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Artykuły w czasopismach na temat "Antiphospholipid syndrome"
Dutra, Livia Almeida, Pedro Braga-Neto, José Luiz Pedroso i Orlando Graziani Povoas Barsottini. "Sneddon's syndrome: case report and review of its relationship with antiphospholipid syndrome". Einstein (São Paulo) 10, nr 2 (czerwiec 2012): 230–32. http://dx.doi.org/10.1590/s1679-45082012000200018.
Pełny tekst źródłaKhamashta, Munther A., i Graham R. V. Hughes. "Antiphospholipid antibodies and antiphospholipid syndrome". Current Opinion in Rheumatology 7, nr 5 (wrzesień 1995): 389–94. http://dx.doi.org/10.1097/00002281-199509000-00005.
Pełny tekst źródłaPavlovic, Dragan, i Aleksandra Pavlovic. "Antiphospholipid syndrome". Srpski arhiv za celokupno lekarstvo 138, nr 9-10 (2010): 651–57. http://dx.doi.org/10.2298/sarh1010651p.
Pełny tekst źródłaIKEDA, Yasuo. "Antiphospholipid Syndrome". Japanese Journal of Thrombosis and Hemostasis 2, nr 2 (1991): 112–21. http://dx.doi.org/10.2491/jjsth.2.112.
Pełny tekst źródłaABE, Nobuya, i Tatsuya ATSUMI. "Antiphospholipid syndrome". Japanese Journal of Thrombosis and Hemostasis 29, nr 3 (2018): 294–306. http://dx.doi.org/10.2491/jjsth.29.294.
Pełny tekst źródłaSantos, Thaís da Silva, Izabel Galhardo Demarchi, Tatiane França Perles Mello, Jorge Juarez Vieira Teixeira i Maria Valdrinez Campana Lonardoni. "Antiphospholipid Syndrome". REVISTA CIÊNCIAS EM SAÚDE 9, nr 4 (25.11.2019): 37–42. http://dx.doi.org/10.21876/rcshci.v9i4.892.
Pełny tekst źródłaICHIKAWA, Kenji, Akito TSUTSUMI, Eiji MATSUURA i Takao KOIKE. "Antiphospholipid Syndrome." Internal Medicine 38, nr 2 (1999): 170–73. http://dx.doi.org/10.2169/internalmedicine.38.170.
Pełny tekst źródłaMakarenko, E. V. "ANTIPHOSPHOLIPID SYNDROME". Health and Ecology Issues, nr 4 (28.12.2017): 4–11. http://dx.doi.org/10.51523/2708-6011.2017-14-4-1.
Pełny tekst źródłaKoike, Takao. "Antiphospholipid syndrome." Ensho 20, nr 5 (2000): 571–80. http://dx.doi.org/10.2492/jsir1981.20.571.
Pełny tekst źródłaArnout, Jef, i Milosz Jankowski. "Antiphospholipid syndrome". Hematology Journal 5 (2004): S1—S5. http://dx.doi.org/10.1038/sj.thj.6200412.
Pełny tekst źródłaRozprawy doktorskie na temat "Antiphospholipid syndrome"
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.
Pełny tekst źródłaAmes, Paul Richard Julian. "Atherogenesis and atherosclerosis in primary antiphospholipid syndrome". Doctoral thesis, Faculdade de Ciências Médicas. UNL, 2013. http://hdl.handle.net/10362/10293.
Pełny tekst źródłaGómez, Puerta José Alfredo. "Antiphospholipid Syndrome: Expanding the Spectrum of Autoimmune Thrombosis". Doctoral thesis, Universitat de Barcelona, 2007. http://hdl.handle.net/10803/2227.
Pełny tekst źródłaThe 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.
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/.
Pełny tekst źródłaDonohoe, 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.
Pełny tekst źródłaGiannakopoulos, 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.
Pełny tekst źródłaTolomeo, 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.
Pełny tekst źródłaLe 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'
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.
Pełny tekst źródłaThis 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
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.
Pełny tekst źródłaPereira, 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.
