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Journal articles on the topic 'Antiphospholipid syndrome'

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Author: Grafiati

Published: 4 June 2021

Last updated: 9 March 2023

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1

Dutra, Livia Almeida, Pedro Braga-Neto, José Luiz Pedroso, and Orlando Graziani Povoas Barsottini. "Sneddon's syndrome: case report and review of its relationship with antiphospholipid syndrome." Einstein (São Paulo) 10, no. 2 (June 2012): 230–32. http://dx.doi.org/10.1590/s1679-45082012000200018.

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The Sneddon's syndrome is a rare disorder characterized by the occurrence of cerebrovascular disease associated with livedo reticularis. The antiphospholipid syndrome is the most frequent type of acquired thrombophilia, defined by the occurrence of thrombosis or pregnancy morbidity in the presence of persistently positive antiphospholipid antibodies. Approximately 80% of Sneddon's syndrome patients have an antiphospholipid antibody marker. These antibodies may play a pathogenetic role in some cases of Sneddon's syndrome, and many authors consider these two syndromes as the same entity. Although clinical features of antiphospholipid syndrome and Sneddon's syndrome may overlap, there is a distinction between clinical and laboratory evidence suggesting that these two entities are different diseases. A recent finding of coagulopathies, including elevated levels of coagulation factor VII, decreased levels of protein S, and activated protein C in Sneddon's syndrome patients suggested a possible biological link between the vasculopathy and a primary coagulopathy. Moreover, the clinical course seems to be progressive in Sneddon's syndrome patients and includes increase of disability and cognitive deterioration, more arterial involvement, and the antiphospholipid syndrome shows a more benign course. Both syndromes share clinical and laboratory features, and whether Sneddon's syndrome represents a spectrum of antiphospholipid syndrome remains unclear. Sneddon's syndrome patients have a worse prognosis and may represent a subgroup of patients who demands more rigorous follow-up. It is important to recognize the Sneddon's syndrome, particularly because stroke episodes may be prevented through appropriate treatment.

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2

Khamashta, Munther A., and Graham R. V. Hughes. "Antiphospholipid antibodies and antiphospholipid syndrome." Current Opinion in Rheumatology 7, no. 5 (September 1995): 389–94. http://dx.doi.org/10.1097/00002281-199509000-00005.

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3

Pavlovic, Dragan, and Aleksandra Pavlovic. "Antiphospholipid syndrome." Srpski arhiv za celokupno lekarstvo 138, no. 9-10 (2010): 651–57. http://dx.doi.org/10.2298/sarh1010651p.

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Antiphospholipid syndrome (APS) is an autoimmune disease with recurrent thromboses and pregnancy complications (90% are female patients) that can be primary and secondary (with concomitant autoimmune disease). Antiphospholipid antibodies are prothrombotic but also act directly with brain tissue. One clinical and one laboratory criterion is necessary for the diagnosis of APS. Positive serological tests have to be confirmed after at least 12 weeks. Clinical picture consists of thromboses in many organs and spontaneous miscarriages, sometimes thrombocytopaenia and haemolytic anaemia, but neurological cases are the most frequent: headaches, stroke, encephalopathy, seizures, visual disturbances, Sneddon syndrome, dementia, vertigo, chorea, balism, transitory global amnesia, psychosis, transversal myelopathy and Guillain-Barre syndrome. About 50% of strokes below 50 years of age are caused by APS. The first line of therapy in stroke is anticoagulation: intravenous heparin or low-weight heparins. In chronic treatment, oral anticoagulation and antiplatelet therapy are used, warfarin and aspirin, mostly for life. In resistant cases, corticosteroids, intravenous immunoglobulins and plasmapheresis are necessary. Prognosis is good in most patients but some are treatment-resistant with recurrent thrombotic events and eventually death.

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4

IKEDA, Yasuo. "Antiphospholipid Syndrome." Japanese Journal of Thrombosis and Hemostasis 2, no. 2 (1991): 112–21. http://dx.doi.org/10.2491/jjsth.2.112.

