA.  (+info)

Musculoskeletal manifestations in a population-based cohort of patients with giant cell arteritis. (10/363)

OBJECTIVE: To define musculoskeletal manifestations occurring in a population-based cohort of patients with giant cell (temporal) arteritis (GCA). METHODS: The records of 128 patients with GCA diagnosed over a 42-year-period (1950-1991) in Olmsted County, MN, were reviewed for the presence and type of musculoskeletal manifestations, their relationship to the onset and course of GCA, and their response to treatment. RESULTS: Fifty-three patients (41%) developed polymyalgia rheumatica: 23 before, 17 concurrently with, and 13 after the diagnosis of GCA. Thirty patients (23%) developed 1 or more peripheral musculoskeletal manifestations. These included peripheral synovitis in 23 patients (6 of whom fulfilled criteria for rheumatoid arthritis), distal extremity swelling with pitting edema in 13, distal swelling without pitting in 5, tenosynovitis in 6, and carpal tunnel syndrome in 2. Fifty-seven episodes of peripheral manifestations occurred in the 30 patients at different times during the course of GCA. In most, the onset of PMR and peripheral manifestations was within 2 years of the diagnosis of GCA. CONCLUSION: Musculoskeletal symptoms in GCA are common and varied. Most appear linked temporally to the underlying GCA, indicating that the nature of this illness and its clinical expression are broader than often considered.  (+info)

New arguments for a vasculitic nature of polymyalgia rheumatica using positron emission tomography. (11/363)

OBJECTIVE: To study the possible contribution of fluorodeoxyglucose (FDG)-positron emission tomography (PET) in the diagnosis of giant cell arteritis and polymyalgia rheumatica. METHODS: A consecutive case series consisting of five patients with polymyalgia rheumatica, six patients with temporal arteritis and 23 age-matched patients with other inflammatory conditions were evaluated with FDG-PET. Studies were performed before therapy with steroids was started. RESULTS: A total of 4/6 patients with giant cell arteritis and 4/5 patients with polymyalgia had increased FDG uptake in their thoracic vessels, compared to 1/23 controls (P < 0.001). Increased vascular FDG uptake in the upper legs was seen in 8/11 patients with giant cell arteritis or polymyalgia compared to 8/23 control patients (P < 0.05), and in the lower legs in 6/11 patients compared to 6/23 controls (P = not significant). CONCLUSIONS: FDG-PET scan is the first non-invasive technique which may indicate large-vessel vasculitis and which can show its extension throughout the body. It strongly suggests that polymyalgia rheumatica is a form of vasculitis.  (+info)

Visual performance in giant cell arteritis (temporal arteritis) after 1 year of therapy. (12/363)

AIMS: To determine if patients with giant cell arteritis (GCA) treated with corticosteroids develop delayed visual loss or drug related ocular complications. METHODS: In a multicentre prospective study patients with GCA (using precise diagnostic criteria) had ophthalmic evaluations at predetermined intervals up to 1 year. The dose of corticosteroid was determined by treating physicians, often outside the study, with the daily dose reduced to the equivalent of 30-40 mg of prednisone within 5 weeks. Subsequently, treatment guidelines suggested that the dose be reduced as tolerated or the patient was withdrawn from steroids in a period not less than 6 months. RESULTS: At presentation, of the 22 patients enrolled, seven patients had nine eyes with ischaemic injury. Four eyes had improved visual acuity by two lines or more within 1 month of starting corticosteroids. No patients developed late visual loss as the steroid dose was reduced. At 1 year the visual acuity, contrast sensitivity, colour vision, and threshold perimetry were not significantly different from the 4-5 week determinations. At 1 year, there were no significant cataractous or glaucomatous changes. At 2 months, there was no difference in systemic complications between patients who received conventional dose (60-80 mg per day) or very high doses (200-1000 mg per day) of corticosteroids at the start or early in the course. CONCLUSIONS: Patients with GCA related visual loss can improve with treatment. Corticosteroids with starting doses of 60-1000 mg per day, with reduction to daily doses of 40-50 mg per day given for 4-6 weeks, and gradual dose reduction thereafter, as clinically permitted, did not result in delayed visual loss. There were no significant drug related ophthalmic complications.  (+info)

