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===={{CMG}}; {{AE}} {{Aneeza Jamshed}}==== | |||
=LIBMAN-SACK ENDOCARDITIS:= | |||
===OVERVIEW:=== | |||
Libman-sack endocarditis is the one of the cardiac manifestations of autoimmune systemic diseases most commonly [[Systemic lupus erythematosus|Systemic Lupus Erythematosus]]. It may also be a finding in malignancy with the non-bacterial non-thrombotic involvement of the valves, most commonly the aortic and mitral valve. The most common complications include embolic phenomenon like cerebrovascular disease and infective endocarditis with valvular insufficeincy. The disease activity and titer of the antibodies in Systemic Lupus Erythematosus can be linked to Libman-sack Endocarditis<ref name="pmidPMID: 20422938">{{cite journal| author=Carrillo-Esper R, Carrillo-Córdova JR, Carrillo-Córdova LD, Carrillo-Córdova CA| title=[Libman-Sacks endocarditis]. | journal=Gac Med Mex | year= 2010 | volume= 146 | issue= 1 | pages= 67-9 | pmid=PMID: 20422938 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20422938 }} </ref>. | |||
<ref name=" | ===HISTORICAL PERSPECTIVES:=== | ||
Libman and Sack in 1924, first coined this term for the sterile verrucous vegetations of the mitral and aortic valves in four patients in New York<ref name="pmidPMID: 19089657">{{cite journal| author=Lee JL, Naguwa SM, Cheema GS, Gershwin ME| title=Revisiting Libman-Sacks endocarditis: a historical review and update. | journal=Clin Rev Allergy Immunol | year= 2009 | volume= 36 | issue= 2-3 | pages= 126-30 | pmid=PMID: 19089657 | doi=10.1007/s12016-008-8113-y | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19089657 }} </ref>. | |||
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===PATHOPHYSIOLOGY:=== | |||
Endothelial dysfunction and hypercoagulable state are the two most important events in the process of non-thrombotic non-bacterial endocarditis (NTBE), that lead to vegetation formation on the valves <ref name="pmidPMID: 32536317">{{cite journal| author=Yoo BW, Lee SW, Song JJ, Park YB, Jung SM| title=Clinical characteristics and long-term outcomes of Libman-Sacks endocarditis in patients with systemic lupus erythematosus. | journal=Lupus | year= 2020 | volume= 29 | issue= 9 | pages= 1115-1120 | pmid=PMID: 32536317 | doi=10.1177/0961203320930097 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32536317 }} </ref>. In Systemic Lupus erythematosus and other autoimmune conditions, the formation of autoantibodies may damage he native valves creating a nidus for the formation of vegetation the vegetations can be small (less than 1mm), histopathologically consisting of fibrin, platelets thrombi, mono-nuclear cells and immune complexes.<ref name="pmidpmid:24029368">{{cite journal| author=Roldan CA, Sibbitt WL, Qualls CR, Jung RE, Greene ER, Gasparovic CM | display-authors=etal| title=Libman-Sacks endocarditis and embolic cerebrovascular disease. | journal=JACC Cardiovasc Imaging | year= 2013 | volume= 6 | issue= 9 | pages= 973-83 | pmid=pmid:24029368 | doi=10.1016/j.jcmg.2013.04.012 | pmc=3941465 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24029368 }} </ref> | |||
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===ETIOLOGY:=== | |||
The major phenomenon involved in the etiology of Lib-man sack endocarditis are Systemic Lupus Erythematosus, Malignancy and Antiphospholipid syndrome. The prevalence of NTBE in malignancy is reported to be '''1.25%''' as compared to 0.25% in general population, among which '''2.7%''' is accounted for by the solid organ malignancies. About '''33%''' prevalence is recorded in patients with either primary or secondary anti-phospholipid syndrome. A significant correlation of '''6% to 11%''' exists between lupus findings and NTBE.<ref name="pmidhttps://doi.org/10.1016/j.jaut.2007.11.011">{{cite journal| author=Schmoldt A, Benthe HF, Haberland G| title=Digitoxin metabolism by rat liver microsomes. | journal=Biochem Pharmacol | year= 1975 | volume= 24 | issue= 17 | pages= 1639-41 | pmid=https://doi.org/10.1016/j.jaut.2007.11.011 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10 }} </ref> | |||
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[[Libman-Sacks endocarditis# | [[Libman-Sacks endocarditis#Etiology|Etiology]] | ||
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Latest revision as of 12:30, 6 April 2021
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aneeza Jamshed, M.B.B.S.[2]
LIBMAN-SACK ENDOCARDITIS:
OVERVIEW:
Libman-sack endocarditis is the one of the cardiac manifestations of autoimmune systemic diseases most commonly Systemic Lupus Erythematosus. It may also be a finding in malignancy with the non-bacterial non-thrombotic involvement of the valves, most commonly the aortic and mitral valve. The most common complications include embolic phenomenon like cerebrovascular disease and infective endocarditis with valvular insufficeincy. The disease activity and titer of the antibodies in Systemic Lupus Erythematosus can be linked to Libman-sack Endocarditis[1].