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5

ABE, Nobuya, and Tatsuya ATSUMI. "Antiphospholipid syndrome." Japanese Journal of Thrombosis and Hemostasis 29, no. 3 (2018): 294–306. http://dx.doi.org/10.2491/jjsth.29.294.

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6

Santos, Thaís da Silva, Izabel Galhardo Demarchi, Tatiane França Perles Mello, Jorge Juarez Vieira Teixeira, and Maria Valdrinez Campana Lonardoni. "Antiphospholipid Syndrome." REVISTA CIÊNCIAS EM SAÚDE 9, no. 4 (November 25, 2019): 37–42. http://dx.doi.org/10.21876/rcshci.v9i4.892.

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Antiphospholipid syndrome (APS) was characterized as an autoimmune condition with the production of antiphospholipid antibodies (aPL) associated with thrombosis and morbidity in pregnancy. The prevalence of aPL in the population ranges from 1% to 5% in patients with APS. The hypotheses regarding pathophysiological mechanisms are strongly related to binding proteins and antiphospholipid antibodies. The exact mechanisms by which they lead to clinical manifestations appear to be heterogeneous, but it is believed which aPL contribute to the cellular activation/coagulation, and so cause the thrombotic events. The treatment of APS should be an individual character and several factors should be taken into accounts, such as a number of antibodies, the age of the patient and the history of thrombotic events.

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7

ICHIKAWA, Kenji, Akito TSUTSUMI, Eiji MATSUURA, and Takao KOIKE. "Antiphospholipid Syndrome." Internal Medicine 38, no. 2 (1999): 170–73. http://dx.doi.org/10.2169/internalmedicine.38.170.

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8

Makarenko, E. V. "ANTIPHOSPHOLIPID SYNDROME." Health and Ecology Issues, no. 4 (December 28, 2017): 4–11. http://dx.doi.org/10.51523/2708-6011.2017-14-4-1.

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Antiphospholipid syndrome is autoimmune acquired thrombophilia associated with the formation of antibodies to phospholipids, which is manifested by recurrent venous or arterial thrombosis and/or pathology of pregnancy. Antiphospholipid antibodies are a heterogeneous group of autoantibodies interacting with phospholipids, which are components of cell membranes and phospholipid-binding proteins of blood plasma. Antiphospholipid syndrome can affect vessels of any caliber and localization, with thrombosis accompanied by no morphological signs of inflammation in the wall of the vessel. Obstetrical pathology is manifested by loss of the fetus, which can occur at any time of pregnancy, as well as other complications of pregnancy, such as preeclampsia and placental insufficiency. Based on the classification criteria, antiphospholipid syndrome is diagnosed if one of the clinical criteria (thrombosis or pregnancy complication) and one of the laboratory criteria including the lupus anticoagulant, antibodies to cardiolipin or β2-glycoprotein I, are revealed. The main tactic of the treatment of patients with antiphospholipid syndrome is to prevent thrombosis. For this purpose, the traditional therapy with anticoagulants and antiaggregants is applied. In addition, new medicines are being developed and evaluated

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9

Koike, Takao. "Antiphospholipid syndrome." Ensho 20, no. 5 (2000): 571–80. http://dx.doi.org/10.2492/jsir1981.20.571.

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10

Arnout, Jef, and Milosz Jankowski. "Antiphospholipid syndrome." Hematology Journal 5 (2004): S1—S5. http://dx.doi.org/10.1038/sj.thj.6200412.

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11

Jallow, T., D. D'Cruz, and H. Lempp. "Antiphospholipid syndrome." BMJ 350, apr02 3 (April 2, 2015): h1426. http://dx.doi.org/10.1136/bmj.h1426.

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12

Greaves, M. "Antiphospholipid syndrome." Journal of Clinical Pathology 50, no. 12 (December 1, 1997): 973–74. http://dx.doi.org/10.1136/jcp.50.12.973.