Pełny tekst źródłaKsiążki na temat "Antiphospholipid syndrome"
Erkan, Doruk, i Silvia S. Pierangeli, red. Antiphospholipid Syndrome. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-3194-7.
Pełny tekst źródłaErkan, Doruk, i Michael D. Lockshin, red. Antiphospholipid Syndrome. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6.
Pełny tekst źródłaA, Khamashta Munther, red. Hughes syndrome: Antiphospholipid syndrome. London: Springer, 2000.
Znajdź pełny tekst źródłaservice), ScienceDirect (Online, red. Antiphospholipid syndrome in systemic autoimmune diseases. Amsterdam: Elsevier, 2009.
Znajdź pełny tekst źródłaA, Asherson Ronald, red. The antiphospholipid syndrome. Boca Raton: CRC Press, 1996.
Znajdź pełny tekst źródłaKhamashta, M. A., Maria L. Bertolaccini i Oier Ateka-Barrutia. Antiphospholipid Syndrome Handbook. London: Springer London, 2010. http://dx.doi.org/10.1007/978-1-84628-735-0.
Pełny tekst źródłaMeroni, Pier Luigi, red. Antiphospholipid Antibody Syndrome. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-11044-8.
Pełny tekst źródłaA, Khamashta Munther, red. Antiphospholipid (Hughes) syndrome. Philadelphia: Saunders, 2006.
Znajdź pełny tekst źródłaA, Khamashta Munther, red. Antiphospholipid (Hughes) syndrome. Philadelphia: Saunders, 2001.
Znajdź pełny tekst źródłaHughes, Graham, i Shirish Sangle. Hughes Syndrome: The Antiphospholipid Syndrome. London: Springer London, 2012. http://dx.doi.org/10.1007/978-0-85729-739-6.
Pełny tekst źródłaCzęści książek na temat "Antiphospholipid syndrome"
Lockshin, Michael D., i E. Nigel Harris. "History of Antiphospholipid Antibody". W Antiphospholipid Syndrome, 3–11. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_1.
Pełny tekst źródłaYelnik, Cécile M., Simone Appenzeller, Giovanni Sanna, Elizabeth Kozora i Maria Laura Bertolaccini. "Neuropsychiatric Manifestations of Antiphospholipid Syndrome". W Antiphospholipid Syndrome, 201–19. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_10.
Pełny tekst źródłaCrowther, Mark, Kimberly J. Legault, David A. Garcia, Maria G. Tektonidou, Amaia Ugarte, Ian N. Bruce, Doruk Erkan i Guillermo Ruiz-Irastorza. "Prevention and Treatment of Thrombotic Antiphospholipid Syndrome". W Antiphospholipid Syndrome, 223–33. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_11.
Pełny tekst źródłade Jesús, Guilherme Ramires, Karen J. Gibbins, Robert M. Silver i D. Ware Branch. "Prevention and Treatment of Obstetric Antiphospholipid Syndrome". W Antiphospholipid Syndrome, 235–46. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_12.
Pełny tekst źródłaUgolini-Lopes, Michelle Remião, Paulo Ricardo Criado, Kurosh Parsi, Reyhan Diz Kucukkaya, Mary-Carmen Amigo, Maria G. Tektonidou i Danieli Andrade. "Treatment of Non-criteria Manifestations in Antiphospholipid Syndrome". W Antiphospholipid Syndrome, 247–66. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_13.
Pełny tekst źródłaBarbhaiya, Medha, Danieli Andrade, Maria Laura Bertolaccini i Doruk Erkan. "Antiphospholipid Syndrome Alliance for Clinical Trials and International Networking (APS ACTION)". W Antiphospholipid Syndrome, 267–76. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_14.
Pełny tekst źródłaZuily, Stéphane, Medha Barbhaiya, Karen H. Costenbader i Doruk Erkan. "15th International Congress on Antiphospholipid Antibodies Task Force on Antiphospholipid Syndrome Classification Report". W Antiphospholipid Syndrome, 279–90. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_15.
