Статті в журналах: "Phospholipid antibody"

1

Wu, X. X., and J. H. Rand. "Antiphospholipid antibody-mediated interference with annexin-V anticoagulant activity." Hämostaseologie 21, no. 02 (2001): 50–53. http://dx.doi.org/10.1055/s-0037-1619508.

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SummaryThe antiphospholipid (aPL) syndrome is a disorder in which vascular thrombosis and/or recurrent pregnancy losses occur together with serologic and coagulation evidence for antibodies directed against anionic phospholipid-protein complexes. Evidence has been developed for the idea that thrombosis in this syndrome may result from disruption of the binding of annexin-V to the phospholipids which line the placental and systemic vasculatures. We hypothesize that annexin-V, a protein known to have high affinity for anionic phospholipids, plays a thromboregulatory role at the vascular-blood interface by shielding anionic phospholipids from complexation with coagulation proteins in circulating blood. We propose that the thrombotic manifestations of the antiphospholipid syndrome are due to disruption of this annexin-V shield by antiphospholipid antibodies, thereby resulting in a net increase of thrombogenic phospholipids exposed to circulating blood. The accumulated data from tissue immunohistochemistry, trophoblast and endothelial cell culture studies, coagulation studies using noncellular phospholipids, and competition studies on artificial phospholipid bilayer are consistent with the hypothesis that the interference with the binding of annexin-V to anionic phospholipid surfaces plays an important role in the mechanism of thrombosis and in pregnancy loss in the antiphospholipid syndrome.

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2

Rauch, J., and AS Janoff. "Antibodies against Phospholipids other than Cardiolipin: Potential Roles for Both Phospholipid and Protein." Lupus 5, no. 5 (October 1996): 498–502. http://dx.doi.org/10.1177/096120339600500534.

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Autoantibodies to phospholipids other than cardiolipin have received less attention, to date, than anti-cardiolipin antibodies. This review focuses on these antibodies and potential roles for both phospholipid and protein in their reactivity. We review data in the literature indicating that antibodies to phosphatidylethanolamine and some lupus anticoagulant antibodies recognize phospholipid-binding proteins in association with phospholipid. Kininogens appear to be involved in the binding of antibodies to phosphatidylethanolamine, while phosphatidylserine-binding proteins, such as prothrombin and annexin V, have been implicated in lupus anticoagulant antibody recognition. These proteins bind to phospholipids that normally reside in the inner monolayer of the cell membrane, suggesting that exposure of these lipids is necessary for protein binding and antibody recognition to occur. In contrast, other autoantibodies, in particular those reactive with erythrocytes, appear to be directed at phospholipids that normally occur in the outer membrane leaflet, such as phosphatidylcholine. In summary, there is clearly accumulating evidence that antibodies to phospholipids other than cardiolipin recognize epitopes on phospholipid-binding proteins. It is not clear whether recognition of these epitopes is due to an increase in antigen density or a change in the protein or phospholipid structure, but it is likely that both protein and phospholipid structure play an important role in the in vivo interactions of these antibodies.

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3

KOIKE, TAKAO. "Anti-phospholipid antibody syndrome." Nihon Naika Gakkai Zasshi 84, no. 9 (1995): 1569–73. http://dx.doi.org/10.2169/naika.84.1569.

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4

Panarelli, P., M. P. Viola-Magni, and E. Albi. "Antiphosphatidylinositol Antibody in Deep Venous Thrombosis Patients." International Journal of Immunopathology and Pharmacology 16, no. 1 (January 2003): 61–66. http://dx.doi.org/10.1177/039463200301600109.

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Antiphospholipid antibodies are a heterogeneous group of immunoglobulins with specificity for a number of phospholipids, phospholipid-binding proteins and phospholipid-protein complexes. The association between antiphospholipid antibodies and a variety of pathologic disorders, such as arterial and venous thrombosis and recurrent pregnancy loss is recognized as Antiphospholipid Syndrome. The immunoassay currently used to detect antiphospholipid antibodies is the anticardiolipin test. Anticardiolipin antibodies are believed to be polyspecific antibodies that cross-react with all the anionic phospholipids. Therefore, testing only for anticardiolipin antibodies does not always permit detection of all antiphospholipid antibodies, specially when only IgG are evaluated. In a selected population of 74 idiopathic and secondary deep venous thrombosis patients, IgG anticardiolipin, antiphosphatidylinositol and antiphosphatidylserine antibodies were detected by solid-phase immunoassays. Our results show that by testing for each antiphospholipid family, many patients, not evidenced by the standard anticardiolipin assay, were found to be antiphospholipid-positive. The anticardiolipin positive patients have always low, moderate or high levels of antiphospholipid antibodies, suggesting that the antiphospholipid positivity is predictive of anticardiolipin positivity. It should be noted that the patients with only antiphosphatidylinositol positive antibody have a story of nervous system pathology. The meaning of these results is at present under discussion.

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5

Stewart, M. W., W. S. Etches, A. S. Russell, J. S. Percy, C. A. Johnston, C. K. Chew, and P. A. Gordon. "Detection of Antiphospholipid Antibodies by Flow Cytometry: Rapid Detection of Antibody Isotype and Phospholipid Specificity." Thrombosis and Haemostasis 70, no. 04 (1993): 603–7. http://dx.doi.org/10.1055/s-0038-1649636.

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SummaryLaboratory diagnosis of antiphospholipid antibodies is important in patients with clinical features of the antiphospholipid syndrome, such as thrombosis and fetal loss. We have developed a novel method for the detection of antiphospholipid antibodies using flow cytometry. Anionic phospholipids cardiolipin, phosphatidylserine and phosphatidylinositol are coated onto polystyrene beads of different sizes, allowing detection and semiquantitation of their respective phospholipid antibody isotypes. The results of the flow cytometric method closely correlate those of the standardised anticardiolipin enzyme-linked immunosorbent assay (ELISA), but the method is quicker and is versatile in its ability to detect IgG, IgM and IgA antibody isotypes at the same time. The method promises to be useful in evaluating the significance of phospholipid specificity and antibody isotypes in patients with the antiphospholipid syndrome.

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6

Gupta, Anuj, Joshika Agarwal, Shilpi Gupta, and Anurag Singh. "Clinical significance of anti-phospholipid antibodies in Henoch Schönlein purpura." International Journal Of Community Medicine And Public Health 8, no. 8 (July 27, 2021): 4037. http://dx.doi.org/10.18203/2394-6040.ijcmph20213041.

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Background: Henoch Schönlein purpura also known as IgA vasculitis is described histologically by IgA deposition in the blood vessel walls and presents with kidney involvement, palpable purpura, arthralgia, and abdominal pain. Our study aims to evaluate the association between anti-phospholipid antibody, anti-cardiolipin antibody, anti-beta(2) glycoprotein 1 antibody and Anti-phosphatidylserine/prothrombin antibodies and IgA vasculitis. Treatment response with intravenous steroids and cyclophosphamide was also studied based on resolution of antibody titer.Methods: We conducted an observational study in three Rheumatology clinics at Ahmedabad, India. Data was collected for a period of 6 months. Diagnosis of IgA vasculitis was determined based on the International Chapel hill consensus conference 2012. Disease activity was assessed based on antibody titer, histological grading and through a pre-determined clinical form to assess objective clinical symptoms. P value of less than 0.05 was considered significantResults: Study evaluated antibody titer of 178 patients. Sixty one percent of the patient's had positive anti-phospholipid antibody titer with predominant antibody subtype as IgG. Inflammatory markers were significantly higher in patient having anti-phospholipid antibody titer. Anti-phospholipid antibody was present in 100 percent patients who had vascular thrombosis. IgG subtype of anti-cardiolipin antibody were found in 60 percent of the patients with renal complication.Conclusions: Anti-phospholipid antibody have a close association with IgA vasculitis. Anti-phospholipid antibody has a significant role in mounting inflammatory response and vascular thrombosis. Combination treatment of intravenous steroids and cyclophosphamide found to be more effective in resolution of titer

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7

Wittevrongel, C., M. Vanrusselt, M. Hoylaerts, J. Vermylen, and J. Arnout. "Beta-2-glycoprotein I Dependent Lupus Anticoagulants Form Stable Bivalent Antibody Beta-2-Glycoprotein I Complexes on Phospholipid Surfaces." Thrombosis and Haemostasis 79, no. 01 (1998): 79–86. http://dx.doi.org/10.1055/s-0037-1614224.

