Complication Of Giant Cell Arteritis Research Articles

Risk factors for cranial ischemic complications in giant cell arteritis.

Cranial ischemic complications (CICs) are among the presenting manifestations of giant cell arteritis (GCA). Yet patients with GCA may develop CICs at a later stage, despite steroid therapy. In the current report we delineate risk factors for CICs, both at presentation and during follow-up, and review the relevant literature. We reviewed charts of 175 patients with GCA. Follow-up data were available for 166 patients. CICs at presentation or developing within 2 weeks of GCA diagnosis were considered GCA related. CICs developing later were considered GCA related only when associated with other GCA-related manifestations or acute-phase reactions. Associations between CICs and other variables were tested by multivariate analysis. At presentation, 43 patients (24.6%) had CICs. Risk factors were transient cerebro-ophthalmic ischemic episodes (COIEs) (odds ratio [OR] 4.3) and male sex (OR 2.5), while the presence of systemic symptoms was "protective" (OR 0.3). During follow-up 8.4% of patients with GCA developed new CICs. Risk factors in these cases were previous CICs at presentation (OR 5.6) and transient COIEs developing during follow-up (OR 14.8). The use of low-dose aspirin was protective (OR 0.2). These data, together with data from the literature review, suggest that GCA patients with transient COIEs and without fever or other systemic symptoms are at increased risk of presenting with CICs. Risk factors for late-developing CICs were CICs at presentation and late-developing transient COIEs.

Giant cell arteritis

Giant cell arteritis (GCA), the most common form of systemic vasculitis in adults, preferentially involves large and medium-sized arteries in patients over the age of 50. The classic manifestations are headache, jaw claudication, polymyalgia rheumatica (PMR), and visual symptoms, but 40% of patients present with a wide range of occult manifestations. Early diagnosis and treatment with prednisone can prevent blindness, the most feared complication of GCA. The pathogenesis of GCA is T-cell dependent and antigen driven. Clinical subsets of GCA appear to result from variable cytokine expression. The risk of developing thoracic aortic aneurysm is increased more than 17-fold in patients with GCA. GCA can also involve large arteries, especially the subclavian and axillary arteries. Color Doppler ultrasound, magnetic resonance imaging, and positron-emission tomography scanning are providing insights into the extent and pathogenesis of the disease but have not replaced temporal artery biopsy as the gold standard for securing the diagnosis. Two recently completed double-blind, placebo-controlled trials concerning whether methotrexate plus prednisone is more effective than prednisone alone reached conflicting conclusions.

Acute-phase response and the risk of developing ischemic complications in giant cell arteritis: Comment on the article by Cid et al

Acute-phase response and the risk of developing ischemic complications in giant cell arteritis: Comment on the article by Cid et al

Acute-phase response and the risk of developing ischemic complications in giant cell arteritis: Comment on the article by Cid et al

Acute-phase response and the risk of developing ischemic complications in giant cell arteritis: Comment on the article by Cid et al

Absence of anti-beta2 glycoprotein I antibodies in giant cell arteritis: a study of 45 biopsy-proven cases.

To search for a relationship between serum anti-beta2 glycoprotein I (anti-beta2GPI) antibodies and the occurrence of ischaemic complications in giant cell arteritis (GCA), since the latter do not correlate with anti-cardiolipin antibodies (ACL), which are frequently observed in GCA. IgG and IgM anti-beta2GPI antibodies and ACL were measured by enzyme-linked immunosorbent assays in sera, collected before treatment, from 45 unselected patients with biopsy-proven GCA, including 15 patients with ischaemic events. IgG and IgM anti-beta2GPI antibodies were not detected in any of the patients, contrasting with the presence of ACL in 51%, of them, without correlation with ischaemia. Anti-beta2GPI antibodies are not detectable in GCA, contrasting with the occurrence of ACL, and ischaemic complications are apparently unrelated to the most frequent anti-phospholipid antibodies.

Platelet-derived growth factor, intimal hyperplasia, and ischemic complications in giant cell arteritis.

To explore whether vasoocclusion in giant cell (temporal) arteritis (GCA) is related to intimal hyperplasia and in situ production of platelet-derived growth factor (PDGF). Temporal artery biopsy specimens from patients with GCA were analyzed for the presence of intimal hyperplasia. Expression of PDGF-A and PDGF-B was assessed by immunohistochemistry and digitized image analysis. PDGF-A and PDGF-B were widely expressed in inflamed arteries. CD68+ macrophages, smooth muscle cells, and multinucleated giant cells produced PDGF, whereas hyperplastic intimal tissue did not. Arteries with marked luminal narrowing and those with no or minimal luminal narrowing differed in the extent and distribution of PDGF expression. Concentric intimal hyperplasia was associated with the accumulation of PDGF-A- and PDGF-B-producing CD68+ macrophages at the media-intima junction. PDGF+,CD68+ macrophages in close proximity to the internal elastic lamina frequently coproduced matrix metalloproteinase 2. Intimal hyperplasia of the temporal artery correlated with ischemic complications of GCA, such as ocular involvement, jaw claudication, and aortic arch syndrome. Production of PDGF has a role in arterial occlusion in GCA. The excessive fibroproliferative response leading to luminal narrowing can be distinguished from the stenosing process in atherosclerosis and postangioplasty restenosis, suggesting that there are different response patterns to arterial injury. In GCA, macrophages at the media-intima border are the dominant source of PDGF. Since vasoocclusion is associated with a number of serious complications in GCA, inhibition of intimal proliferation should be a major goal of treatment.

