Systematic review of case reports of antiphospholipid syndrome following infection

Lupus - Tập 25 Số 14 - Trang 1520-1531 - 2016
Noha Abdel‐Wahab1,2, María A. López-Olivo2, Gineth Paola Pinto-Patarroyo3, María E. Suárez-Almazor2
1Rheumatology and Rehabilitation Department, Assiut University Hospitals, Assiut, Egypt
2Section of Rheumatology and Clinical Immunology, Department of General Internal Medicine, The University of Texas, MD Anderson Cancer Center, Houston, TX, USA
3National Human Genome Research Institute, National Institutes of Health, Bethesda, MD USA

Tóm tắt

Objective The objective of this study was to conduct a systematic review of case reports documenting the development of antiphospholipid syndrome or antiphospholipid syndrome-related features after an infection. Methods We searched Medline, EMBASE, Web of Science, PubMed ePubs, and The Cochrane Library – CENTRAL through March 2015 without restrictions. Studies reporting cases of antiphospholipid syndrome or antiphospholipid syndrome-related features following an infection were included. Results Two hundred and fifty-nine publications met inclusion criteria, reporting on 293 cases. Three different groups of patients were identified; group 1 included patients who fulfilled the criteria for definitive antiphospholipid syndrome (24.6%), group 2 included patients who developed transient antiphospholipid antibodies with thromboembolic phenomena (43.7%), and group 3 included patients who developed transient antiphospholipid antibodies without thromboembolic events (31.7%). The most common preceding infection was viral (55.6%). In cases that developed thromboembolic events Human immunodeficiency and Hepatitis C viruses were the most frequently reported. Parvovirus B19 was the most common in cases that developed antibodies without thromboembolic events. Hematological manifestations and peripheral thrombosis were the most common clinical manifestations. Positive anticardiolipin antibodies were the most frequent antibodies reported, primarily coexisting IgG and IgM isotypes. Few patients in groups 1 and 2 had persistent antiphospholipid antibodies for more than 6 months. Outcome was variable with some cases reporting persistent antiphospholipid syndrome features and others achieving complete resolution of clinical events. Conclusions Development of antiphospholipid antibodies with all traditional manifestations of antiphospholipid syndrome were observed after variety of infections, most frequently after chronic viral infections with Human immunodeficiency and Hepatitis C. The causal relationship between infection and antiphospholipid syndrome cannot be established, but the possible contribution of various infections in the pathogenesis of antiphospholipid syndrome need further longitudinal and controlled studies to establish the incidence, and better quantify the risk and the outcomes of antiphospholipid-related events after infection.

Từ khóa


Tài liệu tham khảo

Miyakis S, 2006, J Thromb Haemost, 4, 295, 10.1111/j.1538-7836.2006.01753.x

Cervera R, 2002, Arthritis Rheum, 46, 1019, 10.1002/art.10187

Juby AG, 1998, Clin Invest Med, 21, 4

Levine JS, 2002, N Engl J Med, 346, 752, 10.1056/NEJMra002974

Mchrani T, 2009, Handbook of systemic autoimmune diseases, 13

Petri M, 2000, J Autoimmun, 15, 145, 10.1006/jaut.2000.0409

Shi W, 1990, Aust N Z J Med, 20, 231, 10.1111/j.1445-5994.1990.tb01025.x

Harel M, 2005, Immunobiology, 210, 743, 10.1016/j.imbio.2005.10.004

10.1177/096120339400300417

Amin NM, 2008, Hematol Oncol Clin North Am, 22, 131, 10.1016/j.hoc.2007.10.001

Blank M, 2002, J Clin Invest, 109, 797, 10.1172/JCI0212337

Shoenfeld Y, 2006, Ann Rheum Dis, 65, 2, 10.1136/ard.2005.045443

Galli M, 1990, Lancet, 335, 1544, 10.1016/0140-6736(90)91374-J

10.1177/096120339200100204

10.1191/0961203303lu394oa

Haneline MT, 2006, Evidence-based chiropractic practice

Michaelis L, 1907, Berl KlinWochenschr, 44, 1635

Wasserman A, Neisser A, 1906, Dtsch Med Wochenschr, 32, 745, 10.1055/s-0028-1142018

Landsteiner K, Muller R, 1907, Wien Klin Wochenschr, 20, 1565

Lynch FW, Boynton RE, 1941, JAMA, 115, 591, 10.1001/jama.1941.02820340013005

Putkonen T, 1952, JAMA, 150, 467, 10.1001/jama.1952.03680050033010

Harvey AM, Shulman LE, 1974, Lupus erythematosus, 4, 196

Koike T, 1984, Clin Exp Immunol, 56, 193

Moore JE, Lutz WB, 1949, J Chron Dis, 1, 297, 10.1016/0021-9681(55)90039-4

Harris EN, 1983, Lancet, 2, 1211, 10.1016/S0140-6736(83)91267-9

Harris EN, 1985, J Clin Lab Immunol, 16, 1

Harris EN, Baguley E, 1987, Br J Rheumatol, 26, 19

Hughes GR, 1986, J Rheumatol, 13, 486

Matsuura E, 1990, Lancet, 336, 177, 10.1016/0140-6736(90)91697-9

McNeil HP, 1990, Proc Natl Acad Sci U S A, 87, 4120, 10.1073/pnas.87.11.4120

Asherson RA, 2003, Ann Rheum Dis, 62, 388, 10.1136/ard.62.5.388

Cervera R, 2004, Ann Rheum Dis, 63, 1312, 10.1136/ard.2003.014175

Flateau C, 2013, Infection, 41, 867, 10.1007/s15010-013-0475-2

Nakayama T, 2014, Case Rep Rheumatol, Article ID 2715

Ramos-Casals M, 2004, Clin Infect Dis, 38, 1009, 10.1086/382537

Asherson RA, 2001, Medicine, 80, 355, 10.1097/00005792-200111000-00002

Cervera R, 2009, J Autoimmun, 32, 240, 10.1016/j.jaut.2009.02.008

Gushiken FC, 1999, Arthritis Rheum, 42, 1189, 10.1002/1529-0131(199906)42:6<1189::AID-ANR15>3.0.CO;2-8

Koike T, 2015, Int J Rheum Dis, 18, 233, 10.1111/1756-185X.12438

Sanghera DK, 1997, Hum Genet, 100, 57, 10.1007/s004390050465

Steinkasserer A, 1993, Hum Genet, 91, 401, 10.1007/BF00217367

Yasuda S, 2005, Arthritis Rheum, 52, 212, 10.1002/art.20741