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SummaryThe precise mechanism by which Beta-2-glycoprotein I (β2GPI-) dependent lupus anticoagulants lengthen phospholipid-dependent clotting reactions is still poorly understood. In order to study this, murine monoclonal antibodies (moabs) against human β2GPI were raised. Eight of the 21 anti-β2GPI moabs, obtained from 2 fusions, fulfilled the criteria for lupus anticoagulant (LA) activity as tested with a variety of sensitive screening assays and confirmatory tests. Seven moabs did not influence any clotting test. The LA positive moabs were found to compete for similar or closely spaced epitopes on immobilized β2GPI. Two moabs with potent LA activity (moabs 22 F 6 and 22 B 3) and 1 moab without LA activity (moab 16 B 3) were selected to study the interaction between antibody, β2GPI and phospholipid. Interactions were investigated by real-time biospecific interaction analysis (BIA) based on plasmon surface resonance technology on a BIA-core instrument using a sensor chip coated with phospholipid. When 22 F 6, the moab with the most pronounced LA activity, was allowed to interact with the phospholipid surface at concentrations between 0 and 400 nmol/l, no appreciable binding could be detected. Likewise, no binding could be measured when β2GPI at concentrations between 0 and 400 nmol/l was passed over the phospholipid coated sensor chip. Combinations of β2GPI and 22 F 6 resulted in significant binding. Similar results were obtained with 22 B 3, another moab with LA activity. A LA negative Moab, 16 B 3, did not cause binding of antibody-β2GPI complexes. Fab’ fragments, derived from moab 22 F 6, inhibited the binding of β2GPI-22 F 6 and β2GPI-22 B 3 in a concentration dependent way, indicating that only bivalent β2GPI-antibody complexes bind with high affinity to phospholipids. Fab’ fragments, derived from moab 22 F 6, also inhibited the LA effect of moabs 22 F 6 and 22 B 3 in diluted plasma. In summary, these experiments indicate that the β2GPI-dependent LA effect depends on the formation of bivalent β2GPI-antibody complexes on phospholipid surfaces.

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8

MATSUURA, EIJI. "Homologous antigen of anti-phospholipid antibody." Japanese Journal of Clinical Immunology 16, no. 6 (1993): 537–44. http://dx.doi.org/10.2177/jsci.16.537.

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9

Kittisupamongkol, W. "The hidden anti-phospholipid antibody syndrome." QJM 101, no. 7 (March 4, 2008): 591. http://dx.doi.org/10.1093/qjmed/hcn063.

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10

Taylor, Pamela V., Sylvia M. Skerrow, and Christopher W. G. Redman. "Pre-eclampsia and anti-phospholipid antibody." BJOG: An International Journal of Obstetrics and Gynaecology 98, no. 6 (June 1991): 604–6. http://dx.doi.org/10.1111/j.1471-0528.1991.tb10382.x.

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11

Kilpatrick, David C. "Pre-eclampsia and anti-phospholipid antibody." BJOG: An International Journal of Obstetrics and Gynaecology 98, no. 12 (December 1991): 1313–14. http://dx.doi.org/10.1111/j.1471-0528.1991.tb15417.x.

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12

Durrani, Omar M., Caroline Gordon, and Philip I. Murray. "Primary Anti-Phospholipid Antibody Syndrome (APS)." Survey of Ophthalmology 47, no. 3 (May 2002): 215–38. http://dx.doi.org/10.1016/s0039-6257(02)00289-8.

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13

LOCKWOOD, C. "ANTI-PHOSPHOLIPID ANTIBODY AND PREGNANCY WASTAGE." Lancet 328, no. 8509 (September 1986): 742–43. http://dx.doi.org/10.1016/s0140-6736(86)90252-7.

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14

d'Oiron, Roseline, Jean-Maurice Lavergne, Renaud Lavend'homme, Abdellah Benhida, Jean-Claude Bordet, Claude Negrier, Kathelijne Peerlinck, Jos Vermylen, Jean-Marie Saint-Remy, and Marc Jacquemin. "Deletion of alanine 2201 in the FVIII C2 domain results in mild hemophilia A by impairing FVIII binding to VWF and phospholipids and destroys a major FVIII antigenic determinant involved in inhibitor development." Blood 103, no. 1 (January 1, 2004): 155–57. http://dx.doi.org/10.1182/blood-2003-04-1321.

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Abstract The C2 domain of factor VIII (FVIII) mediates FVIII binding to von Willebrand factor (VWF) and phospholipids (PLs), thereby determining the stability and the activity of FVIII. A deletion of Ala2201 (Del2201) was identified in the FVIII C2 domain of 2 unrelated patients with mild hemophilia A (FVIII:C 11%-33%). This mutation prevents FVIII binding to a human monoclonal antibody recognizing the C2 domain and inhibiting FVIII binding to VWF and phospholipids. By comparison to healthy FVIII, Del2201 FVIII had a significantly reduced binding to VWF, which likely contributes to reduced FVIII levels in plasma. Del2201 FVIII interaction with phospholipids was evaluated in an FXa generation assay, using various concentrations of synthetic phospholipid vesicles mimicking an activated platelet surface. At the lowest phospholipid concentration allowing FXa generation, Del2201 FVIII activity was reduced 3-fold. This is the first report of a mutation altering FVIII binding to phospholipids and occurring in patients with hemophilia A.

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15

Hassan, Fadi, Mohammad E. Naffaa, Amir Saab, and Chaim Putterman. "Cognitive Impairment in Anti-Phospholipid Syndrome and Anti-Phospholipid Antibody Carriers." Brain Sciences 12, no. 2 (February 5, 2022): 222. http://dx.doi.org/10.3390/brainsci12020222.

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Cognitive impairment is frequently reported among anti-phospholipid syndrome (APS) patients as well as anti-phospholipid antibody (aPL) carriers, but it is less studied than other manifestations of this condition. Moreover, the exact prevalence of cognitive impairment in these patients has not been accurately determined, mainly due to inconsistency in the tools used to identify impairment, small sample sizes, and variability in the anti-phospholipid antibodies measured and positivity cutoffs. The notion of a direct pathogenic effect is supported by the observation that the higher the number of aPLs present and the higher the load of the specific antibody, the greater the risk of cognitive impairment. There is some evidence to suggest that besides the thrombotic process, inflammation-related pathways play a role in the pathogenesis of cognitive impairment in APS. The cornerstone treatments of APS are anti-coagulant and anti-thrombotic medications. These treatments have shown some favorable effects in reversing cognitive impairment, but solid evidence for the efficacy and safety of these treatments in the context of cognitive impairment is still lacking. In this article, we review the current knowledge regarding the epidemiology, pathophysiology, clinical associations, and treatment of cognitive impairment associated with APS and aPL positivity.