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13

Zuo, Yu, Hui Shi, Chun Li, and Jason S. Knight. "Antiphospholipid syndrome." Chinese Medical Journal 133, no. 8 (April 2020): 929–40. http://dx.doi.org/10.1097/cm9.0000000000000705.

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14

Espinosa, Gerard, and Ricard Cervera. "Antiphospholipid syndrome." Arthritis Research & Therapy 10, no. 6 (2008): 230. http://dx.doi.org/10.1186/ar2536.

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15

Asherson, Ronald A., and Ricard Cervera. "Antiphospholipid Syndrome." Journal of Investigative Dermatology 100, no. 1 (January 1993): 21S—27S. http://dx.doi.org/10.1111/1523-1747.ep12355193.

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16

Nash, Michael J., and Hannah Cohen. "Antiphospholipid Syndrome." Medicine 30, no. 10 (October 2002): 31–32. http://dx.doi.org/10.1383/medc.30.10.31.28251.

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17

Austin, Steven, and Hannah Cohen. "Antiphospholipid syndrome." Medicine 34, no. 11 (November 2006): 472–75. http://dx.doi.org/10.1053/j.mpmed.2006.08.012.

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18

Alhasson, Hussam, Abdullah Abdullah, Amr Salama, Richard Alweis, and Timothy Woodlock. "Antiphospholipid Syndrome." American Journal of Therapeutics 27, no. 3 (2020): e328-e330. http://dx.doi.org/10.1097/mjt.0000000000000995.

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19

van Os, G. M. A., R. T. Urbanus, C. Agar, J. C. M. Meijers, and P. G. de Groot. "Antiphospholipid syndrome." Hämostaseologie 30, no. 03 (2010): 139–43. http://dx.doi.org/10.1055/s-0037-1619044.

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SummaryThe antiphospholipid syndrome (APS) is a non-inflammatory autoimmune disease characterized by the presence of antiphospholipid antibodies (aPL) in the plasma of patients with vascular thrombosis, recurrent complications of pregnancy, or both (1, 2). The presence of aPL in plasma of patients can be detected with either a prolongation of phospholipid dependent coagulation tests (lupus anticoagulant, LAC), or with solid phase immune assays against the protein β2-glycoprotein I (β2-GPI) or the phospholipid cardiolipin (anti-β2-GPI antibody ELISA and anti-cardiolipin antibody ELISA, respectively) (3). For a long time there was a lot of confusion on who had the syndrome and who not. To solve this dispute, an international consensus meeting was organized in Sapporo in 1999 to formulate classification criteria for patients with the antiphospholipid syndrome (4). These criteria have been updated in 2004 at another international consensus meeting in Sydney (5). The classification criteria were defined for scientific purposes and were aimed to be used as inclusion criteria in patient related studies. They were specifically not defined for diagnostic purposes. However, current practice is that these criteria are used as a diagnostic tool. This is very unfortunate because the specificity of the different aPL assays to detect the clinical manifestations that characterize APS are disputable. One of the aims of defining the criteria was to initiate studies to determine the value of the different anti-phospholipid antibody assays to serve as biomarker for the risk of thrombosis and pregnancy morbidity. The recent progress made on this important topic will be discussed.

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20

Danowski, Adriana, and Roger A. Levy. "Antiphospholipid syndrome." Revista Brasileira de Reumatologia (English Edition) 53, no. 2 (March 2013): 139–40. http://dx.doi.org/10.1016/s2255-5021(13)70018-x.

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21

Cervera, Ricard. "Antiphospholipid syndrome." Thrombosis Research 151 (March 2017): S43—S47. http://dx.doi.org/10.1016/s0049-3848(17)30066-x.

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22

Ruiz-Irastorza, Guillermo, Mark Crowther, Ware Branch, and Munther A. Khamashta. "Antiphospholipid syndrome." Lancet 376, no. 9751 (October 2010): 1498–509. http://dx.doi.org/10.1016/s0140-6736(10)60709-x.

