ChloroquineV1, Istex, Corpus, bibRecord, 000720

Influence of aspirin on the clinical outcomes of 103 anti-phospholipid antibodies-positive patients

Identifieur interne : 000720 ( Istex/Corpus ); précédent : 000719; suivant : 000721

Influence of aspirin on the clinical outcomes of 103 anti-phospholipid antibodies-positive patients

Auteurs : T. Hereng ; M. Lambert ; E. Hachulla ; M. Samor ; S. Dubucquoi ; C. Caron ; D. Launay ; S. Morell-Dubois ; V. Queyrel ; P.-Y. Hatron

Source :

Lupus [ 0961-2033 ] ; 2008-01.

RBID : ISTEX:7D18D17FA4B6162C90F41ABEA7C821453993C739

English descriptors

Teeft :
- American college, Anticardiolipin antibodies, Antiphospholipid, Antiphospholipid antibodies, Antiphospholipid antibody, Antiphospholipid syndrome, Aplpositive patients, Aptt, Arthritis rheum, Aspirin, Aspirin intake, Aspirin test, Asymptomatic patients, Autoimmune thrombocytopenia, Cohort, Conventional thrombotic risk factors, Erkan, Erythematosus, Fetal death, Figure curve, Higher risk, Idiopathic phenomenon, Immune thrombocytopenic purpura, Internal medicine, Lupus, Lupus antibodies, Lupus anticoagulants, Lupus erythematosus, Marc lambert, Other diseases, Partial thromboplastin times, Patient subgroups, Primary biliary cirrhosis, Primary prevention, Prospective study, Pulmonary embolism, Rheumatoid arthritis, Standard deviation, Statistical analyses, Syndrome, Systemic lupus erythematosus, Systemic sclerosis, Thromb haemost, Thrombosis, Thrombotic, Thrombotic event, Thrombotic events, University hospital, Venous, Venous thrombosis.

Abstract

One hundred and three consecutive asymptomatic anti-phospholipid (aPL) antibody-positive carriers, taking aspirin (n = 75) or not (n = 28), were studied retrospectively to determine whether aspirin could provide primary prevention of anti-phospholipid syndrome (APS) symptoms. All patients positive for anti-cardiolipin antibodies (aCL; >25 UGPL or UMPL) and/or lupus anti-coagulant were followed for a mean of 64 ± 24.7 months. Among aPL-positive patients, 37 had systemic lupus erythematosus (SLE), 20 had prolonged activated partial thromboplastin times, 19 had other connective tissue diseases, 16 had autoimmune thrombocytopenia (AIT), 11 had diverse diseases. Nineteen patients experienced thrombotic event(s) during follow-up. Clinical features, biological parameters and hydroxychloroquine use were comparable for the two groups, but thrombotic events differed (log-rank test; P = 0.02). Four of the 10 SLE patients not taking aspirin developed thrombosis compared with 3/27 SLE patients taking aspirin (log-rank test; P = 0.03). Anti-phospholipid -positive patients with AIT developed fewer thromboses while taking aspirin (log-rank test; P = 0.01). In conclusion, aPL-positive SLE and AIT patients should take aspirin to prevent APS manifestations. Prospective therapeutic trials are needed to confirm aspirin's prophylactic role in such patients. Lupus (2008) 17, 11—15.

Url:

https://api.istex.fr/ark:/67375/M70-641T2Q8M-X/fulltext.pdf

DOI: 10.1177/0961203307084724

Links to Exploration step

ISTEX:7D18D17FA4B6162C90F41ABEA7C821453993C739

Le document en format XML

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<abstract xml:lang="en"><p>One hundred and three consecutive asymptomatic anti-phospholipid (aPL) antibody-positive carriers, taking aspirin (n = 75) or not (n = 28), were studied retrospectively to determine whether aspirin could provide primary prevention of anti-phospholipid syndrome (APS) symptoms. All patients positive for anti-cardiolipin antibodies (aCL; >25 UGPL or UMPL) and/or lupus anti-coagulant were followed for a mean of 64 ± 24.7 months. Among aPL-positive patients, 37 had systemic lupus erythematosus (SLE), 20 had prolonged activated partial thromboplastin times, 19 had other connective tissue diseases, 16 had autoimmune thrombocytopenia (AIT), 11 had diverse diseases. Nineteen patients experienced thrombotic event(s) during follow-up. Clinical features, biological parameters and hydroxychloroquine use were comparable for the two groups, but thrombotic events differed (log-rank test; P = 0.02). Four of the 10 SLE patients not taking aspirin developed thrombosis compared with 3/27 SLE patients taking aspirin (log-rank test; P = 0.03). Anti-phospholipid -positive patients with AIT developed fewer thromboses while taking aspirin (log-rank test; P = 0.01). In conclusion, aPL-positive SLE and AIT patients should take aspirin to prevent APS manifestations. Prospective therapeutic trials are needed to confirm aspirin's prophylactic role in such patients. Lupus (2008) 17, 11—15.</p>
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<title-group><article-title>Influence of aspirin on the clinical outcomes of 103 anti-phospholipid antibodies-positive patients</article-title>
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         <contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Hereng</surname>
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         <contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Lambert</surname>
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         <contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Samor</surname>
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         <contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Dubucquoi</surname>
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         <contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Caron</surname>
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<aff>Hemostasis Laboratory, University Hospital of Lille, Faculty of Medicine and Lille University, 59035 Lille Cedex, France</aff>
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         <contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Launay</surname>
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         <contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Morell-Dubois</surname>
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         <contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Queyrel</surname>
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         <contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Hatron</surname>
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<abstract><p>One hundred and three consecutive asymptomatic anti-phospholipid (aPL) antibody-positive carriers, taking aspirin (<italic>n</italic>
 = 75) or not (<italic>n</italic>
 = 28), were studied retrospectively to determine whether aspirin could provide primary prevention of anti-phospholipid syndrome (APS) symptoms. All patients positive for anti-cardiolipin antibodies (aCL; >25 UGPL or UMPL) and/or lupus anti-coagulant were followed for a mean of 64 ± 24.7 months.</p> 
            <p>Among aPL-positive patients, 37 had systemic lupus erythematosus (SLE), 20 had prolonged activated partial thromboplastin times, 19 had other connective tissue diseases, 16 had autoimmune thrombocytopenia (AIT), 11 had diverse diseases. Nineteen patients experienced thrombotic event(s) during follow-up. Clinical features, biological parameters and hydroxychloroquine use were comparable for the two groups, but thrombotic events differed (log-rank test; <italic>P</italic>
 = 0.02). Four of the 10 SLE patients not taking aspirin developed thrombosis compared with 3/27 SLE patients taking aspirin (log-rank test; <italic>P</italic>
