Immunopathology of cardiac lesions in fatal systemic lupus erythematosus

Bidani, A.; Roberts, Jimmy L.; Schwartz, Melvin M.; Lewis, Edmund J.

doi:10.1016/s0002-9343(80)80010-6

Cited by 158 publications

(83 citation statements)

References 35 publications

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“…Epicardial vasculitis was found at autopsy in another patient who developed hemopericardium during anticoagulation for hemodialysis (23). The histologic findings of fibrosis and/or fibrinous changes in the patients with tamponade described here are similar to those reported among unselected patients in autopsy series, most of whom did not have clinical pericarditis during life (5,9,28). However, in addition, 2 patients of the present series had vascular proliferation, and 1 had frank vasculitis.…”

Section: Discussionsupporting

confidence: 79%

The spectrum of pericardial tamponade in systemic lupus erythematosus: Report of ten patients

Kahl

1992

Arthritis & Rheumatism

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Objective. To describe the range of clinical manifestations and the outcome of pericardial tamponade in patients with systemic lupus erythematosus (SLE).Methods. Patients with pericarditis and with pericardial tamponade were identified from our computerized database of 395 SLE patients. Medical records were reviewed to establish activity of SLE at the time of tamponade, as well as clinical and laboratory features, treatment, and outcome of the tamponade.Results. Pericarditis occurred in 75 patients (19%), with 11 episodes of tamponade in 10 of them (13%; 2.5% of entire series). Tamponade was the initial manifestation of SLE in 4 patients. Seven episodes occurred during active lupus, with nephritis present in 6. Signs of venous congestion, including ascites and facial or peripheral edema, were the most common manifestation of tamponade. Pericardial fluid was exudative, and pericardial tissue demonstrated a range of findings including fibrinous and fibrotic changes, acute and chronic inflammatory infiltrates, and vascular proliferation. Tamponade was fatal in 1 patient, and 2 patients each had recurrent effusions and pericardial thickening.Conclusion. Pericardial tamponade may occur at any point in the course of SLE, and should be considered in patients with unexplained signs of venous con-

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Section: Discussionsupporting

confidence: 79%

The spectrum of pericardial tamponade in systemic lupus erythematosus: Report of ten patients

Kahl

1992

Arthritis & Rheumatism

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“…55 SLE exhibits a number of similarities to the autoimmune disease of MRL mice; for example, both have high levels of circulating antibodies and arteritis and exhibit immune complexes in the vessel wall. 56 Our studies, indicating that autoimmune vasculitis promotes lipid deposition in both large and small coronary arteries, are consistent with the hypothesis that inflammation of the vessel wall may be a promoting factor to the premature atherosclerosis observed in patients with SLE. 36 Supporting this possibility is accumulating evidence from studies with nonhuman primates and humans that chronic, sustained, circulating immune complexes are likely to accelerate atherogenesis, even in the absence of classic risk factors.…”

supporting

confidence: 91%

Immune-complex-mediated vasculitis increases coronary artery lipid accumulation in autoimmune-prone MRL mice.

Qiao¹,

Castellani²,

Fishbein³

et al. 1993

Arterioscler Thromb

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MRLJlpr mice develop severe autoimmune disease and vasculitis by 5 months of age, whereas congenic strain MRL/n mice exhibit much milder vasculitis with a later age of onset When maintained on a high-fat, high-cholesterol (atherogenic) diet, strain MRLJlpr mice exhibited a striking deposition of lipid in both the large and small coronary arteries, whereas strain MRL/n mice exhibited very little lipid accumulation. Neither strain exhibited lipid accumulation on a low-fat chow diet The atherogenic diet induced hyperlipidemia in both strains, but surprisingly the levels of atherogenic apolipoprotein B-containing lipoproteins were much lower in MRLJlpr mice. Immunohistochemical studies revealed that immune complexes (immunoglobulins G and M), T and B lymphocytes, macrophages, granulocytes, apolipoprotein B, and serum amyloid A proteins were present in the walls of the coronary arteries that had vasculitis and lipid accumulation. By 6-7 months of age, MRLJlpr mice had a higher incidence of myocardial infarction in the atherogenic diet group (53%) compared with the chow group (14%), whereas MRL/n mice exhibited no myocardial infarction on either diet These results suggest important interactions between vasculitis, hyperlipidemia, and arterial lipid accumulation. They support the concept that injury to the vessel wall in immune-complex-mediated vasculitis increases lipid deposition in the presence of hyperlipidemia.

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“…ImmunoXuorescence studies demonstrate Wne granular immune complex and complement deposition in the walls and perivascular tissues of myocardial blood vessels supporting the hypothesis that lupus myocarditis is an immune complex-mediated vascular phenomenon [11]. Some reports demonstrate an association between anti-Ro and anticardiolipin antibodies with left ventricular dysfunction [12,13].…”

Section: Discussionmentioning

confidence: 73%

Clinical characteristics of lupus myocarditis in Korea

et al. 2007

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Clinically important myocarditis is an unusual feature in systemic lupus erythematosus (SLE). We describe the clinical characteristics, management and outcomes of Wve SLE patients who developed severe left ventricular dysfunction. Four patients were female with mean age of 36.4 years. Three patients had both lupus myocarditis and lupus nephritis. Four patients had raised anti-dsDNA antibody titer and low complement level and two patients had positive IgG anticardiolipin antibody. Three patients were treated by high-dose corticosteroids, one patient by intravenous pulse methylprednisolone, and one patient by intravenous immunoglobulin and pulse cyclophosphamide with high dose corticosteroids. Left ventricular function improved markedly in four patients and all of them had no recurrence of lupus myocarditis up to follow-up of 33 months. However, one patient, who showed no improvement of left ventricular function, was expired due to sudden cardiac arrest. Lupus myocarditis should be treated by immunosuppressive therapy with high-dose corticosteroids and mostly the prognosis might be good with early treatment.

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Immunopathology of cardiac lesions in fatal systemic lupus erythematosus

Cited by 158 publications

References 35 publications

The spectrum of pericardial tamponade in systemic lupus erythematosus: Report of ten patients

The spectrum of pericardial tamponade in systemic lupus erythematosus: Report of ten patients

Immune-complex-mediated vasculitis increases coronary artery lipid accumulation in autoimmune-prone MRL mice.

Clinical characteristics of lupus myocarditis in Korea

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