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23

Austin, Steven, and Hannah Cohen. "Antiphospholipid syndrome." Medicine 38, no. 2 (February 2010): 101–4. http://dx.doi.org/10.1016/j.mpmed.2009.10.012.

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24

Jayakody Arachchillage, Deepa, and Hannah Cohen. "Antiphospholipid syndrome." Medicine 42, no. 3 (March 2014): 156–61. http://dx.doi.org/10.1016/j.mpmed.2013.12.001.

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25

Clark, Kristina E. N., and Ian Giles. "Antiphospholipid syndrome." Medicine 46, no. 2 (February 2018): 118–25. http://dx.doi.org/10.1016/j.mpmed.2017.11.006.

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26

Petri, Michelle. "Antiphospholipid syndrome." Translational Research 225 (November 2020): 70–81. http://dx.doi.org/10.1016/j.trsl.2020.04.006.

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27

Ravelli, Angelo, and Alberto Martini. "Antiphospholipid Syndrome." Pediatric Clinics of North America 52, no. 2 (April 2005): 469–91. http://dx.doi.org/10.1016/j.pcl.2005.01.001.

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28

Branch, D. Ware, and Munther A. Khamashta. "Antiphospholipid Syndrome." Obstetrics & Gynecology 101, no. 6 (June 2003): 1333–44. http://dx.doi.org/10.1097/00006250-200306000-00031.

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29

Damron, Dana P. "Antiphospholipid Syndrome." Obstetrics & Gynecology 102, no. 4 (October 2003): 873. http://dx.doi.org/10.1097/00006250-200310000-00040.

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30

Branch, Ware. "Antiphospholipid Syndrome." Obstetrics & Gynecology 102, no. 4 (October 2003): 873. http://dx.doi.org/10.1097/00006250-200310000-00041.

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31

Gromnica-Ihle, Erika, and W. Schössler. "Antiphospholipid Syndrome." International Archives of Allergy and Immunology 123, no. 1 (2000): 67–76. http://dx.doi.org/10.1159/000024425.

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32

Keswani, Sanjay C., and Naresh Chauhan. "Antiphospholipid Syndrome." Journal of the Royal Society of Medicine 95, no. 7 (July 2002): 336–42. http://dx.doi.org/10.1177/014107680209500705.

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33

George, Diane, and Doruk Erkan. "Antiphospholipid Syndrome." Progress in Cardiovascular Diseases 52, no. 2 (September 2009): 115–25. http://dx.doi.org/10.1016/j.pcad.2009.06.005.

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34

Nelson, Gregory N. "Antiphospholipid Syndrome." Journal of Hand Surgery 35, no. 11 (November 2010): 1890–92. http://dx.doi.org/10.1016/j.jhsa.2010.07.003.

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35

Manson, J. J., and D. A. Isenberg. "Antiphospholipid syndrome." International Journal of Biochemistry & Cell Biology 35, no. 7 (July 2003): 1015–20. http://dx.doi.org/10.1016/s1357-2725(02)00313-8.

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36

Corban, Michel T., Ali Duarte-Garcia, Robert D. McBane, Eric L. Matteson, Lilach O. Lerman, and Amir Lerman. "Antiphospholipid Syndrome." Journal of the American College of Cardiology 69, no. 18 (May 2017): 2317–30. http://dx.doi.org/10.1016/j.jacc.2017.02.058.

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37

Gezer, Sefer. "Antiphospholipid syndrome." Disease-a-Month 49, no. 12 (December 2003): 696–741. http://dx.doi.org/10.1016/j.disamonth.2003.10.001.

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38

Khamashta, M., and G. R. Hughes. "Antiphospholipid syndrome." BMJ 307, no. 6909 (October 9, 1993): 883–84. http://dx.doi.org/10.1136/bmj.307.6909.883.

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39

Martinez, Alan P., and Mark T. Cunningham. "Antiphospholipid syndrome." Blood Coagulation & Fibrinolysis 27, no. 5 (July 2016): 557–62. http://dx.doi.org/10.1097/mbc.0000000000000550.

