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Academic literature on the topic 'Antiphospholipid syndrome'

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Published: 4 June 2021
Last updated: 9 March 2023

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Journal articles on the topic "Antiphospholipid syndrome"

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

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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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Dissertations / Theses on the topic "Antiphospholipid syndrome"

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Dennen, Gabrielle. "Assessment of perinatal nurses' knowledge of antiphospholipid syndrome and nursing management of pregnant women with antiphospholipid syndrome." Honors in the Major Thesis, University of Central Florida, 2013. http://digital.library.ucf.edu/cdm/ref/collection/ETH/id/841.

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Ames, Paul Richard Julian. "Atherogenesis and atherosclerosis in primary antiphospholipid syndrome." Doctoral thesis, Faculdade de Ciências Médicas. UNL, 2013. http://hdl.handle.net/10362/10293.

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ABSTRACT: In the late seventies the term “Haematological Stress Syndrome” defined some haematological abnormalities appearing in the course of acute and chronic disorders, such as raised plasma levels of fibrinogen (FNG) and factor VIII, reduced fibrinolytic activity and hyperviscosity. In the early nineties the “Membrane stress syndrome hypothesis” proposed the unification of the concepts of haematological stress syndrome with those of oxidation, inflammation and immune activation to explain the pathogenesis of the antiphospholipid syndrome (APS) Antiphospholipid antibodies, coagulation, fibrinolysis and thrombosis. This chapter investigated the occurrence of the “Haematological Stress Syndrome” and thrombosis in 144 participants positive for aPL detected by clotting and immune tests. Among the clotting assays for the detection of lupus anticoagulant, dilute Russell's viper venom time better correlated with a history of venous thrombosis than activated partial thromboplastin time (p<0.0002 vs p<0.009) and was the only test correlated with a history of arterial thrombosis (p<0.01). By regression analysis, serum levels of IgG anticardiolipin antibodies (aCL) associated with the number of venous occlusions (p<0.001). With regards to FNG and von Willebrand factor (vWF), the former rose by 36% (95% CI; 21%, 53%) and the latter by 50% (95% CI; 29%, 75%) at the first venous occlusion and remained unchanged after subsequent occlusions. At variance FNG rose by 45% (95% CI; 31%, 60%) per arterial occlusion and vWF by 27% (95% CI; 10%, 47%) per arterial occlusion throughout. The coagulation/fibrinolytic balance was cross-sectionally evaluated on 18 thrombotic PAPS patients, 18 subjects with persistence of idiopathic aPL and in healthy controls. Markers of thrombin generation prothrombin fragment 1+2 (F1+2), thrombin-antithrombin complex (TAT) and of fibrin turnover D-Dimer (D-D) were higher in thrombotic (p=0.006)and non-thrombotic subjects (p=0.0001) than in controls as were those of D-D (p<0.0001 and p=0.003 respectively). TAT levels did not differ. Gender analysed data revealed blunted tPA release (hence a negative venous occlusion test) in thrombotic females but neither in thrombotic males (p=0.01) nor in asymptomatic subjects of either sex. Also, in both patient groups females had higher mean PAI than males (p<0.0002) and control females (p<0.02). The activity of factor XIII (FXIIIa) was evaluated was evaluated in 29 patients with PAPS, 14 persistent carriers of aPL without thrombosis, 24 thrombotic patients with inherited thrombophilia, 28 healthy controls and 32 patients with mitral and aortic valve prosthesis as controls for FXIII only. FXIIIa was highest in PAPS (p=0.001), particularly in patients with multiple (n=12) than single occlusion (p=0.02) and in correlation with PAI (p=0.003) and FNG (p=0.005). Moreover FXIIIa was strongly associated with IgG aCL and IgG anti-2GPI (p=0.005 for both) in the PAPS group and to a lesser degree in the aPL group (FXIIIa with IgG aCL, p=0.02, with IgG anti-2GPI, p=0.04). Altogether these results indicate: 1) a differential relationship of aPL, vWF and FNG with venous and arterial thrombosis; 2) heightened thrombin generation, accelerated fibrin turnover and fibrinolysis abnormalities also in asymptomatic carriers of aPLs; 3) enhanced FXIIIa that may contribute to atherothrombosis via increased fibrin/fibrinogen cross-linking. Lipid profile, lipid peroxidation and anti-lipoprotein antibodies in thrombotic primary antiphospholipid syndrome. Given the atherogenic lipid profile of SLE, the same possibility was explored in PAPS by comparing high-density lipoprotein (HDL), low-density lipoprotein (LDL), total cholesterol (CHO), apolipoprotein AI (ApoAI), apolipoprotein B (ApoB), triglycerides (TG), anti-lipoprotein antibodies, beta-2-glycoprotein I complexed to oxidized low-density lipoprotein (oxLDL-2GPI) and C-reactive protein (CRP) in 34 thrombotic PAPS patients compared to 36 thrombotic patients with inherited thrombophilia (IT), to 18 subjects persistently positive for antiphospholipid antibodies (aPL) with no underlying autoimmune or non-autoimmune disorders and to 28 healthy controls. Average concentrations of HDL (p<0.0001), LDL (p<0.0001), CHO (p=0.0002), ApoAI (p=0.002) were lower in PAPS whereas average TRY was higher (p=0.01) than other groups. Moreover PAPS showed higher IgG anti-HDL (p=0.01) and IgG anti-ApoAI (p<0.0001) as well as greater average oxLDL-2GPI (p=0.001) and CRP (p=0.003). Within PAPS, IgG anti-HDL correlated negatively to HDL (p=0.004) and was an independent predictor of oxLDL-2GPI (p=0.009). HDL and ApoAI correlated negatively with CRP (p=0.001 and p=0.007, respectively). IgG anti-HDL may hamper the antioxidant and anti-inflammatory effect of HDL favouring low-grade inflammation and enhanced oxidation in thrombotic PAPS. Indeed plasma 8-epi-prostaglandin F2α (a very specific marker of lipid peroxidation) was significantly higher in 10 patients with PAPS than 10 age and sex matched healthy subjects (p=0.0002) and strongly related to the titre of plasma IgG aCL (r=0.89, p=0.0004). Hence oxidative stress, a major player in atherogenesis, also characterises PAPS. Nitric oxide and nitrative stress in thrombotic primary antiphosholipid syndrome. Oxidative stress goes hand in hand with nitrative stress and to address the latter plasma nitrotyrosine (NT, marker of nitrative stress), nitrite (NO2-) and nitrate (NO3-) were measured in 46 thrombotic PAPS patients, 21 asymptomatic but persistent carriers of antiphospholipid antibodies (PCaPL), 38 patients with inherited thrombophilia (IT), 33 patients with systemic lupus erythematosus (SLE) and 29 healthy controls (CTR). Average crude NT was higher in PAPS and SLE (p=0.01) whereas average plasma NO2- was lower in PAPS and average NO3- highest in SLE (p<0.0001). In PAPS, IgG aCL titer and number of vascular occlusions negatively predicted NO2-, (p=0.03 and p=0.001, respectively) whereas arterial occlusions and smoking positively predicted NO3- (p=0.05 and p=0.005). Moreover CRP (an inflammatory marker) positively predicted NT (p=0.004). Nitric oxide metabolites relates to type and number of vascular occlusions and to aPL titers, whereas nitrative stress relates to low grade marker) positively predicted NT (p=0.004). Nitric oxide metabolites relates to type and number of vascular occlusions and to aPL titers, whereas nitrative stress relates to low grade inflammation and both phenomena may have implications for thrombosis and atherosclerosis in PAPS Inflammation and immune activation in thrombotic primary antiphospholipid syndrome. To investigate inflammation and immune activation in thrombotic PAPS high-sensitivity CRP (hs-CRP), serum amyloid A (SAA), oxLDL-2GPI, CRP bound to oxLDL-2GPI (CRP-oxLDL-2GPI) (as inflammatory markers) neopterin (NPT) and soluble CD14 (sCD14) (as immune activation markers) were measured by ELISA in 41 PAPS patients, in 44 patients with inherited thrombophilia (IT) and 39 controls (CTR). Compared to other groups, PAPS presented with higher plasma concentrations of inflammatory, hs-CRP (p=0.0004), SAA (p<0.01), CRP-oxLDL-2GPI (p=0.0004) and immune activation markers, NPT (p<0.0001) and sCD14 (p=0.007). By regression analysis SAA independently predicted thrombosis number (p=0.003) and NPT independently predicted thrombosis type (arterial, p=0.03) and number (p=0.04). These data confirm that low-grade inflammation and immune activation occur and relate to vascular features of PAPS. Antiphosholipid antibodies, haemostatic variables and atherosclerosis in thrombotic primary antiphospholipid syndrome To evaluate whether IgG aCL titre, haemostatic variables and the lipid profile bore any relationship to the intima media thickness (IMT) of carotid arteries high-resolution sonography was applied to the common carotid (CC), carotid bifurcation (CB) and internal carotid (IC) of 42 aPL subjects, 29 with primary thrombotic antiphospholipid syndrome and 13 with persistence of aPL in the absence of any underlying disorder. The following were measured: plasma FNG, vWF, PAI, homocysteine (HC), CHO, TG, HDL, LDL, platelet numbers and aCL of IgG and IgM isotype. By multiple regression analysis, IgG aCL titre independently predicted IMT at all carotid segments examined (p always <0.005). Plasma FNG and HC independently predicted IMT at the CB (p=0.001 and p<0.0001, respectively) and IC (p=0.03 and p<0.0001, respectively). These data strongly support an atherogenic role for IgG aCL in patients with aPL in addition to traditional risk factors. The atherosclerosis hypothesis was investigated in an age and sex-matched case-double-control study including 49 thrombotic PAPS patients (18 M, 31 F, mean age 37 ± 11), 49 thrombotic patients for IT and 49 healthy subjects. Average IMT was always greater in PAPS than control patients (CC: p=0.004, CB: p=0.013, IC: p=0.001). By dividing participants into age tertiles the IMT was greater in the second (CC: p=0.003, CB: p=0.023, IC: p=0.003) and third tertiles (CC: p=0.03, CB: p=0.004, IC: p=0.007). Conclusion: Coagulation activation, fibrinolysis depression, hightened fibrin turnover, oxidative and nitrative stress in parallel with low grade inflammation and immune activation characterise thrombotic PAPS: all these are early atherogenic processes and contribute to the demonstrated premature atherosclerosis that should be considered a clinical feature of PAPS.
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Gómez, Puerta José Alfredo. "Antiphospholipid Syndrome: Expanding the Spectrum of Autoimmune Thrombosis." Doctoral thesis, Universitat de Barcelona, 2007. http://hdl.handle.net/10803/2227.