Platelet‐derived growth factor, intimal hyperplasia, and ischemic complications in giant cell arteritis

Platelet‐derived growth factor, intimal hyperplasia, and ischemic complications in giant cell arteritis

Thoracic aortic aneurysm and rupture in giant cell arteritis. A descriptive study of 41 cases.

To determine the features and outcomes of patients with giant cell arteritis (GCA) who have aneurysms or rupture of the thoracic aorta. Patients with GCA seen over a 40-year period who had aneurysms and/or rupture of the thoracic aorta were identified by assistance of a computerized indexing system. The presence of thoracic aortic aneurysms (TAA), with or without aortic valve insufficiency (AI), was determined by radiographs, computed tomography scans, and ultrasound studies of the thorax, angiograms of the aorta, and postmortem examination. Ten men and 31 women with GCA were found to have TAA and/or rupture. Three developed TAA before GCA was diagnosed, 5 developed aortic findings near the time of the diagnosis, and 33 after the diagnosis of GCA (median of 7 years after diagnosis). Sixteen patients developed acute aortic dissection, which caused death in 8. Nineteen patients also had AI due to aortic root dilation, 15 of whom developed congestive heart failure. Eighteen patients underwent 21 surgical procedures for TAA resection and/or aortic valve replacement or repair. Aortitis was documented histologically in 10 cases. Thoracic aortic complications in GCA are associated with serious outcomes that have been underrecognized and may be fatal. Physicians should be alert to the development of these complications at any time in the course of GCA, even many years after usual symptoms have subsided.

Giant cell arteritis. Epidemiology and treatment.

Giant cell arteritis (GCA) was considered a rare disease 50 years ago; however, it is now known to be an important and significant cause of morbidity and mortality in elderly people. GCA is a generalised arteritis, although the aetiology and pathogenesis of this disorder are poorly understood. It is likely that there are environmental or genetic factors that significantly influence the risk for the disease in different populations. Epidemiological studies have shown the highest incidence in Northern Europe and in Minnesota, US; which are populations of the same descent. Much lower incidence figures have been reported from more Southern regions of Europe and elsewhere. Possibly, the incidence of the disease is increasing as suggested by recent surveys. Glucocorticosteroids are the drugs of choice in all clinical types of GCA. Most studies have been performed with prednisolone. There is no general agreement concerning the initial dosage, but 10 to 40 mg/day is commonly recommended. After a few months the majority of patients can be treated with a low maintenance dosage of prednisolone 5 to 7.5 mg/day. Because of the low dosage required, the frequency of corticosteroid-related adverse effects is relatively low. The median duration of treatment is about 5 years. Nonsteroidal anti-inflammatory drugs, in contrast to corticosteroids, have no proven preventive effect on vascular complications of GCA, and cannot be recommended.

Complications of giant cell arteritis

Polymyalgia rheumatica is a clinical manifestation of giant cell arteritis (GCA) (Bengtsson and Malmvall, 1982). This inflammatory disease involves large and medium-sized arteries. The complications of the disease are mainly caused by arteritic lesions resulting in ischaemia of different organs. Vascular complications are threats to the lives of GCA patients as the disease can involve vital arteries such as the coronaries, the aorta and the cerebral vessels. Fortunately such complications seldom occur in patients who have had a proper diagnosis and corticosteroid treatment. However, series of patients reported before 1950, when corticosteroid treatment became available, include a high frequency of ocular and neurovascular complications. It is now well-established that ischaemic complications of GCA can be prevented by adequate corticosteroid treatment. This chapter will deal mainly with the vascular complications of the disease but it will also discuss the complications in joints. The complications of the disease in the eye and ocular nerve are discussed in Chapter 6. The liver involven~ent of GCA is discussed in Chapter 8, and complications of treatment are discussed in Chapter 9.

Osteoporosis after long‐term corticosteroid treatment of giant cell arteritis

The mineral content of the heel bone, and signs of osteoporosis on X-ray of the spine, were evaluated in 26 patients (20 women and 6 men) with giant cell arteritis (GCA), treated with prednisolone for an average period of 5 years. The mean age was 78 years (range 66-95 years). These results were compared with those obtained from a large population study of individuals aged 72, 75, 82 and 85 years. An increase of obvious and severe spinal osteoporosis from 16 to 85% was observed in the women in the population study between the ages of 72 and 85. No additional osteoporosis that could be attributed to the cortisone treatment was found among the GCA patients. The bone mineral content was not reduced in the patients compared to the general population. We conclude that there is no justification for attempting non-steroid treatment in GCA on account of the risk of osteoporosis. Corticosteroids are the only safe treatment for prevention of complications of GCA.