 = 0.03). Anti-phospholipid -positive patients with AIT developed fewer thromboses while taking aspirin (log-rank test; <italic> P</italic>
 = 0.01). In conclusion, aPL-positive SLE and AIT patients should take aspirin to prevent APS manifestations. Prospective therapeutic trials are needed to confirm aspirin's prophylactic role in such patients. <italic>Lupus</italic>
 (2008) <bold>17</bold>
, 11—15.</p>
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<meta-value>11 PaperInfluence of aspirin on the clinical outcomes of 103 anti-phospholipid antibodies-positive patients SAGE Publications, Inc.200810.1177/0961203307084724 T.Hereng Department of Internal Medicine M.Lambert Department of Internal Medicine, m-lambert@chru-lille.fr E.Hachulla Department of Internal Medicine M.Samor Department of Internal Medicine S.Dubucquoi Immunology Laboratory C.Caron Hemostasis Laboratory, University Hospital of Lille, Faculty of Medicine and Lille University, 59035 Lille Cedex, France D.Launay Department of Internal Medicine S.Morell-Dubois Department of Internal Medicine V.Queyrel Department of Internal Medicine P.-Y.Hatron Department of Internal Medicine *Correspondence: Dr Marc Lambert, Department of Internal Medicine, CHRU de Lille, Hôpital Huriez rue Polonovski, 59035 CHRU Lille Cedex, Received 4 January 2007; accepted 7 September 2007 One hundred and three consecutive asymptomatic anti-phospholipid (aPL) antibody-positive carriers, taking aspirin (n = 75) or not (n = 28), were studied retrospectively to determine whether aspirin could provide primary prevention of anti-phospholipid syndrome (APS) symptoms. All patients positive for anti-cardiolipin antibodies (aCL; >25 UGPL or UMPL) and/or lupus anti-coagulant were followed for a mean of 64 ± 24.7 months. Among aPL-positive patients, 37 had systemic lupus erythematosus (SLE), 20 had prolonged activated partial thromboplastin times, 19 had other connective tissue diseases, 16 had autoimmune thrombocytopenia (AIT), 11 had diverse diseases. Nineteen patients experienced thrombotic event(s) during follow-up. Clinical features, biological parameters and hydroxychloroquine use were comparable for the two groups, but thrombotic events differed (log-rank test; P = 0.02). Four of the 10 SLE patients not taking aspirin developed thrombosis compared with 3/27 SLE patients taking aspirin (log-rank test; P = 0.03). Anti-phospholipid -positive patients with AIT developed fewer thromboses while taking aspirin (log-rank test; P = 0.01). In conclusion, aPL-positive SLE and AIT patients should take aspirin to prevent APS manifestations. Prospective therapeutic trials are needed to confirm aspirin's prophylactic role in such patients. Lupus (2008) 17, 11—15. anti-phospholipid antibody syndrome aspirin prevention systemic lupus erythematosus Introduction Anti-phospholipid syndrome (APS) has been de ned as the occurrence of thrombosis (arterial and/or venous) or fetal loss in patients with anti-phospholipid antibodies (aPL), such as anti-cardiolipin antibodies (aCL) or lupus anti-coagulant (LA).1 Systemic lupus erythematosus (SLE) patients have a higher risk of thrombosis than the general population2 and >30% of them will develop APS during follow-up,2 which sug- gests that primary prevention of thrombosis should be considered for them. Between 1 and 6.5% of blood donors are aCL-positive, and 1.2–3.8% of healthy controls are LA-positive.3 Ginsburg et al.4 showed that healthy men with high aCL titers were at risk for deep venous thrombosis or pulmonary embolism. And Finazzi et al.5 demonstrated that a high IgG-aCL titer was an independent predictor of thrombosis. Because of the aPL frequency in the healthy population and the higher risk of developing thrombosis for aPL-positive patients, it should prove useful to evaluate primary aspirin prophylaxis to pre- vent thrombotic events. We retrospectively studied a cohort of patients found to be aPL-positive on two occasions, with no known thrombotic event at the beginning of follow-up, to determine whether aspirin had an impact on APS manifestations. Patients and methods Patients From 1995 to 2000, an average of 1642 inpatients and outpatients consulting in our internal medicine depart- ment were tested annually for IgG- and IgM-aCL in the Laboratory of Immunology, and 1200 for LA in the Laboratory of Hemostasis. From 1995 to 2000, 12 