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The antiphospholipid syndrome (APS) is an acquired prothrombotic syndrome characterized by venous or arterial thromboses and pregnancy morbidity. It can present as primary APS without any discernable underlying disease, or in association with systemic autoimmune disease [usually systemic lupus erythematosus (SLE)], infections (mainly chronic viral infections) and malignant process, among others. It may also occur rapidly over days or weeks, when it is known as "catastrophic" APS (CAPS).
The first study described one of the largest known cohorts of patients with primary APS from 4 different referral centers. The final study sample included 128 patients with primary APS with a median age of 42 years and mean follow-up of 9 years. After a median disease duration of 8.2 years, 110 (86%) patients remained with primary APS; 11 (8%) patients developed SLE; 6 (5%), LLD; and 1 (1%), myasthenia gravis. At the end of the study, 113 (88%) patients were alive and 15 (12%) patients had died. Our study confirms that progression from primary APS to SLE or LLD is unusual, even after a long follow-up.
In the second study, we evaluated 120 cases of antiphospholipid antibodies associated with malignancies with a mean age of 56 years, The main hematological malignancies found were B-cell lymphoma, spleen lymphoma and chronic myeloid leukemia. The main solid tumors were renal cell carcinoma, primary tumor of unknown origin, lung adenocarcinoma and breast carcinoma. Around one third of patients achieved aPL remission after treatment.
In the third study, we analyzed 15 cases of CAPS that appeared during pregnancy or the puerperium with a mean age at the time of the CAPS event of 27 years. In 7 of the 14 (50%) cases, CAPS appeared during pregnancy, in 6 (43%) cases it presented during puerperium and in 1 (7%) after curettage for a fetal death. The main clinical and serological characteristics were similar to those of patients with CAPS triggered by other factors, however we found some particular features including placental infarctions, pelvic vein thrombosis and myometrial thrombotic microangiopathy and HELLP syndrome.
Final conclusion: Primary APS is a widely recognized distinct entity which rarely progresses to SLE, even after long-term follow-up. APS may also be associated with other chronic disorders, such as solid tumors or hematological malignancies. In cases with the life-threatening variant of APS known as CAPS, pregnancy and the puerperium are periods of high susceptibility for the development of this often fatal form of presentation.
"SINDROME ANTIFOSFOLIPIDICO: EXPANDIENDO EL ESPECTRO CLÍNICA DE LA TROMBOSIS AUTOINMUNE"

El síndrome antifosfolipídico (SAF) es un síndrome protrombótico adquirido caracterizado por trombosis venosas y arteriales y pérdidas fetales recurrentes. Puede estar presente como SAF "primario" cuando no esta asociado a ninguna enfermedad autoinmune [fundamentalmente el lupus eritematoso sistémico (LES)] o en asociación a otros procesos tales como infecciones y procesos neoplásicos, entre otros. También puede manifestarse de una forma acelerada en días o semanas, caracterizado por trombosis de pequeños órganos y fallo multiorgánico, lo que se conoce como SAF "catastrófico".