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16

Umeda, M., K. Igarashi, K. S. Nam, and K. Inoue. "Effective production of monoclonal antibodies against phosphatidylserine: stereo-specific recognition of phosphatidylserine by monoclonal antibody." Journal of Immunology 143, no. 7 (October 1, 1989): 2273–79. http://dx.doi.org/10.4049/jimmunol.143.7.2273.

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Abstract A system based on the direct immunization of phospholipid Ag into mouse spleen has been used to produce mAb against phosphatidylserine (PS). mAb that bind to PS but not to phosphatidylcholine were selected. Remarkable frequency of the production of mAb against PS was observed with the immunization protocol. The mAb exhibited three distinct reactivity profiles ranging from highly specific to broadly cross-reactive. Among 61 hybridomas, 15 mAb were established for further analysis. The reactivities of three typical mAb, designated PS4A7, PS3A, and PSC8, are described. PS4A7 is highly specific to PS and no cross-reaction with other acidic phospholipids was observed. In the experiments using PS derivatives with a modified polar head group, PS4A7 was shown to bind to 1,2-diacyl-sn-glycero-3-phospho-L-serine (PS) but not to 1,2-diacyl-sn-glycero-3-phospho-D-serine or 1,2-diacyl-sn-glycero-3-phospho-L-homoserine, indicating that the antibody recognizes the stereo-specific configuration of serine residue in PS. PS3A binds to both PS and phosphatidylethanolamine, whereas no cross-reaction with other acidic phospholipids was observed. The analysis using the derivatives of PS and phosphatidylethanolamine shows that the antibody recognizes the amino group of the phospholipid Ag and cannot distinguish the conformational structure of serine residue in PS. PSC8 represents the family of mAb that cross-react considerably with other acidic phospholipids.

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17

Rand, JH, X.-X. Wu, AS Quinn, and DJ Taatjes. "The annexin A5-mediated pathogenic mechanism in the antiphospholipid syndrome: role in pregnancy losses and thrombosis." Lupus 19, no. 4 (March 30, 2010): 460–69. http://dx.doi.org/10.1177/0961203310361485.

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Annexin A5 (AnxA5) binds to phospholipid bilayers, forming two-dimensional crystals that block the phospholipids from availability for coagulation enzyme reactions. Antiphospholipid (aPL) antibodies cause gaps in the ordered crystallization of AnxA5 which expose phospholipids and thereby accelerate blood coagulation reactions. The aPL antibody-mediated disruption of AnxA5 crystallization has been confirmed on artificial phospholipid bilayers and on cell membranes including endothelial cells, placental trophoblasts and platelets. Recently, we reported that hydroxychloroquine, a synthetic antimalarial drug, can reverse this antibody-mediated process through two mechanisms: (1) by inhibiting the formation of aPL IgG-β2glycoprotein I complexes; and (2) by promoting the formation of a second layer of AnxA5 crystal ‘patches’ over areas where the immune complexes had disrupted AnxA5 crystallization. In another translational application, we have developed a mechanistic assay that reports resistance to AnxA5 anticoagulant activity in plasmas of patients with aPL antibodies. AnxA5 resistance may identify a subset of aPL syndrome patients for whom this is a mechanism for pregnancy losses and thrombosis. The elucidation of aPL-mediated mechanisms for thrombosis and pregnancy complications may open new paths towards addressing this disorder with targeted treatments and mechanistic assays.

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18

Wu, Xiao-Xuan, and Jacob Rand. "Antibody-Mediated Disruption of the Annexin-V Antithrombotic Shield: A New Mechanism for Thrombosis in the Antiphospholipid Syndrome." Thrombosis and Haemostasis 82, no. 08 (1999): 649–55. http://dx.doi.org/10.1055/s-0037-1615892.

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IntroductionThe antiphospholipid (aPL) syndrome is a condition that manifests in patients as vascular thromboembolism or recurrent pregnancy loss together with laboratory evidence for the presence of antibodies against anionic phospholipid-protein complexes. For a recent comprehensive review, the reader is referred to Hughes et al.1 The syndrome was first proposed to be a distinct entity, called anticardiolipin syndrome, in 1985,2 and was later renamed antiphospholipid syndrome.3 The disorder was classified as “primary” in the absence of a concurrent autoimmune condition, such as systemic lupus erythematosus, or “secondary” in the presence of another such autoimmune disorder. Antiphospholipid antibodies are detected by their reactivity to anionic phospholipids (or protein-phospholipid complexes) in solid phase immunoassays, or by their inhibition of phospholipid-dependent coagulation reactions, known as the “lupus anticoagulant” effect. The ever-expanding, yet still insufficiently integrated, knowledge of this enigmatic disorder makes this area an intriguing subject for investigation.The pathophysiologic mechanism of this syndrome has remained obscure, resulting from the apparent multiplicity of antigenic determinants recognized by the antibodies. In addition, a large number of effects1 have been described for the antibodies in vitro and in cell culture systems. These effects, which include the paradoxical lupus anticoagulant (LAC) phenomenon, are a consequence of the numerous roles played by phospholipids in the hemostasis system and in a multitude of biologic processes. The purpose of this review is to introduce the reader to the current state of knowledge of the role of annexin-V in this disorder.

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19

Shapoorabadi, Farzaneh Ahmadi, Maryam Sadat Mirbagheri Firoozabad, Neda Habibi, and Giti Emtiazi. "Hemolysis, Platelet Aggregation and Antibacterial Activities of Human Antiphospholipid Antibody." Anti-Infective Agents 18, no. 3 (September 11, 2020): 268–74. http://dx.doi.org/10.2174/2211352517666190613111628.

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Background: Anti-phospholipid antibodies have the potential to become an alternative to conventional antibiotics for humans. The Antiphospholipid Syndrome (APS) is an autoimmune disease where the body’s defense system incorrectly reacts against its own phospholipids. APS is distinct through the existence of venous and arterial thromboses, frequently multiple and recurring fetal losses, commonly accompanied by moderate thrombocytopenia. Anti-phospholipid antibodies include lupus anti-coagulant, anti- cardiolipin, anti-beta 2 glycoprotein 1, and anti-prothrombin antibodies. Methods: In this study, the mechanism of action of Anti-phospholipid antibodies against Klebsiella pneumonia and Staphylococcus aureus was investigated in great detail using a unique combination of imaging and biophysical techniques. Antibacterial activity of antiphospholipid antibodies was detected by a diffusion method and the investigation of the complexity of antibody-antigen was done by spectroscopic examination, scanning electron microscopy (SEM), and transmission electron microscopy (TEM) imaging. Results: There was a profound change in the bacteria treated with healthy and patient serum in the optical microscopic study. In all of the studied fields, bacterial treatment with patient serum immediately induced bacterial swelling and cumulative accumulation of the bacteria while no changes were observed in the healthy serum. Anti-bacterial activities of patient serum were detected on the plate. The result of this study showed that after platelet activation by thrombin and incubation with antiphospholipid antibodies, the platelet was aggregated. The transmission electron microscopy (TEM) image showed that the cell wall of Klebsiella pneumonia and Staphylococcus aureus incubated with antiphospholipid had a bizarre shape and antiphospholipid antibodies bound to bacterial membranes. Conclusion: The data indicated that antiphospholipid antibodies with hemolysis activities have an effect on Gram-positive and negative bacteria and these antibodies have the potential to become antibiotic for human.