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40

Annem, Chandrahasa, and Richard A. Furie. "Antiphospholipid Syndrome." JCR: Journal of Clinical Rheumatology 23, no. 5 (August 2017): 278–84. http://dx.doi.org/10.1097/rhu.0000000000000564.

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41

&NA;. "Antiphospholipid Syndrome." Obstetric Anesthesia Digest 26, no. 2 (June 2006): 52–53. http://dx.doi.org/10.1097/00132582-200606000-00008.

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42

Asherson, Ronald A., and Ricard Cervera. "Antiphospholipid Syndrome." Journal of Investigative Dermatology 100, no. 1 (1993): S21—S27. http://dx.doi.org/10.1038/jid.1993.19.

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43

Lim, Wendy. "Antiphospholipid syndrome." Hematology 2013, no. 1 (December 6, 2013): 675–80. http://dx.doi.org/10.1182/asheducation-2013.1.675.

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Abstract The antiphospholipid syndrome (APS) is defined by venous or arterial thrombosis and/or pregnancy morbidity in patients with persistent presence of antiphospholipid antibodies (aPLs). Catastrophic APS is the most severe form of APS, which is associated with rapid development of microvascular thrombosis resulting in multiorgan failure in patients with aPLs. Patients with APS and catastrophic APS are recognized to have a high risk of recurrent thrombosis that can occur despite anticoagulant therapy. Although antithrombotic therapy remains the mainstay of treatment, bleeding manifestations can complicate management and contribute to increased morbidity. Patients with persistently elevated aPL levels, particularly those who exhibit positive testing for lupus anticoagulant, anticardiolipin antibodies, and anti-β2GPI antibodies (triple positivity), appear to be at increased risk for thrombosis and pregnancy complications, whereas isolated positivity for aPLs appears to be associated with low risk. Recognizing that patients with APS have different thrombotic risk profiles may assist clinicians in assessing the risks and benefits of anticoagulation. The optimal type, intensity, and duration of anticoagulation in the treatment of APS remain controversial, particularly for arterial thrombosis and recurrent thrombosis. Future studies that delineate thrombotic risk in APS and evaluate current and novel anticoagulants as well as nonanticoagulant therapies are required.

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44

Keswani, S. C., and N. Chauhan. "Antiphospholipid syndrome." JRSM 95, no. 7 (July 1, 2002): 336–42. http://dx.doi.org/10.1258/jrsm.95.7.336.

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45

Erkan, Doruk, and Michael D. Lockshin. "Antiphospholipid syndrome." Current Opinion in Internal Medicine 5, no. 4 (August 2006): 378–84. http://dx.doi.org/10.1097/01.bor.0000218943.89365.13.

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46

Lau, CS. "Antiphospholipid Syndrome." Vascular Medicine Review vmr-5, no. 1 (February 1994): 33–45. http://dx.doi.org/10.1177/1358863x9400500104.

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47

Vreede, Andrew P., Paula L. Bockenstedt, and Jason S. Knight. "Antiphospholipid syndrome." Current Opinion in Rheumatology 29, no. 5 (September 2017): 458–66. http://dx.doi.org/10.1097/bor.0000000000000410.

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48

Khamashta, M., M. Taraborelli, S. Sciascia, and A. Tincani. "Antiphospholipid syndrome." Best Practice & Research Clinical Rheumatology 30, no. 1 (February 2016): 133–48. http://dx.doi.org/10.1016/j.berh.2016.04.002.

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49

Sammaritano, Lisa R. "Antiphospholipid syndrome." Best Practice & Research Clinical Rheumatology 34, no. 1 (February 2020): 101463. http://dx.doi.org/10.1016/j.berh.2019.101463.

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50

Cuadrado, M. J., and C. Lopez-Pedrera. "Antiphospholipid syndrome." Clinical and Experimental Medicine 3, no. 3 (November 2003): 129–39. http://dx.doi.org/10.1007/s10238-003-0016-x.

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