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Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although corticosteroid treatment is clearly beneficial to patients with temporal arteritis, its exact risk/benefit ratio in these old and side effects-prone patients is unknown. We have thus surveyed that available French and English literature, in order to pool the published series and to evaluate the iatrogenic potential of corticosteroids in this situation. We selected 11 series, yielding a total of 1008 patients. A treatment failure resulted in the death of the patient in five cases. Twenty-seven patients became blind, but only 2 under treatment. The side-effects involved 29% of the patients and are responsible of 29 deaths (2.9%): osteoporosis was the main problem, followed by femoral head necrosis and muscle wasting. Gastroduodenal ulcers were uncommon and generally benign; sigmoid colon diverticulitis was infrequent but dangerous; some infectious complications were noted (herpes zoster, tuberculosis, etc...); high blood pressure and diabetes were common problems. Psychiatric side-effects were rare. Thus, the unwanted effects of corticosteroids in the treatment of temporal arteritis are relatively infrequent and generally not severe, except osteoporosis. They should be systematically prevented by appropriate diet and treatments (e.g., calcium, potassium, and vitamin D supplements).
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PMID:[Benefits of corticosteroids in the treatment of Horton's disease and rhizomelic pseudopolyarthritis: advantages and inconveniences. A meta-analysis]. 134 39

The basal and calcium-stimulated calcitonin response was measured in 10 patients with giant cell arteritis before and 1, 3 and 6 wk after the start of daily treatment with 60 mg of prednisone. The study shows that plasma calcitonin level in response to a calcium injection is increased after 1 wk treatment with prednisone. Later on the calcitonin secretion capacity diminishes significantly compared to the initial level. The phylogenetic old calcitonin system first tries to prevent the occurrence of the process of osteoporosis. Moreover, exhaustion of this system later contributes to the process of steroid osteoporosis.
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PMID:Change of serum calcitonin in patients receiving glucocorticoids: an acute phase study. 239 96

Experimental aneurysmatic dilatation of the rabbit common carotid artery was induced by a single, periarterial application of calcium chloride in vivo. Vessels were fixed in situ after 3 d, 1 wk, 3 wk, 6 wk, and 12 wk by intracardiac perfusion of glutaraldehyde and tissues prepared for light, scanning, and transmission electron microscopy. Progressive focal aneurysmal dilatation was seen limited to the site of calcium application with endothelial damage and thrombus formation in areas of irregular luminal contour. Disruption of the elastic network of the intima and media was seen with varying degrees of intimal fibromuscular hyperplasia and medial disorganization. The calcium-elastic tissue complex was the focus of the inflammatory, arteriosclerotic reaction and subsequent aneurysm formation. The inflammatory cell infiltration initially included primarily neutrophils followed by lymphocytes, plasma cells, monocytes, and multinucleated giant cells. These studies support the hypothesis that disruption of the elastic tissue network of the vascular wall represents an important pathogenetic factor in the initiation of aneurysmal dilatation. In addition, the results of these studies suggest that interaction of calcium with the elastica of the arterial wall may represent an important pathogenetic factor in the initiation of giant cell arteritis.
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PMID:Aneurysm of the rabbit common carotid artery induced by periarterial application of calcium chloride in vivo. 334 36

Patients treated with high-dose or long-term corticosteroids are at risk of accelerated osteoporosis and spontaneous vertebral and traumatic fractures. To assess the efficacy of salmon calcitonin in preventing corticosteroid- induced osteoporosis, 48 patients with newly diagnosed polymyalgia rheumatica, temporal arteritis, and other vasculitides were enrolled in a 2-year, double-blind, randomized, controlled trial. Patients were randomized to receive subcutaneous injections t.i.w. of either 100 IU of salmon calcitonin (25 patients) or placebo (23 patients). After 2 years, 19 and 21 patients, respectively, were evaluable. All patients also received supplemental calcium carbonate (1500 mg daily in divided doses) and vitamin D3 (400 IU daily). Baseline and serial radiologic assessments included dual-energy X-ray absorptiometry (DXA) of the lumbar spine and hip, and spine radiographs to detect vertebral fractures. There were no significant baseline differences between the two study groups. The mean within-subject percentage change in DXA lumbar spine density in the two groups over the 2-year period of the study was only -0.1% (calcitonin plus calcium) versus -0.2% (placebo plus calcium) a nonsignificant difference despite the high mean cumulative corticosteroid doses of 5371 mg and 4680 mg, respectively (NS). The incidence of vertebral fracture was 12.5% (calcitonin plus calcium: 11%, versus placebo plus calcium: 14%, NS), with four fractures in the first year and one fracture in the second year. Higher cumulative cortico-steroid dose was associated with a greater loss in bone density. In rheumatic disease patients starting high-dose, long-term corticosteroids, salmon calcitonin with calcium and vitamin D3 provided no greater bone preservation than that observed with calcium and vitamin D3 alone.
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PMID:A randomized controlled trial of salmon calcitonin to prevent bone loss in corticosteroid-treated temporal arteritis and polymyalgia rheumatica. 899 81