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20

Choi, Hyeok, Sung Soo Ahn, Jason Jungsik Song, Yong-Beom Park, Jaewoo Song, and Sang-Won Lee. "Anti-phospholipid antibody syndrome occurrence in patients with persistent anti-phospholipid antibodies." Rheumatology International 39, no. 8 (May 10, 2019): 1359–67. http://dx.doi.org/10.1007/s00296-019-04318-4.

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21

KILPATRICK, D. "ANTI-PHOSPHOLIPID ANTIBODY SYNDROME AND PRE-ECLAMPSIA." Lancet 334, no. 8669 (October 1989): 987–88. http://dx.doi.org/10.1016/s0140-6736(89)91001-5.

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22

Nikiforow, Sarah, Gilbert Moeckel, and Ursula C. Brewster. "Anti-phospholipid antibody syndrome in the kidney." Kidney International 77, no. 5 (March 2010): 473. http://dx.doi.org/10.1038/ki.2009.484.

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23

Pengo, V., A. Biasiolo, T. Brocco, S. Tonetto, and A. Ruffatti. "Autoantibodies to Phospholipid-binding Plasma Proteins in Patients with Thrombosis and Phospholipid-reactive Antibodies." Thrombosis and Haemostasis 75, no. 05 (1996): 721–24. http://dx.doi.org/10.1055/s-0038-1650355.

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SummaryAnti-phospholipid (aPL) antibodies are defined as antibodies detected in systems employing phospholipids (PL). This general definition is misleading as it comprises a large group of autoimmune phospholipid-reactive antibodies that are directed against specific phospholipid-binding plasma proteins, such as β2-glycoprotein I (β2GPI) and prothrombin. Definition of phospholipid-reacting antibodies according to the plasma protein against which they are directed appears more appropriate and could be useful in understanding clinical events and pathogenic mechanisms. Using ELISA systems we have studied the presence of antibodies directed against specific phospholipid-binding proteins in a series of 22 patients with thrombosis and phospholipid-reactive antibodies of the IgG isotype. High levels of anti-β2GPI IgG were detected in all 22 patients. Normal values were calculated on the basis of OD values at 405 nm (OD405) obtained for 22 age- and sex-matched healthy subjects (cut off value = 0.401). Levels of anti-β2GPI antibodies were linearly correlated with those of cardiolipin-reactive (aCL) antibodies. Eleven out of 22 patients (50%) had values of anti-prothrombin antibodies exceeding the cut-off value of 0.250. No relationship was found between the levels of anti-β2GPI and anti-prothrombin antibodies. Tests for antibodies against two natural inhibitors of blood coagulation, protein C and protein S, revealed elevated levels of anti-protein C IgG and anti-protein S IgG in 4 and 12 patients, respectively. A highly significant correlation between anti-protein C IgG and anti-protein S IgG values as well as between antibody titers against the two studied natural coagulation inhibitors and anti-prothrombin IgG was found. When comparing patients positive for aCL and presence or absence of a previous thrombotic episode (aCL+/T+ vs aCL+/T-), the positivity of anti-P2GPI IgG was found to be statistically associated with thrombosis. Conversely, among patients with previous thromboembolism with or without aCL (aCL+/T+ vs aCL-/T+) the positivity of anti-β2GPI IgG was strictly associated with the positivity of aCL, thus identifying the aPL antibody syndrome. These data demonstrate that anti-β2GPI antibodies are a marker of “autoimmune” thrombosis. Anti-prothrombin antibodies are not a marker of thrombosis and are closely associated with antibodies to protein C and protein S.

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Sheng, Y., A. Sali, H. Herzog, J. Lahnstein, and S. A. Krilis. "Site-directed mutagenesis of recombinant human beta 2-glycoprotein I identifies a cluster of lysine residues that are critical for phospholipid binding and anti-cardiolipin antibody activity." Journal of Immunology 157, no. 8 (October 15, 1996): 3744–51. http://dx.doi.org/10.4049/jimmunol.157.8.3744.

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Abstract beta2-Glycoprotein I (beta2GPI) is a phospholipid-binding serum protein with anticoagulant properties. It plays a vital role in the binding of anti-cardiolipin Abs purified from patients with autoimmune disease when assayed in a cardiolipin (CL) ELISA. Based on a three-dimensional model of beta2GPI, electrostatic calculations, and earlier peptide studies, a highly positively charged amino acid sequence, Lys282-Asn-Lys-Glu-Lys-Lys287, located in the fifth domain of beta2GPI, has been predicted to be the phospholipid binding site. We tested this hypothesis by site-directed mutagenesis of residues in the predicted phospholipid binding site and by assessing the mutants for phospholipid binding and anti-beta2GPI activity. A single amino acid change from Lys286 to Glu significantly decreased the binding of beta2GPI to CL. Double and triple mutants 2k (from Lys286, 287 to Glu286, 287), 2ka (from Lys284, 287 to Glu284, 287), and 3k (from Lys284, 286, 287 to Glu284, 286, 287) possessed no binding of Ab to beta2GPI in a CL ELISA, as well as no inhibitory activity on the binding of iodinated native beta2GPI to CL. These results indicate that the residues Lys284, Lys286, and Lys287 in the fifth domain of beta2GPI are critical for its binding to anionic phospholipids and its subsequent capture for binding of anti-beta2GPI Abs.

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25

R Gomes, Richmond. "Primary Anti-Phospholipid Antibody Syndrome presenting as Multiple Cerebral Venous Sinus Thrombosis: An Arduous Manifestation." Brain and Neurological Disorders 5, no. 2 (June 21, 2022): 01–05. http://dx.doi.org/10.31579/2642-9730/019.

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Lupus anticoagulants (LA) are circulating autoantibodies, primarily directed against phospholipids, that prolong the partial thromboplastin time. Antiphospholipid antibody syndrome (APS) is an autoimmune disorder, mainly found in young females, presenting with vascular thrombosis and/obstetric complications. Thrombosis at anatomically significant sites may lead to considerable morbidity and/or mortality. We here present a 22 years old lady with no prior rheumatological history, presented with sudden onset headache, vomiting, diplopia who later diagnosed with multiple cerebral venous sinus thrombosis (CVST) due to with primaryAPS.MR venography was instrumental in diagnosis. Except for mild headache, the other symptoms responded to anticoagulant. Such massive cerebral venous thrombosis is extremely rare in primary APS.

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Soares, Melina, Sameer Syed, Gustavo Barbero, and Philip E. Thorpe. "ANTIBODY-MEDIATED TARGETING OF “INSIDE-OUT” ANIONIC PHOSPHOLIPIDS IN VIRAL DISEASE (47.21)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S70. http://dx.doi.org/10.4049/jimmunol.178.supp.47.21.

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Abstract The anionic phospholipid phosphatidylserine (PS) is found exclusively in the inner leaflet of the plasma membrane of resting mammalian cells. We hypothesized that certain events that occur during virus replication (eg cell activation or membrane rearrangement) would trigger the exposure of anionic phospholipids on the outer surface of virus- infected cells and subsequently on the enveloped viruses that bud out of these virus- infected cells. We further hypothesized that these exposed anionic phospholipids would serve as targets for anti-viral therapy. We demonstrate here that anionic phospholipids become exposed on the enveloped Pichinde Virus (a model virus for Lassa Fever virus, a potential bioterrorism agent) and on Pichinde virus-infected cells. To detect anionic phospholipids, we used a chimeric monoclonal antibody, bavituximab, that binds anionic phospholipids in a B2-glycoprotein I dependent manner. We show that bavituximab treatment is able to cure overt disease in guinea pigs lethally infected with Pichinde virus. Bavituximab treatment reduced the amounts of virus in multiple tissues and caused direct clearance of virus from the blood. Direct clearance of free virus and antibody-dependent cellular cytotoxicity of virus-infected cells appear to be the major mechanisms that contribute to the anti-viral effect of bavituximab. Bavituximab-treated survivors were immune to reinfection. Furthermore, the murine version of bavituximab, 3G4, shows therapeutic efficacy in a lethal murine model for human cytomegalovirus. Our study demonstrates the promise of anionic phospholipids as targets for new broad-spectrum anti-viral drugs.

