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At least 19 recordsLinked to original sources
PubMed1993

Immunopathogenesis, diagnosis, and treatment of giant cell arteritis, temporal arteritis, polymyalgia rheumatica, and Takayasu's arteritis.

Although the causes of giant cell arteritis, polymyalgia rheumatica, and Takayasu's arteritis are not known, the immune system participates in the pathogenesis of these disorders. Many reports indicate that cellular immunity is active in giant cell arteritis. The diagnosis of Takayasu's arteritis has been advanced by magnetic resonance imaging and ultrasonography. Neither technique has replaced angiography as the gold standard for diagnosis, but both may help monitor the response of Takayasu's arteritis to therapy. The diagnosis of giant cell arteritis with a low erythrocyte sedimentation rate is unusual but is more frequent in patients with a history of polymyalgia rheumatica or corticosteroid use. One recent retrospective study suggests that 20 mg/d of prednisolone is as effective as higher doses in treating giant cell arteritis. Other preliminary studies indicate that methotrexate may effectively spare corticosteroid use in giant cell arteritis and Takayasu's arteritis. Angioplasty for renal artery stenosis in Takayasu's arteritis initially cures 30% of patients and improves the condition in 70%; however, the long-term success rate is 50%. New studies demonstrate that patients with giant cell arteritis and polymyalgia rheumatica have an increased risk of hypothyroidism.

Giant Cell Arteritis↗
PubMed1990

Widespread thrombosis and necrotizing arteritis of the liver in a 69-year-old woman with symptoms simulating those of temporal arteritis.

Autopsy findings of widespread thrombosis and necrotizing arteritis of the liver in a 69-year-old woman who had clinical symptoms suggesting those of temporal (giant cell) arteritis were presented. The lesion of the temporal artery was not of temporal arteritis but of thrombosis, part of widespread thrombosis, which occurred in the small arteries having hypertensive arteriolopathy. This case also had an arteritis of the liver resembling polyarteritis nodosa (PN). The pathologic processes demonstrated in this case suggested that the temporal arteritis-like symptoms may be brought about by occlusion of the temporal artery. Temporal arteritis is a nonfatal and self-limited disease and little information has been obtained from autopsy material. Accordingly, it is necessary to collect autopsy cases of temporal arteritis to investigate this disease through observations of whole bodies. Recently we examined a case which appeared clinically having symptoms of temporal arteritis, but the autopsy revealed that the symptoms were not brought about by temporal arteritis but by thrombosis of the temporal artery. It is the purpose of this paper to present this case and to discuss some problems concerning genesis of symptoms of temporal arteritis.

Aged↗
PubMed1989

Analysis of granulomatous arteritis in MRL/Mp autoimmune disease mice bearing lymphoproliferative genes. The use of mouse genetics to dissociate the development of arteritis and glomerulonephritis.

MRL/Mp mice bearing the lymphoproliferation gene (lpr) spontaneously develop systemic granulomatous arteritis coincident with glomerulonephritis (GNP). Although the association of lpr-dependent lymphoproliferation in these mice seems to be a prerequisite for the development of granulomatous arteritis, the genetic basis is poorly understood. The first approach to this problem was to study the ability of another, nonallelic, lymphoproliferative gene, gld (generalized lymphoproliferative disease), inducing arteritis in MRL/Mp mice. The gld gene was placed on an MRL/Mp background by producing reciprocal (MRL/Mp-+/+ X C3H/Hej-gld/gld)F2 hybrid mice. Seventeen percent of these mice with lymphoproliferation had arteritis and GNP, suggesting that more than one lymphoproliferative gene could induce GNP and arteritis in an MRL/Mp background. Next, the effect of rearrangements in the genetic background of MRL/Mp-lpr/lpr mice by hybridization with non-autoimmune lpr-bearing mice was examined. This was done by making MRL/Mp-lpr/lpr X reciprocal (MRL/Mp-lpr/lpr X C57BL/6-lpr/lpr)F1 mice. Thirty-three percent of these mice developed arteritis, but one third of these did not get GNP, thus showing that susceptibility to arteritis was separate from GNP. The histopathologic features of the arteritis in both the F2 hybrids and the backcross mice were granulomatous and were identical to those seen in MRL/Mp-lpr/lpr mice. These findings suggested that it might be possible to dissociated two components (arteritis and GNP) of a severe autoimmune disease of MRL/Mp mice and to study their pathogenesis separately.

Animals↗
PubMed1977

Giant-cell arteritis, temporal arteritis and polymyalgia rheumatica. A retrospective study of 63 patients.