En el primer estudio se analizó una de las series más amplia y con más largo seguimiento de pacientes con SAF primario. Se incluyeron 128 pacientes con un seguimiento medio de 9 años. Después de una duración media de la enfermedad de 8 años, 110 (86%) pacientes continúan con el diagnóstico de SAF primario, 11 (8%) pacientes desarrollaron un LES, 6 (5%) una forma incompleta de lupus ("lupus-like disease") y 1 (1%) paciente desarrolló una miastenia gravis. La presencia del test de Coombs positivo confiere un riesgo estadísticamente significativo para el desarrollo de LES. . Nuestro estudio confirma que es inusual que un SAF primario evolucione hacia un LES o una forma incompleta de lupus, incluso tras un período largo de seguimiento.
En el segundo estudio se incluyeron un total de 120 casos con anticuerpos antifosfolipídicos (AAF) asociados a procesos neoplásicos. Las principales neoplasias hematológicas relacionadas a los AAF fueron el linfoma de células B, el linfoma esplénico y la leucemia mieloide crónica. Los principales tumores sólidos fueron el carcinoma de células renales, los tumores de primario desconocido, el adenocarcinoma de pulmón y el cáncer de mama. Alrededor de una tercera parte de los paciente negativizaron los AAF después del tratamiento de la neoplasia.
En el tercer estudio se analizaron 15 pacientes con SAF catastrófico que ocurrieron durante el embarazo o el puerperio. Las características clínicas generales del SAF catastrófico durante el embarazo o el puerperio fueron similares a las del SAF catastrófico desencadenado por otros factores a excepción de una tasa mayor de abortos previos. Sin embargo se encontraron una serie de características particulares, como el síndrome de HELLP, la trombosis placentaria, la microangiopatía trombótica de miometrio o la trombosis de la vena pélvica.

CONCLUSIÓN FINAL: El SAF primario es una entidad propia ampliamente reconocida que en raras ocasiones evoluciona a un LES, incluso tras un período largo de seguimiento. El SAF puede asociarse a una serie de procesos crónicos como lo son las neoplasias hematológicas y los tumores sólidos. En aquellos casos con la variante "catastrófica" del SAF, el embarazo y el puerperio, constituyen un período de alta susceptibilidad para el desarrollo de esta variante altamente letal del SAF.
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Poulton, K. S. "Understanding mechanisms of cellular injury in the antiphospholipid syndrome." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1396605/.

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Patients with the Antiphospholipid Syndrome (APS) have circulating antiphospholipid antibodies (aPL) which cause vascular thrombosis (VT) and/or pregnancy morbidity (PM). Previously we have shown that IgG isolated from patients with APS and VT alone (APS-VT) caused activation of p38 MAPK and NFκB signalling pathways and up-regulation of tissue factor (TF) activity in monocytes. These effects were not seen with IgG from patients with APS and PM alone (APS-PM) or healthy controls. TF up-regulation caused by the APS-VT samples was reduced by p38 MAPK, NFκB, and TLR4 inhibitors, thus implicating a TLR4-MyD88 dependent signalling mechanism. Therefore, my PhD aimed to examine whether IgG isolated from patients with different manifestations of the APS have differential effects upon activation of a pregnancy related cell type; trophoblast cells and a thrombotic related cell type; endothelial cells (EC). IgG was purified from the serum of APS-VT patients, APS-PM patients and two control groups. Using a human first trimester trophoblast cell line, HTR-8 cells, I identified that APS-PM but not APS-VT increased TLR4 and TRIF mRNA expression. HTR-8 cell migration was significantly inhibited in cells treated with APS-PM but not APS-VT and this inhibited migration was restored after pre-treatment with a TLR4 inhibitor. I also identified that both APS-VT and APS-PM increased protease-activated receptor (PAR)-1 and PAR-2 mRNA expression in HTR-8 cells, which was not seen in control IgG treated cells. Work carried out in HUVEC identified that only APS-VT phosphorylated p38 MAPK and not APS-PM or healthy controls. When investigating p38 MAPK phosphorylation in HTR-8 cells however, neither APS-PM nor APS-VT phosphorylated p38 MAPK in this pregnancy related cell type. The results obtained in this thesis identify that IgG purified from patients with different clinical manifestations of the APS have differential effects on a pregnancy related cell type than they do on a thrombotic related cell type.
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Donohoe, Siobhan. "An investigation of antiphospholipid antibody associated obstetric complications." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312964.