HISTORICAL PERSPECTIVES:
Libman and Sack in 1924, first coined this term for the sterile verrucous vegetations of the mitral and aortic valves in four patients in New York[2].
PATHOPHYSIOLOGY:
Endothelial dysfunction and hypercoagulable state are the two most important events in the process of non-thrombotic non-bacterial endocarditis (NTBE), that lead to vegetation formation on the valves [3]. In Systemic Lupus erythematosus and other autoimmune conditions, the formation of autoantibodies may damage he native valves creating a nidus for the formation of vegetation the vegetations can be small (less than 1mm), histopathologically consisting of fibrin, platelets thrombi, mono-nuclear cells and immune complexes.[4]
ETIOLOGY:
The major phenomenon involved in the etiology of Lib-man sack endocarditis are Systemic Lupus Erythematosus, Malignancy and Antiphospholipid syndrome. The prevalence of NTBE in malignancy is reported to be 1.25% as compared to 0.25% in general population, among which 2.7% is accounted for by the solid organ malignancies. About 33% prevalence is recorded in patients with either primary or secondary anti-phospholipid syndrome. A significant correlation of 6% to 11% exists between lupus findings and NTBE.[5]
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Libman-Sacks endocarditis Microchapters |
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Differentiating Libman-Sacks Endocarditis from other Diseases |
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Reference
- ↑ Carrillo-Esper R, Carrillo-Córdova JR, Carrillo-Córdova LD, Carrillo-Córdova CA (2010). "[Libman-Sacks endocarditis]". Gac Med Mex. 146 (1): 67–9. PMID 20422938 PMID: 20422938 Check
|pmid=value (help). - ↑ Lee JL, Naguwa SM, Cheema GS, Gershwin ME (2009). "Revisiting Libman-Sacks endocarditis: a historical review and update". Clin Rev Allergy Immunol. 36 (2–3): 126–30. doi:10.1007/s12016-008-8113-y. PMID 19089657 PMID: 19089657 Check
|pmid=value (help). - ↑ Yoo BW, Lee SW, Song JJ, Park YB, Jung SM (2020). "Clinical characteristics and long-term outcomes of Libman-Sacks endocarditis in patients with systemic lupus erythematosus". Lupus. 29 (9): 1115–1120. doi:10.1177/0961203320930097. PMID 32536317 PMID: 32536317 Check
|pmid=value (help). - ↑ Roldan CA, Sibbitt WL, Qualls CR, Jung RE, Greene ER, Gasparovic CM; et al. (2013). "Libman-Sacks endocarditis and embolic cerebrovascular disease". JACC Cardiovasc Imaging. 6 (9): 973–83. doi:10.1016/j.jcmg.2013.04.012. PMC 3941465. PMID pmid:24029368 Check
|pmid=value (help). - ↑ Schmoldt A, Benthe HF, Haberland G (1975). "Digitoxin metabolism by rat liver microsomes". Biochem Pharmacol. 24 (17): 1639–41. PMID https://doi.org/10.1016/j.jaut.2007.11.011 Check
|pmid=value (help).