Objective. To describe characteristics and outcomes of vasculitides associated with malignancies. Methods. The requirement for inclusion in this retrospective, 10-year study was development of vasculitis in patients with a progressing malignancy. Malignancies secondary to immunosuppressants used to treat vasculitis were excluded. The main characteristics of vasculitides were analyzed and compared according to the type of malignancy.
Objective. The prevalence of the involvement of large vessels in giant cell arteritis (GCA) is 3-13%. Aortitis is the most serious complication of GCA. Computed tomodensitometric (CT) scan allows analysis of both the aortic wall and endoluminal part of the aorta. Therefore, we conducted a study using CT scan to analyze aortic abnormalities in patients with recent-onset GCA. Methods. This prospective controlled study compared patients with biopsy-proven GCA with a matched control group based on sex, age, and cardiovascular risk factors. During the 4-week period following diagnosis of GCA, patients underwent an aortic CT scan. The aortic imaging results were blindly compared between both groups. Results. From January 5, 1998 to January 11, 1999, 22 patients and 22 controls were screened by CT scan for aortic involvement. Thickening of the aortic wall was more frequent among patients than controls (45.4% versus 13.6%; P ؍ 0.02). Aortic thickening (mean 3.3 mm) was located on the ascending part of the thoracic aorta in 22.7% of the patients, with no evidence of thickening in the controls (P ؍ 0.05). Thickening of the abdominal aortic wall was noted in 27.3% of the patients and none of the controls (P ؍ 0.02). Conclusion. This study suggests that inflammatory aortic thickening, detected by CT scan, occurs frequently at the time of diagnosis of GCA, and that this condition predominantly occurs on the ascending part of the aorta.
Objective. To describe the clinical, biologic, and histologic features of temporal artery biopsy (TAB)-localized systemic necrotizing vasculitides (SNV), and to assess their frequency among elderly patients undergoing TAB for suspected giant cell (temporal) arteritis (GCA).Methods. The frequency of a TAB localization of SNV was prospectively assessed in a multicenter study of elderly patients undergoing TAB for suspected GCA. All patients with SNV fulfilling the American College of Rheumatology criteria for a specific vasculitic syndrome and with evidence of vasculitis on TAB were included in a retrospective, descriptive study.Results. SNV was diagnosed based on the TAB in 1.4% of the patients with suspected GCA and in 4.5% of the positive (inflamed) TAB specimens. We retrospectively selected 27 patients (18 female, 9 male; mean ؎ SD age 62 ؎ 15 years, range 22-79 years) with SNV and TAB-localized vasculitis. Only 2 of these patients were known to have SNV before TAB localization. Twenty-two patients (81%) had cephalic symptoms, including jaw claudication in 33%, clinically abnormal temporal arteries in 33%, and neuro-ophthalmologic symptoms in 11%. All patients had systemic symptoms suggestive of SNV and histologically proven NV in the TAB specimens (70%) or elsewhere in other biopsy sites (74%). Abnormal biologic results suggestive of SNV were present in 17 patients (63%). For 4 patients, the TAB-documented involvement led to initial misdiagnoses of GCA, and systemic manifestations that developed under steroid therapy revealed the correct diagnosis. The final diagnoses of the patients were polyarteritis nodosa (PAN) (n ؍ 11), Churg-Strauss syndrome (n ؍ 6), micropolyangiitis (n ؍ 3), Wegener's granulomatosis (n ؍ 3), hepatitis B virus-related PAN (n ؍ 2), hepatitis C virus-related cryoglobulinemic vasculitis (n ؍ 1), and rheumatoid vasculitis (n ؍ 1).Conclusion. TAB-localized SNV presents a major diagnostic dilemma because it can mimic GCA. Careful analysis of clinical, biologic, and histologic data should lead to the correct diagnosis and help guide the clinician's choice of appropriate therapy.
Our study suggests for the first time that inflammatory aortic involvement present at onset of GCA could predict a more chronic/relapsing course of GCA, with higher steroid requirements and an increased risk for vascular events in the long term.
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