Regular ArticleLibman–Sacks endocarditis associated with antiphospholipid syndrome and infection☆
Section snippets
Conclusion
Our results show that TLRVYK is one of the target epitopes for anti-β2GPI Abs located on deformed valves from a patient with APS. Previously, we showed that this peptide shares common sequence with different bacterial and viral antigens, and anti-TLRVYK Abs generated as a response to the pathogens could induce experimental APS in naïve mice. Based on these studies and Libman–Sacks report on the infectious history of their patients, we raise the possibility that Libman–Sacks nonbacterial
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Cited by (28)
Neuropsychiatric involvement in systemic lupus erythematosus: A review
2021, Autoimmunity ReviewsCitation Excerpt :In the case of arterial thrombotic recurrences receiving standard anticoagulation, treatment can be optimized by increasing the anticoagulation dose (INR 3–4), changing to low molecular weight heparin or associating antiaggregation with low-dose aspirin, hydroxychloroquine or statins [27]. Libman-Sacks endocarditis is typical in patients with SLE, especially if they are carriers of APS antibodies [31]. Usually the left valves are affected, principally the mitral.
Antiphospholipid syndrome
2019, The Autoimmune DiseasesAntiphospholipid Syndrome: Role of Vascular Endothelial Cells and Implications for Risk Stratification and Targeted Therapeutics
2017, Journal of the American College of CardiologyCitation Excerpt :Ziporen et al. (98) demonstrated deposits of aPLs and complement on deformed heart valves of patients with APS. Blank et al. (99) identified target epitopes of anti-β2-GP1 antibodies on valvular endothelial cell β2-GP1 receptors. These findings suggest that the pathogenesis could include aPL-mediated valvular endothelial cell activation with complement fixation, similar to endothelial cell injury in other vascular beds.
Cardiac manifestations in antiphospholipid syndrome
2007, Autoimmunity ReviewsCitation Excerpt :Some studies suggest that APA may play an important role in the development of vegetations in Libman–Sacks endocarditis [6,8,9,63]. Studies with two β2GPI-related peptides also mimicking common pathogens suggested that Libman–Sacks endocarditis may have infectious origin [63]. In addition, valvular disease is detected in about one-third of APS patients and valvular thrombus formation may exist in APS [58,59].
Cardiac Manifestations in the Antiphospholipid Syndrome
2006, Rheumatic Disease Clinics of North AmericaCitation Excerpt :Shoenfeld and colleagues [26] suggest molecular mimicry between microbial products and β2GPI as a mechanism by which pathogenic aPL may be generated in APS. Blank and colleagues [27] showed that some anti-β2GPI deposited on patients valves are able to recognize a synthetic β2GPI-related peptide (TLRVYK) that shares common sequence with different bacterial and viral antigens, raising the possibility that bacterial antigen induces a crossreacting antibody that leads to Libman-Sacks nonbacterial endocarditis. Qaddoura and colleagues [28] published four cases of primary APS patients with valve disease.
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Contribution to the Conference XIth International Congress on Antiphospholipid Antibodies, 14–18th November 2004, Sydney Australia. This work was supported by a grant given by the Israeli Chief Scientist #4706.