Polymyalgia rheumatica and giant cell arteritis. The dilemma of therapy.

Polymyalgia rheumatica, next to rheumatoid arthritis the most common inflammatory rheumatic disorder of the elderly, is a nonspecific clinical syndrome involving pain in the shoulder and pelvic girdles. Giant cell arteritis appears to localize in elastin-containing arteries and can cause similar myalgias. A relationship exists between the two diseases, as evidenced by their frequent coexistence in the same patient. The symptoms of polymyalgia rheumatica respond to low-dose corticosteroid therapy, while giant cell arteritis requires higher doses to prevent blindness due to involvement of the temporal artery. The key decision in therapy, therefore, concerns the dose and duration of use of steroid for polymyalgic symptoms. In this decision, prevention of the catastrophic complications of giant cell arteritis and avoidance of needless side effects of high-dose steroid therapy in the elderly are competing considerations.

Prognosis of giant cell arteritis including temporal arteritis and polymyalgia rheumatica. A follow-up study on ninety patients treated with corticosteroids.

Ninety patients with giant cell arteritis (GCA) were followed 3-10 years after the diagnosis. The mean observation time was 63 months. Thirteen patients died. Corticosteroids were administered to all but one patient; 35 were still on treatment after a mean observation period of 59 months. In 38 patients, 94 flare-ups of the disease were recorded during corticosteroid treatment, most of them occurring during the first year of treatment and when a low dose of prednisolone had been given. Thirty-three relapses, 76% within 3 months, occurred in 28 patients after withdrawal of treatment. One patient relapsed after more than ten years of disease. Polymyalgia rheumatica was the most common symptom of flare-up or relapse, regardless of the clinical picture at the time of diagnosis. The duration of treatment should be individualized. One year of treatment is enough in a few patients, whereas others need steroid therapy for more than four years. The rate of intercurrent disease and complications of GCA or its treatment was low. No patient developed severe eye damage due to GCA. The mortality rate was in fact lower than expected with regard to age and sex.

Polymyalgia rheumatica and giant cell arteritis

Summary The cardinal features for the diagnosis of polymyalgia rheumatica are as follows: o 1. Age . Patients are at least 55 years of age and usually older than 60. 2. Symptoms . Patients complain of proximal, symmetric muscle aching and stiffness without weakness, often accompanied by constitutional symptoms, such as fatigue or fever. 3. Physical examination . The musculoskeletal system usually is within normal limits despite severe symptoms. 4. Laboratory . There is a striking elevation of the ESR. A mild anemia may be present. 5. Therapeutic response . Treatment with small doses of steroids, such as prednisone, 10 mg daily for 4 days, produces a rapid, dramatic, subjective improvement and eventual fall in the ESR. 6. Exclusions . Other diseases causing myalgia should be excluded, such as infection, rheumatoid arthritis, systemic lupus erythematosus, malignancy or polymyositis. 7. Self-limited disease . Disease activity manifested by symptoms and elevation of the ESR should remit after about 2 years. Many patients with polymalgia rheumatica apparently have underlying giant cell arteritis. Every patients should be investigated carefully for other manifestations of giant cell arteritis as follows: o 1. Symptoms . Temporal or other headache, any ocular symptoms or extremity claudication may result from other vessel involvement. 2. Signs . The temporal arteries should be examined carefully for thickening, tenderness, nodularity and diminished or absent pulsations. The patient should be examined for any arterial bruits. 3. Biopsy . Temporal artery biopsy seldom is necessary diagnostically and usually will not alter therapy, since a negative biopsy cannot exclude the diagnosis. Indications for biopsy are fever of unknown origin or equivocal diagnosis because of psychogenic or other factors. Guidelines for management are: o 1. Initial treatment . Patients with polymyalgia rheumatica can be started on low doses of prednisone, e.g., 10 mg daily, with gradual increase in dose if necessary to control symptoms and the ESR. Patients with manifestations of temporal or ophthalmic arteritis probably are treated more safely by higher initial doses, such as prednisone, 40–60 mg daily, with gradual reduction to lower maintenance doses. 2. Follow-up . Maintenance steroids should be the lowest dose that will render the patient essentially symptom-free and keep the ESR within normal limits. Exacerbations of myalgias or constitutional symptoms, the appearance of symptoms or signs of temporal or ophthalmic arteritis or rises in the ESR call for increased steroid doses. After 6 months, periods of stability should lead to attempts to taper and eventually to discontinue steroids, as the disease has run its course. The ESR must be monitored carefully. The most important point is that polymyalgia rheumatica is a treatable disease that can be missed easily. Recognition and treatment of this illness in an older patient who has been prematurely incapacitated can produce complete amelioration of symptoms and perhaps save him from visual loss or other serious complications of giant cell arteritis. Few other rheumatic or any other diseases can be so gratifying to treat.