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Giannakopoulos, Bill Clinical School St George Hospital Faculty of Medicine UNSW. "Investigations on beta 2-glycoprotein I and antiphospholipid antibodies." Publisher:University of New South Wales. Clinical School - St George Hospital, 2008. http://handle.unsw.edu.au/1959.4/41440.

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An outline of the work contained in this thesis is presented. The first chapter is a critical review of the literature pertaining to the pathophysiological mechanisms operational with regards to the antiphospholipid syndrome (APS). The syndrome is characterised by venous and arterial thrombosis, and recurrent fetal loss, in association with the persistent presence of antibodies targeting the main autoantigen beta 2-glycoprotein I (β2GPI). The second chapter reviews the literature delineating the diverse physiological functions of β2GPI, and then relates them to its role in our current understanding of the pathophysiology of APS. The third chapter presents a critical review of the evidence base for the diagnosis and management of APS. The fourth chapter describes the interaction between β2GPI and the glycoprotein Ib alpha (GPIbα) subunit of the platelet receptor GPIb-IX-V. GPIbα is an important platelet adhesion receptor, which mediates multiple additional functions on the platelet surface, including binding coagulation factor XI (FXI). The implication of the interaction between β2GPI and GPIbα on platelet activation and the release of thromboxane in the presence of anti-β2GPI antibodies is explored, as well as the intracellular pathways via which this activation occurs. The relevance of these findings to understanding APS pathogenesis, in particular thrombosis, is discussed. The fifth chapter delineates the interaction between the fifth domain of β2GPI and FXI and its activated form factor XIa (FXIa). The ability of FXIa to cleave β2GPI between lysine (Lys) 317 and threonine (Thr) 318, and modulate its function is reported. The sixth chapter describes the ability of β2GPI to inhibit FXIa autoproteolytic hydrolysis at the specific FXIa residues arginine (Arg) 507, Arg532 and Lys539. This interaction with β2GPI stabilizes FXIa activity over time, and leads to enhanced FXIa mediated fibrin formation. This is a novel physiological function of β2GPI with important implications. Recent epidemiological studies by others have emphasized the critical role of FXIa in pathological thrombus propagation. The seventh chapter defines the relevance of the FXIa residues Arg507, Arg532 and Lys539 to FXIa mediated inactivation by the main FXIa inhibitor Protease Nexin 2 (PN2), and by Antithrombin III (ATIII). Insights into future directions for research are presented and discussed within each individual chapter.
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Tolomeo, Tanya. "The role of beta2-glycoprotein I-reactive T cells in antiphospholipid syndrome." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=19246.

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Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by the presence of autoantibodies to phospholipid (PL)-binding proteins, such as beta2-glycoprotein I (beta2GPI), and clinical manifestations including thrombosis and/or recurrent pregnancy loss. Beta2GPI-reactive T cells have been shown to be activated in patients with APS, but the mechanism responsible for this activation remains unclear. Recent studies have proposed that exposure of a cryptic epitope on beta2GPI, as a consequence of binding to PL, leads to the activation of beta2GPI-autoreactive T cells in APS patients. To test this hypothesis, we evaluated the development of beta2GPI-reactive T cells in a murine model of aPL production. C57BL/6 mice were immunized repeatedly with human beta2GPI in the presence of lipopolysaccharide (LPS) to induce aPL production. High levels of circulating aPL were observed as early as the second immunization, but splenic T cell reactivity to beta2GPI was not detectable in vitro until after the fourth immunization. Splenic T cells from mice producing high levels of aPL proliferated in response to native human beta2GPI, alone or bound to anionic PL, but PL-bound beta2GPI appeared to be a more potent antigen. Beta2GPI-reactive T cells produced IL-2 and IFN-gamma, but not IL-4 or IL-10, suggesting a TH1 bias of this T cell response. These results demonstrate that T cell reactivity to beta2GPI can develop in nonautoimmune individuals repeatedly exposed to this antigen in a proinflammatory context (e.g., LPS). Our data further suggest that the beta2GPI-reactive T cells induced in this model have a TH1 bias and may be more reactive to a PL-dependent epitope on beta2GPI than to native beta2GPI.
Le syndrome antiphospholipide (SAPL) est une maladie autoimmune caractérisée par la présence d'auto-anticorps antiphospholipides (aPL) dirigés contre des protéines liant les phospholipides anioniques dont la beta2-glycoproteine I (beta2GPI), ainsi que par des manifestations cliniques incluant la thrombose et la perte foetale récurrente. Il a été démontré que des lymphocytes T spécifiques à la beta2GPI étaient activés chez les patients atteints du SAPL. Cependant, le mécanisme responsable de cette activation lymphocytaire reste nébuleux. Des études récentes ont proposé que l'exposition d'épitopes cryptiques de la beta2GPI, suite à la liaison de cette glycoprotéine à des phospholipides anioniques, engendre l'activation de lymphocytes T autoréactifs spécifiques à la beta2GPI chez les patients atteints du SAPL. Afin de vérifier cette hypothèse, nous avons évalué le développement de lymphocytes T spécifiques à la beta2GPI dans un modèle murin de production d'aPL. Des souris C57BL/6 ont été immunisées à répétition avec de la beta2GPI humaine en présence de lipopolysaccharide (LPS) dans le but d'induire la production d'aPL. Des titres élevés d'aPL circulants ont été observés dès la deuxième immunization, tandis que les lymphocytes T spécifiques à la beta2GPI n'ont été détectés que suite à la quatrième immunisation. Ainsi, les lymphocytes T provenant de la rate des souris produisant des niveaux élevés d'aPL ont proliféré en réponse à la forme native de beta2GPI et encore plus fortement en réponse au complexe beta2GPI-PL. Ces lymphocytes T réactifs à la beta2GPI ont démontré une production d'interleukine 2 et d'interféron gamma. Cependant, aucune interleukine 4 ou 10 n'
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8

