Morphology of vascular, renal, and heart lesions in the antiphospholipid syndrome: Relationship to pathogenesis

被引:18
作者
Amigo M.-C. [1 ]
García-Torres R. [1 ]
机构
[1] Department of Rheumatology, Instituto Nacional de Cardiologìa Ignacio Chàvez, Juan Badiano # 1, Tlalpan, Mèxico, Distrito Federal
关键词
Heart Lesion; Lupus Anticoagulant; Renal Vein Thrombosis; Rheumatol; Systemic Lupus Erythematosus;
D O I
10.1007/s11926-000-0089-4
中图分类号
学科分类号
摘要
A growing body of evidence suggests that aPL are not only serological markers of the antiphospholipid syndrome (APS), but may also directly contribute to the development of thrombosis and other manifestations, including the APS vasculopathy. The latter has been documented in leptmeninges, lung, skin, myocardium, peripheral arteries, and kidney. Renal lesions, a common feature of primary antiphospholipid syndrome (PAPS), include occlusion of principal renal arteries or their main branches, TMA, cortical ischemia, and renal vein thrombosis. Within the cardiac manifestations associated with aPL, valvular involvement is the most common. Histologic findings in valve specimens are consistent with a noninflammatory lesion characterized by intravalvular capillary thrombosis, laminar or verrucous superficial thrombosis, vascular proliferation, fibrosis, and calcification. Even though there is general consensus that endothelial damage triggers the chain of events that results in valve thickening, fusion, rigidity, and ultimately functional abnormalities, we believe that more experimental work remains to be done on the initial valve insult in APS. © 2000, Current Science Inc.
引用
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页码:262 / 270
页数:8
相关论文
共 60 条
[1]  
Bowles C.A., Vasculopathy associated with the antiphospholipid antibody syndrome, Rheum Dis Clin North Am, 16, pp. 471-480, (1990)
[2]  
Alegre V.A., Winkelmann R.K., Histopathologic and immunofluorescence study of skin lesions associated with circulating lupus anticoagulant, J Am Acad Dermatol, 19, pp. 117-124, (1988)
[3]  
Alarcon-Segovia D., Cardiel M.H., Reyes E., Antiphospholipid arterial vasculopathy, J Rheumatol, 16, pp. 762-767, (1989)
[4]  
Hughson M.D., McCarty G.A., Brumback R.A., Spectrum of vascular pathology affecting patients with the antiphospholipid syndrome, Human Pathol, 26, pp. 716-724, (1995)
[5]  
Roubey R.A.S., Mechanisms of autoantibody-mediated thrombosis, Lupus, 7, pp. 114-119, (1998)
[6]  
Comp P.C., De B.L.E., Esmon N.L., Et al., Human thrombomodulin is inhibited by IgG from two patients with non-specific anticoagulants [Abstract], Blood, 62, (1983)
[7]  
Oosting J.D., Derksen R.H., Bobbink I.W., Et al., Antiphospholipid antibodies directed against a combination of phospholipid with prothrombin, protein C, or protein S: an explanation for their pathogenic mechanism?, Blood, 81, pp. 2618-2625, (1993)
[8]  
Matsuda J., Gohchi K., Kawasugi K., Et al., Inhibitory activity of anti-b2-glycoprotein 1 antibody on factor Va degradation by activated-protein C and its cofactor protein S, Am J Hematol, 49, pp. 89-91, (1995)
[9]  
Stankiewickz A.J., Steiner M., Lally E.V., Et al., Abnormally high level of C4b binding protein and deficiency of free fraction of protein S in a patient with systemic lupus erythematosus and recurrent thromboses, J Rheumatol, 18, pp. 82-87, (1991)
[10]  
Ruiz-Arguelles G., Ruiz-Arguelles A., Alarcon-Segovia D., Et al., Natural anticoagulants in systemic lupus erythematosus. Deficiency of protein S bound to C4bp associates with recent history of venous thromboses, antiphospholipid antibodies, and the antiphospholipid syndrome, J Rheumatol, 18, pp. 552-558, (1991)