Cases reported "Arteritis"

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1/11. Systemic granulomatous arteritis associated with Epstein-Barr virus infection.

    A 61-year-old woman initially presented with symptoms and findings reminiscent of infectious mononucleosis, and her illness then took a rapidly fatal course. autopsy revealed widespread granulomatous arteritis, with multinucleated giant cells but without eosinophils and fibrinoid necrosis, affecting small arteries and arterioles and infiltration of haemophagocytic histiocytes into many organs. in situ hybridization with Epstein-Barr virus (EBV)-specific oligonucleotide probes showed positive signals in the infiltrating immune cells and epithelial and endothelial cells of the affected organs. EBV-associated haemophagocytic syndrome (EBV-AHS) with systemic granulomatous arteritis was diagnosed. From the immunophenotypes of the infiltrating immune cells, a possible role of CD4 T-cells in the pathogenesis of this haemophagocytic syndrome and granulomatous vasculitis was suggested.
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2/11. The features of glomerulitis in the acute stage of panarteritis nodosa. Developmental process of glomerulitis and correlation between glomerular and vascular lesions.

    In order to determine the morphological characteristics of certain vascular and glomerular lesions and the correlation between them, we attempted three-dimensional observation using serial sections of an autopsy kidney, from a patient with panarteritis nodosa in the acute phase. Fibrinoid necrotizing vasculitis spread from arcuate arteries to arterioles in a segmental, eccentric pattern, especially occurring at bifurcations. Segmental arteriolitis often originated in extraglomerular capsular arteriole and spread into the intraglomerular capsular arteriole and glomerular capillaries, directly leading to necrotizing glomerulitis. Some of the glomerulitis connected directly with extracapsular arteriolitis was segmental and eccentric in distribution. Most of the glomerulitis had a tendency to originate in the hilar arteriole, which was near bifurcations between the arteriole and glomerular capillaries. Segmental glomerulitis was found to consist of four elements: glomerular tuft necrosis with fibrin exudation, crescents, rupture or dissolution of Bowman's capsule, and pericapsulitis. It is suggested that the segmental inflammatory attacks, repeated more than twice, give rise to widespread and almost global necrotizing glomerulitis.
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3/11. Segmental mediolytic arteritis. A clinicopathologic and ultrastructural study of two cases.

    We describe the histopathologic and ultrastructural changes in two cases of segmental mediolytic arteritis (SMA) and summarize the clinical and pathologic findings in previous reports. SMA is initiated by the transformation of the arterial smooth-muscle cytoplasmic contents into a maze of dilated vacuoles containing edema-like fluid. With vacuolar rupture, the smooth-muscle cells are disrupted and the mediolytic process completed. Mediolysis is accompanied by fibrin deposition and hemorrhages at the adventitio-medial junction and within the media. inflammation is inconstant and limited to the periadventitial tissues. Transmural mediolysis leads to the formation of arterial wall gaps--defects in the vascular wall bridged by a serofibrinous layer. The serosal and intramural arteries and arterioles of the jejunum and the epicardial coronary arteries were the targets of SMA in this report. SMA occurs in two clinical settings: (a) in abdominal muscular arteries and arterioles of predominantly elderly patients presenting either with ischemic bowel disease or shock, and (b) in the coronary arteries of neonates in conditions associated with severe hypoxemia. We conclude that SMA is the result of an inappropriate vasospastic response expressed in a splanchnic vascular bed undergoing vasoconstriction as a response to shock or severe hypoxemia.
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4/11. Unusual causes of arterial insufficiency.

    Most patients with vascular insufficiency in the legs suffer from atherosclerosis. Thus, it is easy to miss the diagnosis in occasional patients with disease due to other causes. Mechanical and functional disorders which affect major arteries or arterioles are described.
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5/11. Disseminated visceral giant cell arteritis: histopathologic description and differentiation from other granulomatous vasculitides.

    Disseminated visceral giant cell arteristic, a previously unknown entity, was observed in four autopsied patients, all men, aged 33, 67, 59 and 45 years. None of the patients had temporal arteritis, collagen disease, sarcoidosis, hepatitis or other infections, and vasculitis was diagnosed only after death. All had giant cell arteritis of extracranial arteries and arterioles in at least three of the following organs: the heart, lungs, kidneys, liver, pancreas, and stomach in various combinations. Despite some histopathologic similarities, disseminated visceral giant cell arteritis can be distinguished from other necrotizing and granulomatous vasculitides by the type of vessels principally affected and the presence or absence of giant cells, vascular fibrinoid necrosis and eosinophilic infiltrates. The observations suggest that it is a distinctive type of systemic vasculitis.
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6/11. Segmental retinal periarteritis with branch arterial occlusion.