The initial clinical symptoms, the course of the disease, and the effect of corticosteroid treatment have been analyzed in a retrospective study of 63 patients with temporal arteritis or polymyalgia rheumatica. The relationship between the physical examination of the temporal regions, the ophthalmological examination, and biopsy from the temporal artery with respect to the diagnostic value were examined. Histological examination of biopsy specimens from the temporal artery in 58 patients revealed arteritis in 46. Half of the patients had only local symptoms from the temporal regions; one fourth presented such symptoms as well as myalgias, and one fourth had myalgias only. Patients presenting local symptoms of temporal arteritis as well as of myalgias had always had myalgias as the initial symptom and developed local symptoms of temporal arteritis 1-24 months later. Permanent reduction of vision occurred in 20% of the patients. Symptoms of generalized arteritis were observed in several patients. The overlapping of the clinical symptoms, the positive biopsy findings in patients with polymyalgia rheumatica as the only local symptom and the identical reaction to corticosteroid treatment support the conception of temporal arteritis and polymyalgia rheumatica as two manifestations of the same disease. The physical and the ophthalmological examinations were of limited diagnostic value. Positive biopsy findings were seen in 25 patients with noraml palpatory findings, and in 46 patients without eye symptoms the ophthalmoscopic examination revealed no signs of arteritis. If the first biopsy from the temporal artery is negative, biopsy from the contralateral temporal artery should be performed. Correctly timed corticosteroid treatment in adequate doses can prevent reduction of vision in giant-cell arteritis. The treatment is a long-term therapy, its average duration in the present study being more than two years.

Adrenal Cortex Hormones↗
PubMed1997

Large vessel vasculitis (giant cell arteritis, Takayasu arteritis).

Giant cell arteritis and Takayasu arteritis are separate but similar idiopathic diseases clinically characterized by constitutional symptoms, shared surrogate markers of systemic inflammation and indistinguishable granulomatous pan-arteritis of large vessels. This review emphasizes and analyses changing perceptions about the diseases. Recent series suggest that aortic involvement in giant cell arteritis may be more common than was previously appreciated. The case for and against inflammatory arthritis in giant cell arteritis is discussed. Ethnic new geographical variation in Takayasu arteritis-disease expression is reviewed. New philosophies of treatment are presented for both diseases. Prognosis in giant cell arteritis and its relationship to treatment is analysed. The utility of the laboratory for diagnosis and monitoring disease activity is appraised for each.

Animals↗
PubMed1996

Clinical differentiation between giant cell (temporal) arteritis and Takayasu's arteritis.

OBJECTIVE: To determine whether giant cell (temporal) arteritis (GCA) can be differentiated from Takayasu's arteritis on the basis of clinical findings. METHODS: A comparative study contrasting 217 patients with GCA to 63 patients with Takayasu's arteritis was conducted, using the prospectively gathered large multicenter data set of the American College of Rheumatology Vasculitis Criteria Databank. Logistic regression and recursive partitioning were used to assess the capability of a variety of variables to separate these 2 vasculitic disorders. RESULTS: Age of 40 years at onset of disease was the most discriminatory single variable. Excluding age at onset, ethnic background and a combination of clinical signs indicating upper limb vascular impairment, shoulder stiffness, and tender scalp led to correct classifications of 95% in both GCA and Takayasu's arteritis. Vascular insufficiency of the upper extremities, a key feature of Takayasu's arteritis, was noted in 15% of patients with GCA, although to a lesser degree. CONCLUSION: Although similar in many respects, GCA and Takayasu's arteritis were easily definable and separable disorders, even when the typical age barrier of 40 years at onset of disease was excluded. These findings strengthen the concept that they are distinct disease entities.

Age of Onset↗
PubMed1981

The epidemiology of giant cell arteritis including temporal arteritis and polymyalgia rheumatica. Incidences of different clinical presentations and eye complications.

During a period of three years in Göteborg, Sweden, 126 cases of giant cell arteritis (GCA) were diagnosed. Histologic evidence of arteritis was found on temporal artery biopsy in 74 (59%). The total annual incidence of GCA was calculated to be 9.3 per 100,000 inhabitants. In the age group over 50, incidence was 28.6 per 100,000. For histologically proven GCA, the incidence was 5.5 per 100,000 of the total population. The corresponding figure in the age group over 50 was 16.8 per 100,000. Twenty-six patients (21%) had a clinical presentation of temporal arteritis, and 23 (18%) had a combined picture of temporal arteritis and polymyalgia rheumatica (PMR). Sixty-seven (53%) had the PMR syndrome without any temporal symptoms, and 10 patients (8%) had a "silent" presentation with only general symptoms. The PMR syndrome was more common among women with GCA (79%) than among men (56%). The group of patients without muscular symptoms contained an equal number of men and women. Eye complications were seen in 15 patients (12%). In 6, the ocular symptoms were transient, while 9 suffered from permanent loss of vision. In 3 of these patients, temporal artery biopsy revealed no evidence of arteritis, and 5 had no clinical signs of localized temporal arteritis.