575 patients were aCL- and/or LA-positive on two con- secutive occasions. Among them, 108 had not experi- enced any known thrombosis or obstetrical event when aPL positivity was con rmed. To determine whether they had APS, aPL-positive women were referred to our outpatient consultation: they were always asked about obstetrical complications to con rm or refute the diagnosis. The 108 patients are referred to henceforth as asymptomatic aPL-positive patients. Three of them were lost to follow-up and two patients received long- term anti-coagulation: one patient with neuropsychi- atric manifestations during an SLE are was prescribed corticosteroids, cyclophosphamide and warfarin because of high aPL levels; the other received low-molecular-weight heparin and aspirin during pregnancy. Therefore, the characteristics of 103 aPL- positive patients, from their initial consultation in our department (when aPL were rst detected) until December 2005, were analysed, retrospectively. For the 10 patients not followed in our department until December 2005, they or their treating physician were contacted by phone to update their les concerning thrombotic events and treatment until that date. De nitions of the diseases Systemic lupus erythematosus was classi ed accord- ing to the criteria of the American College of Rheumatology.6 Autoimmune thrombocytopenia (AIT) was classi ed according to standardized crite- ria.7 Some patients were investigated because of their prolonged activated partial thromboplastin times (APTT), which led to LA detection. Migraine was de ned according to the international classi cation of headache disorders.8 During follow-up, APS was clas- si ed according to the Sapporo criteria.1 Myocardial infarction was diagnosed based on typical electrocar- diographic features and elevated creatine kinase. Stroke diagnosis was based on clinical manifestations and abnormal cerebral computed tomography (CT) scan or cerebral magnetic resonance imaging. Deep vein thrombosis was diagnosed ultrasonographically, and pulmonary embolism based on lung scintigraphy and/or pulmonary CT scan. Anti-phospholipid measurements Anti-cardiolipin antibodies titers were determined using the Inova-QuantaliteTM commercial kit (Inova, San Diego, CA, USA) with quanti cation of IgG and IgM subfractions in standardized units. Only samples containing >25 UGPL or UMPL were considered aCL-positive. The revised criteria of the Subcommittee on Lupus anti-coagulants/anti-phospholipid antibodies, using diluted thromboplastin time, activated cephalin time and the Rosove index were applied to detect the presence of LA.9 Treatments Hydroxychloroquine was prescribed for continuous use to all SLE patients. Because no international rec- ommendations on aspirin use in aPL-positive patients were available between 1995 and 2000, aspirin use was left to the discretion of the treating physician without randomization. No oral anti-coagulation was prescribed to asymptomatic aPL-positive patients. Statistical analysis Statistical analyses were performed on data obtained after aPL con rmation. We used SPSS software ver- sion 11.0.1. Data are expressed as means ± standard deviation, n (%) or median (range). Comparisons between patient subgroups were performed using Students' t-test and nonparametric Mann–Whitney tests. Differences between percentages were estimated using χ2 or Fisher's exact test, when necessary. Survival probability was analysed with Kaplan–Meier curves and log-rank tests. A P < 0.05 was considered signi cant. Results One hundred and three aPL-positive patients were evaluated (91 women, 12 men). Their mean age at the time of the rst aPL determination was 41.7 ± 16.7 years. The mean duration of follow-up was 64 ± 24.7 months, with 83% of the patients having been followed for ≥50 months. Associated diseases in aPL-positive patients were: SLE (n = 37), AIT (n = 16), rheuma- toid arthritis (RA, n = 8), systemic sclerosis (SSc, n = 7), Sjögrens' syndrome (n = 4) or other diseases (n = 11). Prolonged APTT was the only abnormality in 20 patients. The main characteristics of the 103 aPL-positive patients studied as a function of aspirin intake are reported in Table 1: 75 took aspirin and 28 did not. Nineteen patients developed 24 APS manifestations during follow-up: 12 arterial thromboses (10 strokes, two myocardial infarctions), nine venous thromboses (seven deep vein thromboses, two pulmonary