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Uzgiris, Egidijus E. "Antibody crystallization on phospholipid films: Dynamics and the effects of antibody conformation." Journal of Cellular Biochemistry 29, no. 3 (1985): 239–51. http://dx.doi.org/10.1002/jcb.240290308.

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28

Deb, Sudip Ranjan, Ahmedul Kabir, Tanzia Khanum, Md Golam Ur Rahman, Anowar Hossain, Md Alamin, and Rafiya Afroz. "Digital Symmetrical Peripheral Gangrene: A Rare Male PresentAtion of AntiPhospholipid Anti Body Syndrome." Journal of Dhaka Medical College 24, no. 2 (September 15, 2016): 152–55. http://dx.doi.org/10.3329/jdmc.v24i2.29628.

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Anti-phospholipid antibody syndrome can be defined as the occurrence of venous and arterial thrombosis with or without recurrent miscarriage in association with laboratory evidence of persistent Antiphospholipid antibody / antibody to beta-2-Glycoprotein-1 / anti cardiolipin antibody /lupus anticoagulant (usually associated with SLE). It occurs usually in female who can present with recurrent miscarriage and fetal loss. Anti-phospholipid Antibody can be also found in some autoimmune diseases and post viral infections. Even certain drugs; e.g. phenothiazine, can cause it. Arterial thrombosis may lead to peripheral limb ischemia, stroke, and myocardial infarct. And venous thrombosis may be found in the form of DVT, pulmonary embolism & thrombosis in vessels supplying the abdominal organ.J Dhaka Medical College, Vol. 24, No.2, October, 2015, Page 152-155

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Harris, EN, and SS Pierangeli. "Functional Effects of Anticardiolipin Antibodies." Lupus 5, no. 5 (October 1996): 372–77. http://dx.doi.org/10.1177/096120339600500507.

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The ‘lupus anticoagulant’ phenomenon is the best documented functional effect of antiphospholipid (aPL) antibodies, occurring either by inhibition of the prothrombinase and/or Factor X activation reactions. Understanding the mechanism by which aPL antibodies inhibit phospholipid dependent coagulation reactions may yield important clues about their ‘thrombogenic effects’ in vivo. We conducted a series of studies to determine the specificity, diversity, and mechanism by which aPL antibodies inhibit phospholipid dependent reactions. Results showed that purified immunoglobulins with lupus anticoagulant and anti-cardiolipin activities were absorbed by negatively charged phospholipids and both activities were recovered from the phospholipid-antibody precipitate. Purified aPL antibodies inhibited the prothrombinase reaction in a plasma free system in which β2-glycoprotein 1 (β2-GP1) was absent. Affinity purified aPL antibodies had 25–50 times the inhibitory activity of immunoglobulin preparations. The phospholipid binding proteins, β2-GP1 and placental anticoagulant protein I (PAP I), independently inhibited the prothrombinase reaction, and when these proteins were combined with aPL, inhibition of the prothrombinase reaction was additive. Antibodies of syphilis had no inhibitory effect, partially accounted for by lack of specificity for phosphotidylserine (PS). Although aPL antibodies inhibited the protein C activation reaction, there was no correlation of these activities with inhibition of the prothrombinase reaction. Together, these results show that aPL exert their effects by interaction with negatively charged phospholipids, in particular phosphotidylserine, but lack of correlation between inhibition of the prothrombinase and protein C activation reactions, suggests that the nature of the coagulation protein is also important.

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30

Mohammadi, Milad, Beatrice Oehler, Jan Kloka, Corinna Martin, Alexander Brack, Robert Blum, and Heike L. Rittner. "Antinociception by the anti‐oxidized phospholipid antibody E06." British Journal of Pharmacology 175, no. 14 (June 7, 2018): 2940–55. http://dx.doi.org/10.1111/bph.14340.

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31

de Groot, Philip G. "Mechanisms of anti-phospholipid antibody formation and action." Thrombosis Research 127 (February 2011): S40—S42. http://dx.doi.org/10.1016/s0049-3848(11)70011-1.

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32

Cheng, Hwee-Ming, and Kok-Kien Wong. "Anti-phospholipid antibody isotypes in normal human sera." Immunology Letters 23, no. 3 (January 1990): 183–86. http://dx.doi.org/10.1016/0165-2478(90)90189-w.

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33

Sangle, Nikhil A., and Kristi J. Smock. "Antiphospholipid Antibody Syndrome." Archives of Pathology & Laboratory Medicine 135, no. 9 (September 1, 2011): 1092–96. http://dx.doi.org/10.5858/2010-0325-rsr.1.

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Antiphospholipid antibodies are directed against phospholipid-protein complexes and include lupus anticoagulant, anticardiolipin antibodies, and anti–beta-2 glycoprotein I antibodies. Antiphospholipid antibody syndrome is a common cause of acquired thrombophilia and is characterized by venous or arterial thromboembolism or pregnancy morbidity and the presence of antiphospholipid antibodies. Antibodies should be demonstrable on at least 2 occasions separated by 12 weeks. Heterogeneity of the autoantibodies and absence of gold standard assays makes interpretation of laboratory results a challenge for both laboratorians and clinicians. This review discusses the key laboratory and clinical aspects of antiphospholipid antibody syndrome. Particular focus is given to lupus anticoagulant detection, in view of recently updated laboratory guidelines.

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Kuypers, FA, RA Lewis, M. Hua, MA Schott, D. Discher, JD Ernst, and BH Lubin. "Detection of altered membrane phospholipid asymmetry in subpopulations of human red blood cells using fluorescently labeled annexin V." Blood 87, no. 3 (February 1, 1996): 1179–87. http://dx.doi.org/10.1182/blood.v87.3.1179.bloodjournal8731179.

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The phospholipids of the human red cell are distributed asymmetrically in the bilayer of the red cell membrane. In certain pathologic states, such as sickle cell anemia, phospholipid asymmetry is altered. Although several methods can be used to measure phospholipid organization, small organizational changes have been very difficult to assess. Moreover, these methods fail to identify subpopulations of cells that have lost their normal phospholipid asymmetry. Using fluorescently labeled annexin V in flow cytometry and fluorescent microscopy, we were able to identify and quantify red cells that had lost their phospholipid asymmetry in populations as small as 1 million cells. Moreover, loss of phospholipid organization in subpopulations as small as 0.1% of the total population could be identified, and individual cells could be studied by fluorescent microscopy. An excellent correlation was found between fluorescence-activated cell sorter (FACS) analysis results using annexin V to detect red cells with phosphatidylserine (PS) on their surface and a PS-requiring prothrombinase assay using similar red cells. Cells that bound fluorescein isothiocyanate (FITC)-labeled annexin V could be isolated from the population using magnetic beads covered with an anti-FITC antibody. Evaluation of blood samples from patients with sickle cell anemia under oxygenated conditions demonstrated the presence of subpopulations of cells that had lost phospholipid asymmetry. While only a few red cells were labeled in normal control samples (0.21% +/- 0.12%, n = 8), significantly increased (P < .001) annexin V labeling was observed in samples from patients with sickle cell anemia (2.18% +/- 1.21%, n = 13). We conclude that loss of phospholipid asymmetry may occur in small subpopulations of red cells and that fluorescently labeled annexin V can be used to quantify and isolate these cells.