Blindness↗
PubMed1992

Giant cell arteritis of the female genital tract with temporal arteritis.

The clinical and pathological features of a patient with giant cell arteritis of the uterus and ovaries are described. A 61 year old woman had fever and weight loss over a period of eight months. A hysterectomy with bilateral salpingo-oophorectomy was performed for a large cystic ovarian mass. Histological examination showed a benign ovarian cyst and unexpected giant cell arteritis affecting numerous small to medium sized arteries in the ovaries and myometrium. The diagnosis of temporal arteritis was confirmed by a random temporal artery biopsy, despite the absence of symptoms of temporal arteritis. This observation is compared with previously reported cases and the relation between granulomatous arteritis of the genital tract and temporal arteritis is discussed. The main differential diagnosis in this localisation was represented by Wegener's granulomatosis and periarteritis nodosa.

Female↗
PubMed1986

Temporal arteritis with giant cell aortitis, coronary arteritis, and myocardial infarction.

Extracranial giant cell arteritis occurs in 10% to 15% of patients with temporal arteritis and polymyalgia rheumatica. Aorta and its major branches are most often involved and death may result from an unsuspected ruptured aortic aneurysm or aortic dissection. Involvement of coronary arteries by giant cell arteritis resulting in death from myocardial infarction is extremely rare. This article describes one such case: an 84-year-old man who died of acute myocardial infarction with the unexpected autopsy finding of giant cell aortitis and coronary arteritis, and who, three years earlier, had sudden onset of bilateral blindness and biopsy-proven temporal arteritis.

Age Factors↗
PubMed1976

[Takayasu-Onishi arteritis. II. Relations of Takayasu-Onishi arteritis with other non-specific arteritides].

Takayasu-Onishi arteritis (T.O.) is similar to Hutchison-Horton arteritis (H.H.) on histological, clinical, laboratory, and pathogenetic grounds. Both probably depend on immunitary dysreactivity, their different clinical expression being attributable to differences in the district involved and the age of the subject. Both are preceded or accompanied by rheumatism. An interesting relation can be made out between temporal arteritis and "rheumatic polymyalgia" or, more aptly, "rhizomelic polymyalgia" (Ballabio, 1975). The latter (of rheumatic origin) may accompany arteritis - Hamrin, indeed, has suggested their unification in the description "arteritic polymyalgia". It is uncertain whether vasculopathy in the course of collagen disease, rheumatic arteritis, and polyarteritis nodosa can be identified with T.O., even though a common immunological basis can be made out. The difference between T.O. and thromboangiitis obliterans, on the other hand, is quite clear at the present time.

Aortic Arch Syndromes↗
PubMed1980

The clinical pictures of giant cell arteritis. Temporal arteritis, polymyalgia rheumatica, and fever of unknown origin.

In a prospective study, 68 hospitalized patients were diagnosed as having giant cell arteritis. Temporal artery biopsy was performed in all patients and showed histologic evidence of arteritis in 42 (62%). Twenty-six patients had a negative biopsy but met the clinical criteria for the diagnosis. Four different clinical pictures were recognized. Thirteen patients (19%) had symptoms of localized temporal arteritis without muscular discomfort. The polymyalgia rheumatica syndrome without signs of localized arteritis was seen in 33 patients (49%). Seventeen (25%) had symptoms of both polymyalgia rheumatica and temporal arteritis. Five patients (7%) had general symptoms only, such as fever, anorexia, and fatigue, without muscular or arteritic symptoms.

Aged↗
PubMed1990

Giant cell arteritis (temporal arteritis) affecting the breast: report of two cases and review of published reports.

The breast is an infrequently recognised site of primary giant cell arteritis. Two cases of giant cell arteritis affecting the breast are described and 11 previously described cases are reviewed. All cases presented with single or multiple breast masses, leading to a diagnosis before biopsy of suspected breast carcinoma. Symptoms similar to those of polymyalgia rheumatica occurred in about half of these patients, though the significance of these symptoms was only appreciated in retrospect. Clinical or pathological evidence of giant cell arteritis outside the breast (temporal artery, thyroid artery) was noted in a minority of cases. Seven patients received corticosteroid treatment, and all patients recovered without complications. Two patients had an adenocarcinoma of the breast contiguous with the giant cell arteritis. Giant cell arteritis affecting the breast may be underrecognised and should be considered in older women with polymyalgia rheumatica-like symptoms and tender breast mass(es).