emboli), three obstetrical events (one fetal death secondary to eclampsia associated with a retroplacental hematoma, one fetal death at 32 weeks of gestation, one pre- eclampsia). Mean rst aPL determination to thrombosis interval was 32.2 ± 17 months (range, 3–72 months). These 19 patients were diagnosed as having SLE (n = 7), AIT (n = 5), an isolated APTT inhibitor 13 Table 1 Characteristics of asymptomatic aPL carriers as a function of aspirin use during follow-up aOther diseases were: temporal arteritis (n = 5), Raynauds' phenomenon (n = 3), primary biliary cirrhosis (n = 2), Graves' disease (n = 1). SD, standard deviation; SLE, systemic lupus erythematosus; APTT, activated partial thromboplastin time; AIT, autoimmune thrombocytopenia; RA, rheumatoid arthritis; SSc, systemic sclerosis; LA, lupus anti-coagulant; aCL, anti-cardiolipin; APS, anti-phospholipid syndrome; de ned as known arterial and/or venous thrombosis and/or obstetrical events, according to the Sapporo criteria.1 (n = 2), Sjögren's syndrome (n = 2), idiopathic Raynaud's phenomenon (n = 2) and one with primary biliary cirrhosis. According to our univariate analysis, the frequencies of aCL Ig G and aCL Ig M were signi cantly higher in patients taking aspirin (P = 0.018 and P = 0.012, respectively). Aspirin was signi cantly associated with a thrombotic event (P = 0.02). Comparisons of patients taking aspirin or not during follow-up showed (Table 1) comparable SLE rates, LA frequency, IgG- and IgM- aCL levels and use of hydroxychloroquine. However, they differed signi cantly for thrombotic events [Figure 1(a); Kaplan–Meier curve, log-rank test, P = 0.02]. Among SLE patients, four of the 10 not taking aspirin developed a thrombosis during follow-up versus three of the 27 SLE taking aspirin (Figure 1(b); Kaplan–Meier curve, log-rank test, P = 0.03). Four of the six AIT patients not taking aspirin suffered a throm- botic event versus one of the 10 taking aspirin during follow-up (Figure 1(c); Kaplan–Meier curve, log-rank test, P = 0.01). No severe bleeding event occurred in any of the cohort patients during follow-up, including those with AIT. Conventional thrombotic risk factors were comparable between aPL-positive patients taking aspirin or not, respectively, 34.6% (n = 26) and 39.2% (n = 11) (Table 2). Discussion The results of this analysis showed that the frequency of APS symptoms was lower in aPL-positive patients taking aspirin, particularly those with SLE or AIT. In our department, all rheumatology inpatients and outpa- tients are systematically tested for aPL, which can explain the high number of aPL-positive patients with- out APS manifestations. However, low aPL frequen- cies in apparently healthy populations have been reported.2,3 Although aPL in APS patients have been associated with the occurrence and recurrence of thrombotic events, only limited data are available concerning primary prevention of these events. Unfortunately, our analysis was retrospective with- out randomization of aspirin and with several biases. Aspirin use was left to the discretion of the treating physician and so 27.1% of our patients were not taking aspirin. Moreover, patients taking aspirin had higher frequencies of IgG- and IgM-aCL and therefore, should have a higher risk of thrombosis. The livedo frequency in our cohort was low (7.7%) but similar to that of Erkan et al. (11–12%).10 Although our results must be interpreted with caution, they support the use of aspirin in aPL-positive SLE and AIT patients to prevent thrombotic events. 14 Figure 1 Kaplan-–Meier curves of thrombotic event-free sur- vival for the entire aPL-positive population [(a), n = 103], only SLE patients [(b), n = 37] and only AIT patients [(c), n = 16] according to aspirin intake. Age, sex, conventional thrombotic risk factors, APS- associated manifestations (livedo, thrombocytopenia), SLE frequency, hydroxychloroquine use did not differ Table 2 Conventional thrombotic risk factors in the 103 aPL-positive patients Values are expressed as n (%). between aPL-positive patients taking aspirin or not, but they differed signi cantly for thrombotic complications. The frequency of conventional thrombotic risk factors was similar to that of observed in the prospective pri- mary prevention trial by Erkan et al.10 Unfortunately, hypercholesterolemia rates of our patient subgroups could not be compared, but Erkan et al. reported rates