Apart from the therapy of autoimmune diseases, corticosteroids have an important position in the treatment of rheumatoid arthritis. Corticosteroids are used after the failure of non-steroidal antiinflammatory agents or of the basis therapies to control the illness. When the rheumatoid arthritis is accompanied by a systemic disease, they will be used earlier and in higher dosages. For polymyalgia rheumatica, independently of an association with temporal arteritis, corticosteroids are the therapy of choice. Risks of long-time corticosteroid therapy are a higher incidence of infection and bone demineralisation, especially in postmenopausal women. A careful prevention with Calcium and Vitamin D must be carried out systematically. The demineralisation can be limited by the use of Deflazacort, a corticosteroid, which decreases the loss of calcium.
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PMID:[Systemic corticosteroid therapy in rheumatology, advantages and risks]. 974 32

The prevention and treatment of glucocorticoid-induced osteoporosis is a major concern for rheumatologists since inflammatory joint disease is among the most common reasons for long-term glucocorticoid therapy. We used a randomized placebo-controlled design to evaluate the efficacy of one-year cyclical etidronate therapy in preventing bone loss in 83 glucocorticoid-treated patients with rheumatoid arthritis, polymyalgia rheumatica, or giant cell arteritis. Glucocorticoid treatment duration was shorter than three months, and the starting dose was greater than 7.5 mg of prednisone-equivalent per day. Etidronate was given according to the standard cyclical schedule, i.e. 400 mg/d for periods of 14 days separated by 76-day intervals during which patients took 500 mg of supplemental calcium per day. The primary evaluation criterion was the change in lumbar spine bone mineral density after one year of etidronate therapy. Bone mineral density decreased by 1.94 +/- 0.61% in the placebo group and increased by 0.86 +/- 0.6% in the etidronate group, yielding a between-group difference of 2.8 +/- 0.86% (P = 0.002). The difference was largest in postmenopausal women (3.38 +/- 1.11%; P = 0.004). At the femoral neck, there was a smaller bone mineral density decrease in the etidronate than in the placebo group, but the difference (1.11 +/- 1.13%) was not statistically significant. The most common side effects were gastrointestinal symptoms and showed no difference between the two groups. Four fractures (including one vertebral fracture) occurred in the placebo group versus two (including one vertebral) in the etidronate group. Etidronate prevents glucocorticoid-induced lumbar spine bone loss in patients with rheumatoid arthritis, polymyalgia rheumatica, or giant cell arteritis.
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PMID:Evaluation of the efficacy of etidronate therapy in preventing glucocorticoid-induced bone loss in patients with inflammatory rheumatic diseases. A randomized study. 1033 77

Diagnosis and management of giant cell (temporal) arteritis (GCA) should be performed by physicians who can accurately monitor the ophthalmologic, neurologic, and systemic sequelae of the disease as well as the numerous side effects of systemic corticosteroids, which are typically necessary for treatment. When the diagnosis of giant cell arteritis is seriously entertained, early treatment with adequate doses of oral or intravenous corticosteroids should not be delayed until laboratory confirmation has been obtained. Unilateral or bilateral temporal artery biopsy should be performed on all patients with suspected GCA. A positive biopsy result mandates that higher doses of corticosteroids be used during the first 2 months, which comprise the critical period for risk of new ocular ischemia. A definitive, biopsy-proven diagnosis requires at least 6 months, and typically 12 months, of corticosteroid therapy. Common pitfalls include increasing the dose and prolonging the use of corticosteroids in response to increases in the erythrocyte sedimentation rate (ESR) unrelated to GCA or visual blurring that may be related to benign tear film abnormalities, corticosteroid-induced lens changes, and other ophthalmic conditions. The muscle stiffness of polymyalgia rheumatica (PMR) must be distinguished from the osteoarthritis and other painful conditions common in the elderly. After corticosteroid therapy has begun, continuing ophthalmologic evaluation is necessary to evaluate the effectiveness of treatment and whether ocular complications, such as glaucoma or cataract, develop. Careful attention must be given to early detection and prevention of systemic side effects of corticosteroid treatment. Patients may be given gastrointestinal protective agents, such as histamine (H(2))-blocking agents; vitamin D and calcium; oral hypoglycemic agents; and, if necessary, insulin and antihypertensive drugs. If bone density measurements warrant, hormones/supplementation to prevent or reverse osteoporosis may be prescribed. After the initial diagnosis and first 4 weeks of treatment, elevation of the ESR or C-reactive protein alone should generally not be used as signs of disease activity nor as a reason to increase the daily dose of steroids. If symptoms or signs of disease activity occur, the dose should be raised regardless of test results. Even with vigorous physician-patient education, however, a patient is occasionally unable to provide adequate historical information about response to therapy, and the physician is forced to rely on laboratory values as a measure of disease activity. After initial high-dose corticosteroid therapy, patients without a classic history and with negative biopsy results will generally receive a rapid taper to low doses of corticosteroids. The role of repeated temporal artery biopsy in the clinical management of GCA is unclear. Despite persistence of PMR and, in some cases, histologic evidence of inflammation in temporal arteries, patients do not frequently have recurrence of symptomatic GCA after 6 months or more of corticosteroid therapy. Under these circumstances, late vision loss is rare.
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PMID:Giant Cell Arteritis. 1109 95