Miranda, Sébastien. "Modulation de la dysfonction endothéliale et de l'altération du glycocalyx endothélial au cours du Syndrome des Antiphospholipides primaire artériel.Approche translationnelle et aspects pharmacologiques Infliximab improves endothelial dysfunction in a mouse model of antiphospholipid syndrome: role of reduced oxidative stress. New insights into antiphospholipid related endothelial dysfunction by assessment of vascular glycocalyx layer. Results from a preliminary case control study." Thesis, Normandie, 2019. http://www.theses.fr/2019NORMR006.

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Ce travail a permis chez des patients atteints d'un SAPL artériel primaire mais également dansdes modèles de cultures cellulaires et dans un modèle murin de SAPL de confirmer l'existence d'unedysfonction endothéliale et de montrer pour la première fois l’altération du GCX endothélial.L'implication de l’altération du GCX dans la survenue d'une dysfonction endothéliale, d'un étatpro-thrombotique permanent à distance de toute poussée de la maladie a pu être établie de façondirecte tant au niveau clinique qu'expérimental tout comme son association au développement d'uneathérosclérose précoce infra clinique.L'approche pharmacologique a montré l'effet favorable d'un traitement par un anticorpsmonoclonal anti-TNFα sur la dysfonction endothéliale vasomotrice et d'en caractériser lesmécanismes d'action dans le SAPL. Ainsi, son administration se traduit principalement par laréduction du stress oxydant en modulant la voie de la NADPH oxydase, en diminuant l'expression dela NOS inductible et en luttant contre le découplage de la NOS endothéliale.De même, l'utilisation de l'hydroxychloroquine dans le modèle expérimental de SAPL a pourla première fois, montré un effet protecteur de ce traitement sur la fonction endothéliale, en restaurantune vasorelaxation normale et un niveau de génération de thrombine basal après injection d'anticorpsantiphospholipides humains purifiés.Enfin, le rôle clé de l’héparanase dans l’altération du GCX a pu être démontré et sa modulationtant par l’hydroxychloroquine que par des agents spécifiques laisse entrevoir un effet protecteurendothélial bénéfique qu’il faudra évaluer dans des essais cliniques futurs
This transversal work conducted among antiphospholipid patients, mice and cells confirmedthe existence of an endothelial dysfunction and bring first evidence that glycocalyx shedding couldbe an important part of the pathophysiology of the disease. Glycocalyx shedding is associatedwith prothrombotic state, endothelial dysfunction and led to subclinical atherosclerosis.In this study, we have demonstrated that TNF alpha was responsible of increased oxidative stress anddecreased relaxation response of mesenteric arteries in mice. Anti TNF alpha was able to improve theendothelial function as well as the oxidative stress but failed to improve the eNOS mRNA transcription.Then we have investigated the ability of hydroxychloroquine to prevent the prothrombotic state in miceand cells. The results demonstrated that HCQ completely reversed the prothrombotic state as well as theendothelial function.Finally, we have demonstrated that antiphospholipid antibodies were associated with glycocalyxshedding. This shedding was triggered by an increased heparanase activity in mice and cells. Usingspecific siRNA against heparanase improved the tissue factor expression and the thrombin generationin endothelial cells exposed to antiphospholipid antibodies.Taken together our finding bring evidences that heparanase could be an important target in thepathophysiology of the antiphospholipid antibodies
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9

Harris, Simon Leigh. "The antigenic binding site of antibodies to factor XII associated with antiphospholipid syndrome." Thesis, University of Kent, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399595.