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35

Rand, Jacob H. "Pathophysiology of Anti-PL Syndrome in Thrombosis." Blood 114, no. 22 (November 20, 2009): SCI—45—SCI—45. http://dx.doi.org/10.1182/blood.v114.22.sci-45.sci-45.

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Abstract Abstract SCI-45 The antiphospholipid (aPL) syndrome (APS) is an enigmatic autoimmune thrombotic disorder that was initially identified through astute clinical observations and the development of a quantitative test for aPL antibodies. The condition is marked by 2 types of assays: 1) immunoassays that were derived from the “biologic false positive syphilis” test and 2) coagulation assays that detect “lupus anticoagulants” (LAs), which are inhibitors of phospholipid-dependent coagulation reactions. The most recent consensus investigational criteria for diagnosing APS require that patients have evidence for thrombosis and/or pregnancy complications attributable to placental insufficiency and also laboratory evidence for persistent (aPL) antibodies, detected by high levels of IgG or IgM antibodies against cardiolipin and β2-glycoprotein I (β2GPI) and/or through abnormal LA assays. The thrombotic disorder requires long term anticoagulant treatment, which is accompanied by the risk of bleeding complications. Several mechanisms have been postulated and can be classified as involving: 1) aPL antibody-mediated inhibition of endogenous anticoagulant mechanisms; 2) aPL antibody-triggered signaling events on target cells (vascular endothelial cells, monocytes, platelets and trophoblasts) that promote proadhesive and prothrombotic phenotypes; and 3) aPL antibody-mediated complement activation. At present, it appears that the APS diagnostic entity actually includes several distinct subsets that reflect the actions of heterogeneous antibodies directed against different epitopes of phospholipid-binding proteins which then may yield different clinical sequelae. We have accumulated significant data indicating that a major one of these mechanisms involves aPL antibody-mediated disruption of annexin A5 (AnxA5) activity. AnxA5 is a potent anticoagulant protein whose anticoagulant properties are a consequence of its high affinity for anionic phospholipid. The protein forms 2-dimensional crystals on phospholipid surfaces that shield the phospholipids from availability for coagulation reactions. AnxA5 appears to play a thrombomodulatory role on the surfaces of cells lining the placental and systemic vasculatures. It is highly expressed on the apical membranes of placental syncytiotrophoblasts, the location where maternal blood interfaces with fetal cells. aPL antibody-antigen complexes disrupt the ordered crystallization of AnxA5, displace the protein from phospholipid membrane surfaces and thereby accelerate coagulation reactions. This effect of the antibodies has been demonstrated on artificial bilayers, on cultured trophoblasts and on endothelial cells and platelets. This disruption has been appears to be a consequence of aPL antibodies that recognize a specific epitope within domain I of β2GPI, the key antigen recognized by aPL antibodies. Based upon these data, we developed a novel clinical assay “the AnxA5 resistance (A5R) test” to identify patients who have antibodies that interfere with the anticoagulant activity of AnxA5. Initial studies indicate that a large proportion of APS patients have evidence for A5R. It therefore appears possible that measurement for A5R may provide a mechanistic assay for APS. We are also developing treatments to target this mechanism and protect AnxA5 from antibody-mediated disruption which may open novel nonanticoagulant approaches to treating APS. Disclosures Off Label Use: The presentation will include research on in vitro effects of hydroxychloroquine; the drug is not FDA approved for the treatment of patients with antiphospholipid syndrome who do not also have concurrent systemic lupus erythematosus or rheumatoid arthritis.

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Viall, C. A., L. W. Chamley та Q. Chen. "116. TROPHOBLAST ANTIPHOSPHOLIPID ANTIBODY INTERNALISATION BY A β2 GLYCOPROTEIN I-ANIONIC PHOSPHOLIPID-MEGALIN COMPLEX". Reproduction, Fertility and Development 22, № 9 (2010): 34. http://dx.doi.org/10.1071/srb10abs116.

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Women with antiphospholipid antibodies (aPL) are at an increased risk of preeclampsia, recurrent miscarriage, stillbirth and intrauterine growth restriction. Antiphospholipid antibodies may predispose to these pathologies by damaging the placenta, although exactly how is not understood. Recently, a novel pathogenic mechanism was suggested by work which showed that aPL are specifically internalised by placental trophoblasts where they caused aberrant trophoblast death. Internalisation may occur via an endocytic receptor called megalin in a process that seems to involve at least one of the two components of the antigen for aPL, the anionic phospholipid-binding protein β2 glycoprotein I (β2GPI). However, whether internalisation is also dependent upon anionic phospholipids is unknown. Identifying the receptor pathway responsible for aPL internalisation may provide insight into the pathogenesis of aPL in the placenta. To investigate the process of aPL internalisation, first trimester placental explants were cultured with fluorescently-labeled monoclonal aPL, or a control antibody and/or β2GPI or acetylated β2GPI, which can not bind anionic phospholipids. The explants were then sectioned and the localisation of the aPL, β2GPI, or acetylated β2GPI was determined by confocal microscopy. The localisation of megalin expression in placental explants was determined by immunohistochemistry. Megalin was expressed throughout the syncytiotrophoblast but more strongly in some regions. After an overnight incubation, both aPL and β2GPI, but not control antibodies were co-localised in the cytoplasm of the syncytiotrophoblast. Acetylated β2GPI was not internalised and partially blocked aPL uptake. These results suggest that aPL are internalised into the synctiotrophoblast by a receptor-dependent mechanism involving β2GPI, anionic phospholipids and megalin. This work forms the first step to understanding how aPL are internalised by trophoblasts. Further investigation of this mechanism and the subsequent intracellular effects of aPL may lead to a new therapeutic strategy for aPL-positive pregnant women by preventing the pathogenic effect of aPL on the placenta.

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37

Aleman, Maria M., Siddharth Jindal, Nina Leksa, Robert Peters, and Joe Salas. "Phospholipid-Independent Activity of Fviiia Mimetic Bispecific Antibodies in Plasma." Blood 132, Supplement 1 (November 29, 2018): 2461. http://dx.doi.org/10.1182/blood-2018-99-119226.