Aged↗
PubMed2000

Thrombocytosis in temporal arteritis rising platelet counts: a red flag for giant cell arteritis.

OBJECTIVES: To determine whether early recognition and detection of thrombocytosis in patients with giant cell arteritis can help secure an earlier diagnosis, and whether it can help differentiate cases of arteritic optic neuropathy from other forms of optic neuropathy. METHODS: Medical and ophthalmologic records from 1993 to 1998 of the authors' patients with biopsy-proven temporal arteritis versus the authors' patients with nonarteritic anterior ischemic optic neuropathy and idiopathic demyelinating optic neuritis were prospectively collected. Past and present blood analyses were collected, and platelet counts were compared between patients with giant cell arteritis and control populations. This was done to determine whether thrombocytosis could help with the diagnosis and differentiation of these different disease states. RESULTS: There was a significant difference in the frequency of thrombocytosis in patients with giant cell arteritis (13 out of 19 patients), with or without arteritic ischemic optic neuropathy, as compared with those with nonarteritic anterior ischemic optic neuropathy (zero out of 30 patients), idiopathic optic neuritis (zero out of 26 patients), and healthy age-matched controls (one out of 22 control subjects). This difference was especially helpful in patients whose sedimentation rates were within the normal range (adjusting for age). Also noted was the finding that the rise in the platelet counts was not acute, but rather it was a slow gradual increase for approximately 12 months before the onset of significant systemic or visual symptoms. CONCLUSION: Thrombocytosis should be considered an important marker in patients being referred for evaluation of ischemic optic neuropathy, diplopia, amaurosis fugax, headache, or even generalized malaise. Westegren sedimentation rates <50 mm/hr are often erroneously viewed as nondiagnostic or equivocal in the elderly and just followed. An over-the-phone review of patients' sedimentation rates, complete blood counts, and platelet counts can lead to expedited evaluation and treatment of patients who may be at high risk of visual loss from temporal arteritis. Thrombocytosis should lower a physician's threshold to acutely treat patients for possible arteritic ischemic optic neuropathy until the disease is definitely ruled out.

Aged↗
PubMed1995

Characterization of the arteritis induced by infusion of rats with UK-61,260, an inodilator, for 24 h. A comparison with the arteritis induced by fenoldopam mesylate.

Administration of fenoldopam mesylate (FM), a dopaminergic agonist, or of cyclic cAMP phosphodiesterase inhibitors (PDE III), for example theophylline and caffeine, induces arteritis in the rat. In this study we characterized the arteritis induced by UK-61,260, an investigational inotropic agent with vasodilatory properties which displays an inhibitory action on cyclic AMP phosphodiesterase, in comparison with lesions induced by FM. The compounds were administered to Sprague-Dawley rats by intravenous infusion over 24 h (FM and UK-61,260), orally or subcutaneously (UK-61,260); the rats were killed and necropsied for pathological examination at various times between 0 h and 28 days post-infusion. Infusion of UK-61,260 at doses of 100, 300 or 400 mg/kg produced arteritis mainly in the mesenteric arteries and occasionally in the renal, pancreatic, gastric and coronary arteries. There were no arterial lesions after infusion of 30 mg/kg, or after administration of 30, 100 or 200 mg/kg per day subcutaneously for 7 days, or after acute administration of 100, 300, 400 or 600 mg/kg orally. Infusion of rats with 72 or 144 mg/kg FM produced arteritis over a wider range of tissues than did UK-61,260. However, the arterial lesions produced by infusion of either drug have the same initial aspect and a similar evolution with time. Immediately after the end of the infusion, minimal necrosis and haemorrhage occurred in the media only, without involvement of the endothelium or the perivascular space. This indicates that the media of the artery is the primary site of injury. The lesions seen 1 and 3 days post-infusion were characterized by severe medial necrosis and haemorrhage with perivascular acute inflammation and appeared macroscopically as haemorrhagic spots on the vessels. On days 7, 14 and 28 post-infusion, no medial necrosis or haemorrhage were present, while perivascular chronic inflammation and moderate smooth muscle hyperplasia were seen. It appeared, therefore, that the lesions underwent repair in 28 days, but footprints of the damage were still present 28 days post-infusion. The similarity between arteritis induced in rats by fenoldopam or by UK-61,260, at doses inducing PDE III inhibition, is consistent with the view that they have a similar pathogenesis. In our view it is probable that these pharmacologically and chemically distinct drugs trigger an increase in intracellular levels of cAMP which in turn triggers vascular damage. The arterial changes observed in the current study after acute administration may explain the increased incidence of polyarteritis nodosa occurring in long term toxicity studies with FM or PDE III inhibitors.

Administration, Oral↗