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Pereira, Delgado Alves Jose Antonio. "Oxidative stress and vascular disease in systemic lupus erythematosus and primary antiphospholipid syndrome." Thesis, University College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.412911.

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Books on the topic "Antiphospholipid syndrome"

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Erkan, Doruk, and Silvia S. Pierangeli, eds. Antiphospholipid Syndrome. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-3194-7.

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Erkan, Doruk, and Michael D. Lockshin, eds. Antiphospholipid Syndrome. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6.

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A, Khamashta Munther, ed. Hughes syndrome: Antiphospholipid syndrome. London: Springer, 2000.

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service), ScienceDirect (Online, ed. Antiphospholipid syndrome in systemic autoimmune diseases. Amsterdam: Elsevier, 2009.

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A, Asherson Ronald, ed. The antiphospholipid syndrome. Boca Raton: CRC Press, 1996.

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Khamashta, M. A., Maria L. Bertolaccini, and Oier Ateka-Barrutia. Antiphospholipid Syndrome Handbook. London: Springer London, 2010. http://dx.doi.org/10.1007/978-1-84628-735-0.

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Meroni, Pier Luigi, ed. Antiphospholipid Antibody Syndrome. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-11044-8.

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A, Khamashta Munther, ed. Antiphospholipid (Hughes) syndrome. Philadelphia: Saunders, 2006.

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A, Khamashta Munther, ed. Antiphospholipid (Hughes) syndrome. Philadelphia: Saunders, 2001.

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Hughes, Graham, and Shirish Sangle. Hughes Syndrome: The Antiphospholipid Syndrome. London: Springer London, 2012. http://dx.doi.org/10.1007/978-0-85729-739-6.

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Book chapters on the topic "Antiphospholipid syndrome"

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Lockshin, Michael D., and E. Nigel Harris. "History of Antiphospholipid Antibody." In Antiphospholipid Syndrome, 3–11. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_1.

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Yelnik, Cécile M., Simone Appenzeller, Giovanni Sanna, Elizabeth Kozora, and Maria Laura Bertolaccini. "Neuropsychiatric Manifestations of Antiphospholipid Syndrome." In Antiphospholipid Syndrome, 201–19. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_10.

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Crowther, Mark, Kimberly J. Legault, David A. Garcia, Maria G. Tektonidou, Amaia Ugarte, Ian N. Bruce, Doruk Erkan, and Guillermo Ruiz-Irastorza. "Prevention and Treatment of Thrombotic Antiphospholipid Syndrome." In Antiphospholipid Syndrome, 223–33. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_11.

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de Jesús, Guilherme Ramires, Karen J. Gibbins, Robert M. Silver, and D. Ware Branch. "Prevention and Treatment of Obstetric Antiphospholipid Syndrome." In Antiphospholipid Syndrome, 235–46. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_12.

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Ugolini-Lopes, Michelle Remião, Paulo Ricardo Criado, Kurosh Parsi, Reyhan Diz Kucukkaya, Mary-Carmen Amigo, Maria G. Tektonidou, and Danieli Andrade. "Treatment of Non-criteria Manifestations in Antiphospholipid Syndrome." In Antiphospholipid Syndrome, 247–66. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_13.

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Barbhaiya, Medha, Danieli Andrade, Maria Laura Bertolaccini, and Doruk Erkan. "Antiphospholipid Syndrome Alliance for Clinical Trials and International Networking (APS ACTION)." In Antiphospholipid Syndrome, 267–76. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_14.

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Zuily, Stéphane, Medha Barbhaiya, Karen H. Costenbader, and Doruk Erkan. "15th International Congress on Antiphospholipid Antibodies Task Force on Antiphospholipid Syndrome Classification Report." In Antiphospholipid Syndrome, 279–90. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_15.

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Soybilgic, Arzu, Cassyanne L. Aguiar, M. Patricia Massicotte, Gili Kenet, E. Ann Yeh, Laura Andreoli, Tadej Avcin, and Barry L. Myones. "15th International Congress on Antiphospholipid Antibodies Task Force on Pediatric Antiphospholipid Syndrome Report." In Antiphospholipid Syndrome, 291–306. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_16.