of 4–10% in aPL-positive patients.10 Although aspirin was not randomly prescribed in our cohort, the clinical and biological pro les of patients taking aspirin or not were comparable except for aCL IgG and aCL IgM, which suggests no between-group major bias. Moreover, their aPL pro les, initially and during follow-up, were similar to those obtained in the prospective study by Giron-Gonzalez et al.11 In our study, 18% of the patients developed thrombosis with a mean time to thrombosis of 32.2 months, which is sim- ilar to that reported by McClain et al.,12 who found that aCL detection preceded the rst thrombotic event by a mean of 37 months in SLE patients. It is important to keep in mind that seven of our 19 patients who developed APS symptoms during follow-up had SLE and ve had AIT. SLE patients must be analysed separately. Thus considering only our SLE patients, 18.9% (7/37) experienced throm- botic events during follow-up, compared with 30–50% previously reported.12–16 This difference could be explained by our patient's aspirin use. Indeed APS fre- quency in our SLE patients not taking aspirin (40%) is in accordance with literature values. However, few sta- tistical analyses have examined the impact of aspirin on the prevention of APS symptoms in aPL-positive SLE patients. Wahl et al.17 conducted a Markov-decision analysis to evaluate prophylactic aspirin in SLE patients and concluded that it should be prescribed to all SLE patients, especially aPL carriers, to prevent arterial and venous thrombotic manifestations. However, their recommendations were based on a the- oretical analysis. Erkan et al.18 concluded that aspirin use seemed to prevent thromboses in aPL-positive patients in their cohort in which 78% of their 56 aPL- positive patients had SLE. But that study had not been 15 designed to evaluate the prophylactic effect of aspirin. In our study, SLE patients taking aspirin suffered signi cantly fewer thrombotic APS-de ning events during follow-up. Despite our small SLE population, our results suggest that aspirin would be useful for primary prevention of thrombosis in aPL-positive SLE patients. Although hydroxychloroquine has lipid- lowering properties, its preventive effect on thrombosis has not been clearly established19,20 and could not be con rmed in our study. About 33% of our aPL-positive AIT patients experi- enced thrombotic events, compared with 45% reported previously.21,22 These APS symptoms occurred signi - cantly less frequently in our AIT patients taking aspirin, in accordance with Diz-Kucukkaya et al.21 Only seven of our patients without SLE or AIT developed APS-de ning thrombotic events: two with prolonged APTT, two with Sjögrens' syndrome, two with idiopathic Raynaud's phenomenon and one with primary biliary cirrhosis. It is dif cult to determine aspirin's impact for these patients. Indeed, Giron- Gonzalez et al.11 reported that their 178 aPL-positive patients, with biological evidence of an APTT inhibitor without connective tissue disease, did not develop any thrombosis during 36 months of follow-up without aspirin, but 12 of them had received enoxaparin because of prolonged immobilization. Most recently, Erkan et al. published the results of their prospective study on APS primary prevention with aspirin and con- cluded that aPL-positive individuals do not bene t from low-dose aspirin.10 However, the SLE-patient subgroup was not analysed separately. Therefore, no de nitive conclusion can be drawn about the in uence of aspirin in this setting. Thus, the results of our retrospective study and those of others17,18 suggest that prospective therapeutic trials are needed to determine the real prophylactic impact of aspirin as preventive therapy in aPL-positive patients with SLE or AIT. Acknowledgments The authors thank Valerie Deken, Biostatistics Department, University Hospital of Lille for conducting the statistical analyses. The rst two authors, Thomas Hereng and Marc Lambert, contributed equally to this work. References Wilson WA, Gharavi AE, Koike T. et al. International consensus statement on preliminary classification criteria for definite antiphospholipid syndrome: report of an international workshop. Arthritis Rheum 1999; 42: 1309—1311. Petri M. Epidemiology of the antiphospholipid antibody syndrome. J Autoimmun 2000; 15: 145—151. Vila P., Hernandez MC, Lopez-Fernandez MF, Battle J. Prevalence, follow-up and clinical