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Abstract Introduction: An important coagulation regulatory mechanism is localization of clotting complexes to exposed phosphatidylserine (PS) on cell surfaces. All components of the intrinsic tenase complex (factor (F)VIIIa, FIXa, and FX) bind to PS. FVIIIa mimetic bispecific antibodies are drugs in development for hemophilia A that aim to mimic the cofactor function of FVIIIa by bringing together FIXa and FX to generate FXa. However, these antibodies differ from FVIII in many ways including no requirement of activation and a lack of direct PS binding. Emicizumab is a bispecific antibody currently on the market for hemophilia A patients with inhibitors. It binds to factor FIX, FIXa, FX, and FXa with micromolar affinities in solution. Previously, we have shown that in-house preparations of sequence-identical emicizumab (SI-Emi) showed similar weak affinities to its antigens and similar in vitro activity to published emicizumab results by one-stage clotting, chromogenic FXa generation, and thrombin generation. However, in chromogenic FXa generation using antibody concentrations in the range of the mean steady state plasma concentration of patients on emicizumab prophylaxis [~360 nM, (Oldenburg, et al., NEJM 2017)], SI-Emi maintained 28% of its activity even in the absence of PS-containing phospholipid vesicles. Another FVIIIa mimetic antibody, BS-027125, was discovered by our group and binds with low nanomolar affinity to FIX, FIXa and FX, with no detectable binding to FXa. In one-stage clotting, BS-027125 achieved clot times similar to physiological levels of FVIII, but had poor activity in thrombin generation at these concentrations. Furthermore, it too maintained small amounts of phospholipid-independent activity in chromogenic FXa generation. Given the artificial nature of the chromogenic FXa generation assay, and that activity of prothrombinase is PS-dependent thereby precluding omission of phospholipids from thrombin generation assays, we developed an assay to detect FXa generation in a plasma milieu by FVIIIa mimetic antibodies or FVIII with and without phospholipid vesicles. Methods: FVIIIa mimetic antibodies or recombinant FVIII (rFVIII) were incubated with thrombin for 5 minutes, quenched with hirudin, then spiked into platelet-free congenital hemophilia A plasma treated with additional hirudin. FXIa (to generate FIXa in situ) with and without PC:PE:PS (40:40:20 molar ratio) phospholipid vesicles was added and reactions were triggered with a solution of CaCl2 and fluorogenic FXa substrate (Mes-D-LGR-ANSN(C2H5)2). Substrate cleavage was monitored kinetically on a fluorescent plate reader. Substrate cleavage by FXIa could not be detected, yet another unknown plasma peptidase did cleave substrate at a constant low rate that was background subtracted. Results: In the absence of phospholipid vesicles, SI-Emi maintained 51±3.7% of its FXa generation activity at all concentrations tested (3.8±0.4 versus 8.0±1.1 RFU/min at 333 nM). BS-027125 showed very low activity (0.43±0.12 RFU/min at 50 nM) in the presence of phospholipid vesicles, however, in the absence of phospholipid vesicles, BS-027125 activity was not detectable above baseline. Nearly all rFVIII activity (>99%) was lost in the absence of phospholipid vesicles (0.14±0.04 versus 15.1±1.8 RFU/min at 0.3 IU/mL). Addition of annexin V was sufficient to block all rFVIII activity in the presence or absence of phospholipid vesicles, but could not block SI-Emi activity. Furthermore, addition of rivaroxaban, a direct FXa inhibitor, confirmed that detection of substrate cleavage was due to FXa activity. Conclusions: In the absence of phosphatidylserine-containing phospholipid vesicles, SI-Emi promoted the generation of FXa in plasma triggered with FXIa. The activity of BS-027125 was too low in this assay to clearly determine its phospholipid-independent activity. These results suggest SI-Emi has mis-regulated (PS-independent) procoagulant activity due to a lack of phospholipid localization of the antibody-FIXa-FX complex. Given the weak affinity of SI-Emi for its antigens, the exact mechanism enabling this activity is unclear. Further study of this phenomenon and its relevance to overall thrombin generation and in vivo activity are needed. Disclosures Aleman: Bioverativ, a Sanofi company: Employment. Jindal:Bioverativ, a Sanofi company: Employment. Leksa:Bioverativ a Sanofi company: Employment. Peters:Bioverativ a Sanofi company: Employment, Equity Ownership. Salas:Bioverativ a Sanofi company: Employment, Equity Ownership.

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Marciniak, E., and EH Romond. "Impaired catalytic function of activated protein C: a new in vitro manifestation of lupus anticoagulant." Blood 74, no. 7 (November 15, 1989): 2426–32. http://dx.doi.org/10.1182/blood.v74.7.2426.2426.

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Abstract Lupus anticoagulant (LA), an antibody against anionic phospholipid with anticoagulant laboratory manifestations, is paradoxically associated with a high incidence of thrombosis. In the present study we analyzed the phospholipid- and platelet-dependent degradation of factor Va following clotting in plasma from 15 consecutive patients with LA to provide evidence for a distinct procoagulant effect of the antibody. After clotting with 25 micrograms phospholipid/mL, all samples containing LA showed markedly decreased rates of factor Va degradation (k = 0.01 to 0.14 min-1 v 0.27 to 0.35 min-1 in controls). Also with higher phospholipid concentrations (up to 100 micrograms/mL), as well as in the presence of platelets (5 to 33 x 10(7)/mL), significantly less of the procoagulant activity disappeared per unit of time in samples with LA than in controls. Plasma with LA was to a variable extent capable of decreasing or abolishing factor Va inhibition in normal plasma. Most importantly, exogenous activated protein C failed to correct the ineffective factor Va destruction despite adequate protein S levels. These data suggest that LA prevents the formation of the complex essential for rapid proteolysis of factor Va both on phospholipid and on the platelet membrane, thereby compromising the catalytic function of activated protein C. Our findings offer a new opportunity for a more comprehensive evaluation of patients with antiphospholipid antibody in defining the pathogenesis of thrombosis in this clinical condition.

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39

Marciniak, E., and EH Romond. "Impaired catalytic function of activated protein C: a new in vitro manifestation of lupus anticoagulant." Blood 74, no. 7 (November 15, 1989): 2426–32. http://dx.doi.org/10.1182/blood.v74.7.2426.bloodjournal7472426.

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Анотація:

Lupus anticoagulant (LA), an antibody against anionic phospholipid with anticoagulant laboratory manifestations, is paradoxically associated with a high incidence of thrombosis. In the present study we analyzed the phospholipid- and platelet-dependent degradation of factor Va following clotting in plasma from 15 consecutive patients with LA to provide evidence for a distinct procoagulant effect of the antibody. After clotting with 25 micrograms phospholipid/mL, all samples containing LA showed markedly decreased rates of factor Va degradation (k = 0.01 to 0.14 min-1 v 0.27 to 0.35 min-1 in controls). Also with higher phospholipid concentrations (up to 100 micrograms/mL), as well as in the presence of platelets (5 to 33 x 10(7)/mL), significantly less of the procoagulant activity disappeared per unit of time in samples with LA than in controls. Plasma with LA was to a variable extent capable of decreasing or abolishing factor Va inhibition in normal plasma. Most importantly, exogenous activated protein C failed to correct the ineffective factor Va destruction despite adequate protein S levels. These data suggest that LA prevents the formation of the complex essential for rapid proteolysis of factor Va both on phospholipid and on the platelet membrane, thereby compromising the catalytic function of activated protein C. Our findings offer a new opportunity for a more comprehensive evaluation of patients with antiphospholipid antibody in defining the pathogenesis of thrombosis in this clinical condition.

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40

Lee, Yong Min, Min Woo Lee, Young Hoon Lee, and Seung-Kook Baek. "Bilateral Frosted Branch Angiitis in Anti-phospholipid Antibody Syndrome." Journal of the Korean Ophthalmological Society 63, no. 7 (July 15, 2022): 630–36. http://dx.doi.org/10.3341/jkos.2022.63.7.630.