Pełny tekst źródłaSoybilgic, Arzu, Cassyanne L. Aguiar, M. Patricia Massicotte, Gili Kenet, E. Ann Yeh, Laura Andreoli, Tadej Avcin i Barry L. Myones. "15th International Congress on Antiphospholipid Antibodies Task Force on Pediatric Antiphospholipid Syndrome Report". W Antiphospholipid Syndrome, 291–306. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_16.
Pełny tekst źródłaCervera, Ricard, Ignasi Rodríguez Pintó, Gerard Espinosa, Tamir Shragai, Miri Blank, Yehuda Shoenfeld, Ilan Krause i Thomas L. Ortel. "15th International Congress on Antiphospholipid Antibodies Task Force on Catastrophic Antiphospholipid Syndrome Report". W Antiphospholipid Syndrome, 307–16. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_17.
Pełny tekst źródłaAndrade, Danieli, Ricard Cervera, Hannah Cohen, Mark Crowther, Maria J. Cuadrado, Guillaume Canaud, David A. Garcia i in. "15th International Congress on Antiphospholipid Antibodies Task Force on Antiphospholipid Syndrome Treatment Trends Report". W Antiphospholipid Syndrome, 317–38. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55442-6_18.
Pełny tekst źródłaStreszczenia konferencji na temat "Antiphospholipid syndrome"
Vrbanec, Kristina, Igor Antončić, David Bonifačić, Siniša Dunatov i Lidija Tuškan-Mohar. "Antiphospholipid syndrome". W 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.
Pełny tekst źródłaMohammed, Mohammed H., i Mark S. Lingenfelter. "Catastrophic Antiphospholipid Syndrome (CAPS): A Rare Fatal Complication Of Antiphospholipid Syndrome". W 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.
Pełny tekst źródłaSantos 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 i Eutilia Andrade Medeiros Freire. "CATASTROPHIC ANTIPHOSPHOLIPID SYNDROME: CASE REPORT". W SBR 2021 Congresso Brasileiro de Reumatologia. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2021.2198.
Pełny tekst źródłaAydi, Z., Z. Hadj Ali, I. Rachdi, F. Daoud, H. Zoubeidi, B. BenDhaou i F. Boussema. "59 Antiphospholipid syndrome: about 62 cases". W 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.
Pełny tekst źródłaWorm Furtado, Andrea, Afonso Guilherme Schmidt, Larissa Vargas Cruz, André Lucas Ribeiro, Augusto Emílio Hinterholz, Larissa Martinelli Dullius, Vanessa Hax, Ilka Benedet Lineburger i Ricardo Machado Xavier. "Catastrophic antiphospholipid syndrome with hemorrhagic alveolitis". W SBR 2021 Congresso Brasileiro de Reumatologia. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2021.1891.
Pełny tekst źródłaPombo, ME, R. Merino, D. Pascual, MV Cuesta, A. Aguado i J. García-Consuegra. "AB0102 Antiphospholipid syndrome (aps) in children". W 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.
Pełny tekst źródłaMELO, 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 i FERNANDA MAGALHÃES DE MORAES LOPES. "CATASTROPHIC ANTIPHOSPHOLIPID SYNDROME WITH FAVORABLE OUTCOME". W 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-047.
Pełny tekst źródłaKhawaja, M., L. Magder i M. Petri. "PS4:67 Losing antiphospholipid antibody positivity post thrombosis in secondary antiphospholipid syndrome". W 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.
Pełny tekst źródłaKiefer, M., L. Schweiger i B. Moulton. "Diffuse Alveolar Hemorrhage in Primary Antiphospholipid Syndrome". W 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.
Pełny tekst źródłaEstévez, M., A. Argibay, L. Rodriguez, M. Freire, B. Gimena, J. Fernández-Martín i A. Rivera. "FRI0289 Cerebrovascular disease in the antiphospholipid syndrome". W 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.
Pełny tekst źródłaRaporty organizacyjne na temat "Antiphospholipid syndrome"
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, sierpień 2021. http://dx.doi.org/10.37766/inplasy2021.8.0074.
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