significance of the anticardiolipin in normal subjects. Thromb Haemost 1994; 72: 209—213. Ginsburg KS, Liang MH, Newcomer L. et al. Anticardiolipin antibodies and the risk for ischemic stroke and venous thrombosis. Ann Intern Med 1992 ; 117: 997—1002. Finazzi G., Brancaccio V., Moia M. et al. Natural history and risk factors for thrombosis in 360 patients with antiphospholipid antibodies: a four-year prospective study from the Italian registry. Am J Med 1996; 100: 530—536. Hochberg MC Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum 1997; 40: 1725. Cines DB, Blanchette VS Immune thrombocytopenic purpura. N Engl J Med 2002; 346: 995—1008. Headache Classification Subcommittee of the International Headache Society. The International Classification of Headache disorders, 2nd edition, Cephalalgia, 2004; 24: 9—160. Brandt JT, Barna LK, Triplett DA Laboratory identification of lupus anticoagulants: results of the Second International Workshop for Identification of Lupus Anticoagulants, on behalf of the Subcommittee on Lupus Anticoagulants/Antiphospholipid Antibodies of the ISTH. Thromb Haemost 1995; 74: 1597—1603. Erkan D., Harrison MJ, Levy R., Peterson M., Petri M., Sammaritano L. et al. Aspirin for primary thrombosis prevention in the antiphospholipid syndrome: a randomized, double-blind, placebo-controlled trial in asymptomatic antiphospholipid antibody-positive individuals. Arthritis Rheum 2007; 56: 238—291. Giron-Gonzalez JA, Garcia Del Rio E, Rodriguez C, Rodriguez-Martorell J, Serrano A. Antiphospholipid syndrome and asymptomatic carriers of antiphospholipid antibody: prospective analysis of 404 individuals. J Rheumatol 2004; 31: 1560—1567. McClain MT, Arbuckle MR, Heinlen LD et al. The prevalence, onset, and clinical significance of antiphospholipid antibodies prior to diagnosis of systemic lupus erythematosus. Arthritis Rheum 2004; 50: 1226—1232. Love PE, Santoro SA Antiphospholipid antibodies, anticardiolipin and the lupus anticoagulant in systemic lupus erythematosus (SLE) and in non-SLE disorders. Ann Intern Med 1990; 112: 682—689. Papadopolous E., Magder L., Petri M. Antiphospholipid antibodies and venous thrombosis (VT) in SLE. Arthritis Rheum 1999; 42: S369. Shah NM, Khamashta MA, Atsumi T., Hughes Grv. Outcome of patients with anticardiolipin antibodies: a 10 year follow-up of 52 patients. Lupus 1998; 7: 3—6. de Bandt M. , Benali K., Guillevin L. et al. Longitudinal determination of antiphospholipid antibodies in lupus patients without previous manifestations of antiphospholipid syndrome: a prospective study. J Rheumatol 1999; 26: 91—96. Wahl DG, Bounameaux H., de Moerloose P., Sarasin FP Prophylactic antithrombotic therapy for patients with systemic lupus erythematosus with or without antiphospholipid antibodies: do the benefits outweigh the risks? A decision analysis. Arch Intern Med 2000; 160: 2042—2048. Erkan D., Yazici Y., Peterson MG, Sammaritano L., Lockshin MD A cross-sectional study of clinical thrombotic risk factors and preventive treatments in antiphospholipid syndrome. Rheumatology 2002; 41: 924—929. Bruce IN `Not only...but also': factors that contribute to accelerated atherosclerosis and premature coronary heart disease in systemic lupus erythematosus. Rheumatology 2005; 44: 1492—1502. Ho KT, Ahn CW, Alarcón GS et al. Systemic lupus erythematosus in a multiethnic cohort (LUMINA): XXVIII. Factors predictive of thrombotic events. Rheumatology 2005; 44: 1303—1307. Diz-Kucukkaya R., Hacihanefioglu A., Yenerel M. et al. Antiphospholipid antibodies and antiphospholipid syndrome in patients presenting with immune thrombocytopenic purpura: a prospective cohort study. Blood 2001; 98: 1760—1764. Atsumi T., Furukawa S., Amengual O., Koike T. Antiphospholipid antibody associated thrombocytopenia and the paradoxical risk of thrombosis. Lupus 2005; 14: 499—504.</meta-value>
</custom-meta>
</custom-meta-wrap>
</article-meta>
</front>
<back><ref-list> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Wilson WA</surname>
</name>
, <name name-style="western"><surname>Gharavi AE</surname>
</name>
, <name name-style="western"><surname>Koike T.</surname>
</name>
 et al. <article-title>International consensus statement on preliminary classification criteria for definite antiphospholipid syndrome: report of an international workshop</article-title>
. <source>Arthritis Rheum</source> 
               <year>1999</year>
; <volume>42</volume>