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Cervera, Ricard, Ignasi Rodríguez Pintó, Gerard Espinosa, Tamir Shragai, Miri Blank, Yehuda Shoenfeld, Ilan Krause, and Thomas L. Ortel. "15th International Congress on Antiphospholipid Antibodies Task Force on Catastrophic Antiphospholipid Syndrome Report." In Antiphospholipid Syndrome, 307–16. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_17.

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Andrade, Danieli, Ricard Cervera, Hannah Cohen, Mark Crowther, Maria J. Cuadrado, Guillaume Canaud, David A. Garcia, et al. "15th International Congress on Antiphospholipid Antibodies Task Force on Antiphospholipid Syndrome Treatment Trends Report." In Antiphospholipid Syndrome, 317–38. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_18.

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Conference papers on the topic "Antiphospholipid syndrome"

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Vrbanec, Kristina, Igor Antončić, David Bonifačić, Siniša Dunatov, and Lidija Tuškan-Mohar. "Antiphospholipid syndrome." In NEURI 2015, 5th Student Congress of Neuroscience. Gyrus JournalStudent Society for Neuroscience, School of Medicine, University of Zagreb, 2015. http://dx.doi.org/10.17486/gyr.3.2236.

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Mohammed, Mohammed H., and Mark S. Lingenfelter. "Catastrophic Antiphospholipid Syndrome (CAPS): A Rare Fatal Complication Of Antiphospholipid Syndrome." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3178.

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Santos Melo, Tâmara, Robson Antônio Gonçalves, Valéria Bezerra da Silva, Gabriela Almeida Barbosa, Danielle Christinne Soares Egypto, Maria Roberta Melo Pereira Soares, Ana Karla Guedes de Melo, Sandra Rejane Cabral Batista, Alessandra de Sousa Braz, and Eutilia Andrade Medeiros Freire. "CATASTROPHIC ANTIPHOSPHOLIPID SYNDROME: CASE REPORT." In SBR 2021 Congresso Brasileiro de Reumatologia. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2021.2198.

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Aydi, Z., Z. Hadj Ali, I. Rachdi, F. Daoud, H. Zoubeidi, B. BenDhaou, and F. Boussema. "59 Antiphospholipid syndrome: about 62 cases." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.59.

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Worm Furtado, Andrea, Afonso Guilherme Schmidt, Larissa Vargas Cruz, André Lucas Ribeiro, Augusto Emílio Hinterholz, Larissa Martinelli Dullius, Vanessa Hax, Ilka Benedet Lineburger, and Ricardo Machado Xavier. "Catastrophic antiphospholipid syndrome with hemorrhagic alveolitis." In SBR 2021 Congresso Brasileiro de Reumatologia. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2021.1891.

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Pombo, ME, R. Merino, D. Pascual, MV Cuesta, A. Aguado, and J. García-Consuegra. "AB0102 Antiphospholipid syndrome (aps) in children." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.236.

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MELO, ELISA FERNANDES DE, VINICIUS VERLANGIERI SOUBIHE, RAYLANE SHELLYDA DE ALMEIDA ANATE, NATÁLIA ENGLER RAVASIO, LAÍS HELENA BITTENCOURT RIBEIRO SOUBHIA, ALINE GIMENEZ GUERRA, LARISSA ALMEIDA CAMPOS ESTEVES, NATHÁLIA FARIA DE PAULA, and FERNANDA MAGALHÃES DE MORAES LOPES. "CATASTROPHIC ANTIPHOSPHOLIPID SYNDROME WITH FAVORABLE OUTCOME." In 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-047.

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Khawaja, M., L. Magder, and M. Petri. "PS4:67 Losing antiphospholipid antibody positivity post thrombosis in secondary antiphospholipid syndrome." In 11th European Lupus Meeting, Düsseldorf, Germany, 21–24 March 2018, Abstract presentations. Lupus Foundation of America, 2018. http://dx.doi.org/10.1136/lupus-2018-abstract.113.

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Kiefer, M., L. Schweiger, and B. Moulton. "Diffuse Alveolar Hemorrhage in Primary Antiphospholipid Syndrome." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6627.

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Estévez, M., A. Argibay, L. Rodriguez, M. Freire, B. Gimena, J. Fernández-Martín, and A. Rivera. "FRI0289 Cerebrovascular disease in the antiphospholipid syndrome." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.4509.

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Reports on the topic "Antiphospholipid syndrome"

1

Yang, Mingfei. Was Antiphospholipid Syndrome A Risk Factor of Stroke? A Systemic Review and Meta-analysis of Cohort Studies Published in the 21st Centur. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0074.

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