Skeletal muscle mitochondrial function in polymyalgia rheumatica and in giant cell arteritis. (13/363)

OBJECTIVE: To ascertain whether mitochondrial function is impaired in polymyalgia rheumatica (PMR) and giant cell arteritis (GCA). PATIENTS AND METHODS: Thirteen patients suffering from isolated PMR, 19 from GCA (eight with and 11 without PMR) and 25 healthy people submitted to orthopaedic surgery were included. Skeletal muscle was obtained from the quadriceps by open biopsy. Mitochondrial histological abnormalities were assessed on Gomori's trichrome staining and on cytochrome c oxidase and succinic dehydrogenase reactions. Biochemical studies consisted of polarographic measurement of oxidative activity using complex I, II, III and IV substrates, and spectrophotometric determination of individual enzymatic activity of such complexes. RESULTS: We did not find differences among groups either with respect to the percentage of histological or histochemical abnormalities [P = not significant (NS) for all stainings and reactions], oxidative capacity (P = NS for all substrates) or individual enzymatic activities (P = NS for all complexes). CONCLUSION: Skeletal muscle mitochondria remain histologically and functionally unaffected in PMR and in GCA.  (+info)

Giant cell arteritis of the cervical radicular vessels presenting with diaphragmatic weakness. (14/363)

The clinical and histopathological details of a patient who succumbed to giant cell arteritis (GCA) of the cervical radicular vessels are described. The initial clinical presentation, with diaphragmatic weakness, has not previously been reported. Normal inflammatory indices and the unusual presentation prevented diagnosis during life, but GCA should be considered in the differential diagnosis of any unexplained neuropathic or radiculopathic syndrome, as corticosteroid therapy may lead to recovery. This is the first account of the pathological findings in cervical radiculopathy associated with GCA.  (+info)

Giant cell arteritis associated with rheumatoid arthritis monitored by magnetic resonance angiography. (15/363)

A 57-year-old Japanese woman with well controlled rheumatoid arthritis visited our hospital with a severe bitemporal headache and marked fatigue. Based on the classification criteria by the American College of Rheumatology, she was diagnosed as having giant cell arteritis. Magnetic resonance (MR) angiography was performed, from which stenotic changes in the bilateral superficial temporal arteries were strongly suspected. Corticosteroid therapy was quickly started. The patient followed an uneventful course with no complications. Therapeutic effect was confirmed by MR angiographic findings obtained 4 weeks after the initiation of therapy.  (+info)

Formation of new vasa vasorum in vasculitis. Production of angiogenic cytokines by multinucleated giant cells. (16/363)

Inflammation of the arterial wall in giant cell arteritis induces a series of structural changes, including the formation of new vasa vasorum. To study the regulation of neoangiogenesis in giant cell arteritis, temporal arteries were examined for the extent and localization of microvessel generation and for the production of angiogenic factors. In normal arteries, vasa vasorum were restricted to the adventitia, but in inflamed arteries, capillaries emerged in the media and the intima. These capillaries displayed a distinct topography with a circumferential arrangement in the external one-third of the intima. Neovascularization was closely correlated with the formation of lumen-obstructing intima, the fragmentation of the internal elastic lamina, and the presence of multinucleated giant cells. Comparison of tissue cytokine transcription in temporal arteries of giant cell arteritis patients with and without up-regulated neoangiogenesis identified interferon-gamma and vascular endothelial growth factor but not fibroblast growth factor-2 as mediators associated with vasa vasorum proliferation. Giant cells and CD68-positive macrophages at the media-intima junction were found to be the major cellular sources of vascular endothelial growth factor. These data demonstrate that formation of new vasa vasorum in vasculitis is regulated by inflammatory cells and not by arterial wall cells, raising the possibility that it represents a primary disease mechanism and not a secondary hypoxia-induced event. Increased neovascularization in interferon-gamma-rich arteries suggests that the formation of new vasa vasorum is determined by the nature of the immune response in the arterial wall, possibly resulting from the generation and functional activity of multinucleated giant cells.  (+info)