Patients with a suspected diagnosis of giant cell arteritis (GCA) should be started on high-dose corticosteroid therapy without delay. A temporal artery biopsy should be performed after initiation of therapy to confirm the diagnosis. Patients with acute visual or neurologic symptoms present a neuro-ophthalmic emergency. Therapy should be initiated immediately with high-dose intravenous methylprednisolone sodium succinate and followed by high-dose oral prednisone. Treatment may begin with high-dose oral prednisone in patients without visual or neurologic symptoms. Calcium, vitamin D, and peptic ulcer prophylaxis should accompany steroid therapy, as indicated. The following treatments should be considered for patients with suspected GCA and acute visual or neurologic signs or symptoms: intravenous methylprednisolone sodium succinate (250 mg intravenously every 6 hours) should be given for 3 days, followed by oral prednisone (80 mg per day or 1 mg/kg) for 4 to 6 weeks. Prednisone should then be tapered by 10 mg per day every month. Most patients require 1 year of therapy to avoid relapse. Taper and duration should be modified according to erythrocyte sedimentation rate, C-reactive protein, and signs and symptoms of GCA. Rheumatologic consultation and follow-up is often helpful for these patients. For patients with suspected GCA and no acute visual or neurologic signs or symptoms, therapy may begin directly with oral prednisone (80 mg per day or 1 mg/kg) with same taper and duration based on laboratory values and clinical signs and symptoms.
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PMID:Giant Cell Arteritis. 1466 69

Medial arterial calcification, which has been increasingly recognized in end-stage renal disease (ESRD) patients, has been associated with acutely symptomatic vascular complications including calcific uremic arteriolopathy (calciphylaxis) and ischemic changes in the extremities. This report describes a 50-year-old ESRD patient on maintenance hemodialysis in whom medial arterial calcification developed with features mimicking the findings of temporal arteritis. He complained of persistent bilateral temporal area headaches with associated symptoms of blurred vision; pain in his shoulders, hips, and knees; and intermittent symptoms consistent with jaw claudication. He was not receiving calcium or vitamin D supplements. Superficial temporal arteries were dilated, tortuous, nodular, and tender to palpation. Ophthalmologic examination was unremarkable, except for the presence of peripapillary atrophy. Temporal artery biopsy results showed medial arterial calcification with mild inflammatory changes. No giant cells were identified. Additional long-term complications of medial arterial calcification have included the development of painful ischemic ulceration of the glans penis and extensive mitral annulus calcification detected by echocardiography. The findings in this patient show that clinical manifestations of medial artery calcification associated with ESRD can mimic those seen with other vascular diseases.
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PMID:Medial arterial calcification mimicking temporal arteritis. 1538 38

To examine whether excessive protein O-GlcNAcylation plays a role in the dysfunction of the diabetic heart, we delivered adenovirus expressing O-GlcNAcase (Adv-GCA) into the myocardium of STZ-induced diabetic mice. Our results indicated that excessive cellular O-GlcNAcylation exists in the diabetic heart, and that in vivo GCA overexpression reduces overall cellular O-GlcNAcylation. Myocytes isolated from diabetic hearts receiving Adv-GCA exhibited improved calcium transients with a significantly shortened T(decay) (P<0.01) and increased sarcoplasmic reticulum Ca2+ load (P<0.01). These myocytes also demonstrated improved contractility including a significant increase in +dL/dt and -dL/dt and greater fractional shortening as measured by edge detection (P<0.01). In isolated perfused hearts, developed pressure and -dP/dt were significantly improved in diabetic hearts receiving Adv-GCA (P<0.05). These hearts also exhibited a 40% increase in SERCA2a expression. Phospholamban protein expression was reduced 50%, but the phosphorylated form was increased 2-fold in the diabetic hearts receiving Adv-GCA. We conclude that excess O-GlcNAcylation in the diabetic heart contributes to cardiac dysfunction, and reducing this excess cellular O-GlcNAcylation has beneficial effects on calcium handling and diabetic cardiac function.
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PMID:Adenovirus-mediated overexpression of O-GlcNAcase improves contractile function in the diabetic heart. 1589 Sep 78


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