    An 18-year-old woman complained of acute visual field loss in the right eye due to branch arterial occlusion. Similar disease occurred in the left eye two years later. Extensive laboratory examination revealed no factor of etiologic significance, and no sign of uveitis was observed. The retinal arterioles around the optic disc were segmentally inflamed angiographically, which led to their obstruction. Corticosteroid therapy (betamethazone, 3.0 mg/day) improved the arteriolitis within two weeks.
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7/11. Isolated benign cerebral vasculitis.

    A young woman south medical care for headache, nausea, and evolving focal neurologic signs. The CSF was normal; cerebral angiography showed segmental narrowing and irregularity of intraparenchymal arterioles. Isolated cerebral vasculitis was the clinical diagnosis made by careful exclusion; the illness reponded well to steroids and there was later angiographic evidence of healing.
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8/11. Pulmonary vasculitis with hypereosinophilia and episodic pulmonary hypertension: report of three siblings.

    Three siblings with eosinophilia who developed pulmonary hypertension are reported. They consisted of a 3 year old boy (case 1), a 9 year old boy (case 2) and a 13 year old girl (case 3), all of whom died within an 18 month period of severe episodic attacks of pulmonary hypertension and the resultant low cardiac output. Marked peripheral eosinophilia was found in cases 1 and 2, and mild eosinophilia in case 3. Open lung biopsy of case 1 revealed pulmonary arteritis with massive eosinophilic infiltration and intimal thickening of muscular arteries of 300-1500 microns in diameter. At autopsy, cases 2 and 3 showed almost similar findings, comprising widespread obliteration of the pulmonary arteries by concentric intimal thickening, medial hypertrophy and recanalized thrombi of arterioles. Rarely, there were foci of granulomas in the thickened intima surrounding birefringent foreign bodies. There were small areas of infarction in the lungs and heart due to arterial thrombi. Vascular lesions other than those in the lungs were mild and almost limited to the branches of the coronary arteries. Therefore, the present cases appear to be a single disease of pulmonary hypertension secondary to endothelial injury and the resultant intimal fibrosis probably evoked by toxic substances, although such agents were not confirmed.
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9/11. Unexplained pulmonary hypertension with pulmonary arteritis in rheumatoid disease.

    The case is described of a 24-year-old woman who died after suffering from rheumatoid arthritis for eight years. During the last four months of her life there was clinical evidence of pulmonary hypertension. At necropsy the heart showed right ventricular hypertrophy but no congenital defect. Microscopic examination of the lungs disclosed evidence of hypertensive pulmonary vascular disease with medial hypertrophy and intimal fibrosis of muscular pulmonary arteries together with hypertensive changes in the pulmonary arterioles. Some of the muscular pulmonary arteries also showed fibrinoid necrosis of their media and acute arteritis. It was concluded that the fibrinoid necrosis was a minifestation of severe hypertensive pulmonary vascular disease rather than being a primary rheumatoid arteritis of the lung.
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10/11. Pan-nephritis (glomerulonephritis, arteriolitis, and tubulointerstitial nephritis) associated with predominant mesangial C1q deposition and hypocomplementemia: a variant type of C1q nephropathy?

    A 35-year-old man showed acute nephritic syndrome manifested as proteinuria, hematuria, and hypocomplementemia after upper respiratory infection. A renal biopsy showed mild to moderate mesangial proliferative glomerulonephritis with an accumulation of mononuclear cells in the capillary loop and with the deposition of C1q (graded as 3 ), immunoglobulin (Ig) G, C3 (2 ), IgA, IgM, and fibrinogen (weak to 1 ), and mononuclear cell infiltration of the glomerular hilus, arterioles, and proximal tubules, which was a peculiar form of renal lesion. The mesangial deposition of C1q has been well documented in lupus nephritis, membranoproliferative glomerulonephritis, and endocapillary glomerulonephritis. The clinical signs and laboratory data in our patient ruled out these diseases. Although an immunofluorescence study showed these similarities to Clq nephropathy, the histopathological features of the peculiar arteriolitis and tubulointerstitial nephritis and laboratory findings of hypocomplementemia, as well as the good response to oral steroid therapy, differed from typical C1q nephropathy. The current patient appears to be a very rare phenotype of nephritis, being the only 1 case in almost 2,800 renal biopsies.
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