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Purpose: We report a case of bilateral frosted branch angiitis caused by anti-phospholipid antibody syndrome.Case summary: A 60-year-old female complained of worsening vitreous floaters and decreased visual acuity in both eyes. The initial best-corrected visual acuity (BCVA) was 0.8 in the right eye and 0.05 in the left. On slit-lamp examination, inflammatory findings were observed in the anterior chamber and vitreous body of both eyes. On fundus examination, vascular sheathing in the shape of a frosted branch was observed in the posterior pole and peripheral retina in both eyes. Optical coherence tomography indicated macular edema in the left eye. Staining and leakage of dye along the vascular sheathing were observed in both eyes with fluorescein angiography. On suspicion of panuveitis, we conducted a blood test and started eye drops and oral steroid therapy. However, vitreous inflammation, macular edema, and vascular sheathing increased; thus, we proceeded with systemic steroid therapy. We conducted blood tests at 8-week intervals; lupus anticoagulant was negative but anticardiolipin antibody and anti- ß2 glycoprotein-I antibody were positive. We diagnosed the patient with bilateral frosted branch angiitis caused by anti-phospholipid antibody syndrome. During the follow-up period, the BCVA remained steady at 0.5 in the right eye and 0.3 in the left eye, without symptom recurrence.Conclusions: Bilateral frosted branch angiitis, a rare disease, is known to respond well to systemic steroid treatment. However, if accompanied by primary anti-phospholipid antibody syndrome, as in the case presented, it may have an atypical prognosis.

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Schousboe, Inger, та Margit Søe Rasmussen. "Synchronized Inhibition of the Phospholipid Mediated Autoactivation of Factor XII in Plasma by β2-glycoprotein I and Anti-β2-glycoprotein I". Thrombosis and Haemostasis 73, № 05 (1995): 798–804. http://dx.doi.org/10.1055/s-0038-1653871.

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SummaryLupus anticoagulants are a group of antibodies commonly found in patients with autoimmune diseases such as systemic lupus erythematosus. Lupus anticoagulants inhibit phospholipid dependent coagulation and may bind to negatively charged phospholipids. Recent studies have suggested an association between anti-β2-glycoprotein I and a lupus anticoagulant, whose activity is frequently dependent on the presence of β2-glycoprotein I. Based on these observations, the effect of anti-β2-glycoprotein I on the autoactivation of factor XII in plasma was investigated. Autoactivation initiated by the presence of negatively charged phospholipids, but not by sulfatide, was strongly inhibited by immunoaffinity purified anti-β2-glycoprotein I. The dose-response curve of anti-β2-gly coprotein I was identical with that of a precipitating antibody, showing no inhibition at low and high antibody dilutions and maximal inhibition at an intermediate dilution. At high antibody concentrations, an increased rate of factor Xlla activation was observed. This increase was of the same magnitude as the decreased rate observed in plasma supplemented with the same amount of β2-glycoprotein I as in the plasma itself. This confirms the inhibitory effect of β2-GP-I on the contact activation and shows that inhibition is effective on the autoactivation of factor XII in plasma. The inhibitory action of β2-glycoprotein I was independent of the inhibition caused by the anti- β2-glycoprotein I/β2-glycoprotein I complex suggesting a synchronized inhibition of factor XII autoactivation by β2-glycoprotein I and anti-β2-gly coprotein I. The inhibition caused by the antibody is suggested to be caused by a reduced availability of negatively charged phospholipids due to the binding of the anti-β2- GP-I/β2-GP-I complex. This complex may be a lupus anticoagulant.

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42

Petri, M. "Update on anti-phospholipid antibodies in SLE: the Hopkins’ Lupus Cohort." Lupus 19, no. 4 (March 30, 2010): 419–23. http://dx.doi.org/10.1177/0961203309360541.

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Anti-phospholipid antibodies are common in patients in the Hopkins’ Lupus Cohort: 47% have anti-cardiolipin, 32.5% anti-β2-glycoprotein I and 26% lupus anticoagulant (by dRVVT confirmatory testing). Systemic lupus erythematosus patients with the lupus anticoagulant at baseline have a 50% chance of a deep venous thrombosis/pulmonary embolus in the next 20 years. Anti-phospholipid antibodies differ in their association with thrombosis: the lupus anticoagulant is most strongly associated with arterial and venous thrombosis and is the only anti-phospholipid antibody associated with myocardial infarction. Anti-phospholipid antibodies are not associated with atherosclerosis. Lupus (2010) 19, 419—423.

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Uddin, MN, AKMB Karim, N. Akter, M. Ahmed, M. Orin, SA Tanni, M. Asaduzzaman, et al. "Anti-Phospholipid Antibody Syndrome with Subdural Hematoma: A Case Report." Pulse 10, no. 1 (October 19, 2018): 25–28. http://dx.doi.org/10.3329/pulse.v10i1.38608.

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A 33-year-old man with anti-phospholipid antibody syndrome associated with Budd Chiari syndrome and subdural hematoma. He developed venous thrombosis in his hepatic vein (stenting done) when laboratory studies demonstrated prolongation of activated partial thromboplastin time (APTT). Subdural hematoma demonstrated with Computed tomography (CT) of brain. Laboratory studies revealed thrombocytopenia, prolonged bleeding time and APTT, positive antinuclear antibody and positive test results for both lupus anticoagulant and an anti-cardiolipin antibody, namely antiphospholipid antibodies. Based on these findings, we consider that the tendency of this bleeding may have been due to antiphospholipid antibodies, attacking the platelet membranes and that the bridging veins in the subdural space may be the site at which the bleeding tendency easily appears. Antiphospholipid antibody syndrome accompanied by hemorrhagic complications had rarely been reported. We suggest that special attention should be given to hemorrhagic complications in patients with antiphospholipid antibody syndrome associated with fragility of the vessels and/or platelet dysfunction and on anticoagulant (warfarin).Pulse Vol.10 January-December 2017 p.25-28

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FUNAUCHI, Masanori, Masafumi SUGIYAMA, Shinnya IKOMA, Motoki OHNO, Kinnya HAMADA, and Atsushi HORIUCHI. "Thrombocytopenia in the Criteria for Anti-Phospholipid Antibody Syndrome." Internal Medicine 37, no. 9 (1998): 797–98. http://dx.doi.org/10.2169/internalmedicine.37.797.

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45

MATSUDA, SHIGEZO. "Recent knowledge on correspondent antigen of anti-phospholipid antibody." Japanese Journal of Clinical Immunology 19, no. 1 (1996): 27–38. http://dx.doi.org/10.2177/jsci.19.27.

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46

KOIKE, TAKAO. "Diagnosis and treatment of the anti-phospholipid antibody syndrome." Nihon Naika Gakkai Zasshi 87, no. 3 (1998): 466–69. http://dx.doi.org/10.2169/naika.87.466.

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47

Vaidya, S., C. C. Wang, C. Gugliuzza, and J. C. Fish. "ANTI-PHOSPHOLIPID ANTIBODY SYNDROME AND POST-TRANSPLANT RENAL THROMBOSIS." Transplantation 65, Supplement (May 1998): 153. http://dx.doi.org/10.1097/00007890-199805131-00296.

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48

Rauch, Joyce. "Platelet Phospholipid Antigen–Antibody Interactions: Detection and Biological Relevance." Transfusion Medicine Reviews 4, no. 2 (April 1990): 110–14. http://dx.doi.org/10.1016/s0887-7963(90)70255-6.

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Gharavi, Azzudin E., and Michael D. Lockshin. "Enhancement of anti-phospholipid antibody activity by Tween 20." Journal of Immunological Methods 114, no. 1-2 (November 1988): 277. http://dx.doi.org/10.1016/0022-1759(88)90185-8.

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Cheng Hwee Ming and Yap Sook Fan. "Enhancement of anti-phospholipid antibody activity by Tween 20." Journal of Immunological Methods 109, no. 2 (May 1988): 253–55. http://dx.doi.org/10.1016/0022-1759(88)90250-5.

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