: <fpage>1309</fpage>
—<lpage>1311</lpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Petri M.</surname>
</name> 
               <article-title>Epidemiology of the antiphospholipid antibody syndrome</article-title>
. <source>J Autoimmun</source> 
               <year>2000</year>
; <volume>15</volume>
: <fpage>145</fpage>
—<lpage>151</lpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Vila P.</surname>
</name>
, <name name-style="western"><surname>Hernandez MC</surname>
</name>
, <name name-style="western"><surname>Lopez-Fernandez MF</surname>
</name>
, <name name-style="western"><surname>Battle J.</surname>
</name> 
               <article-title>Prevalence, follow-up and clinical significance of the anticardiolipin in normal subjects</article-title>
. <source>Thromb Haemost</source> 
               <year>1994</year>
; <volume>72</volume>
: <fpage>209</fpage>
—<lpage>213</lpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Ginsburg KS</surname>
</name>
, <name name-style="western"><surname>Liang MH</surname>
</name>
, <name name-style="western"><surname>Newcomer L.</surname>
</name>
 et al. <article-title>Anticardiolipin antibodies and the risk for ischemic stroke and venous thrombosis</article-title>
. <source>Ann Intern Med</source> 
               <year>1992</year>
 ; <volume>117</volume>
: <fpage>997</fpage>
—<lpage>1002</lpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Finazzi G.</surname>
</name>
, <name name-style="western"><surname>Brancaccio V.</surname>
</name>
, <name name-style="western"><surname>Moia M.</surname>
</name>
 et al. <article-title>Natural history and risk factors for thrombosis in 360 patients with antiphospholipid antibodies: a four-year prospective study from the Italian registry</article-title>
. <source>Am J Med</source> 
               <year>1996</year>
; <volume>100</volume>
: <fpage>530</fpage>
—<lpage>536</lpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Hochberg MC</surname>
</name> 
               <article-title>Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus</article-title>
. <source>Arthritis Rheum</source> 
               <year>1997</year>
; <volume>40</volume>
: <fpage>1725</fpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Cines DB</surname>
</name>
, <name name-style="western"><surname>Blanchette VS</surname>
</name> 
               <article-title>Immune thrombocytopenic purpura</article-title>
. <source>N Engl J Med</source> 
               <year>2002</year>
; <volume>346</volume>
: <fpage>995</fpage>
—<lpage>1008</lpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Headache Classification Subcommittee of the International Headache Society.</surname>
</name> 
               <article-title>The International Classification of Headache disorders</article-title>
, <edition>2</edition>
nd edition, <source>Cephalalgia</source>
, <year>2004</year>
; <volume>24</volume>
: <fpage>9</fpage>
—<lpage>160</lpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Brandt JT</surname>
</name>
, <name name-style="western"><surname>Barna LK</surname>
</name>
, <name name-style="western"><surname>Triplett DA</surname>
</name> 
               <article-title>Laboratory identification of lupus anticoagulants: results of the Second International Workshop for Identification of Lupus Anticoagulants, on behalf of the Subcommittee on Lupus Anticoagulants/Antiphospholipid Antibodies of the ISTH</article-title>
. <source>Thromb Haemost</source> 
               <year>1995</year>
; <volume>74</volume>
: <fpage>1597</fpage>
—<lpage>1603</lpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Erkan D.</surname>
</name>
, <name name-style="western"><surname>Harrison MJ</surname>
</name>
, <name name-style="western"><surname>Levy R.</surname>
</name>
, <name name-style="western"><surname>Peterson M.</surname>
</name>
, <name name-style="western"><surname>Petri M.</surname>
</name>
, <name name-style="western"><surname>Sammaritano L.</surname>
</name>
 et al. <article-title>Aspirin for primary thrombosis prevention in the antiphospholipid syndrome: a randomized, double-blind, placebo-controlled trial in asymptomatic antiphospholipid antibody-positive individuals</article-title>
. <source>Arthritis Rheum</source> 
               <year>2007</year>
; <volume>56</volume>
: <fpage>238</fpage>
—<lpage>291</lpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Giron-Gonzalez JA</surname>
</name>
, <article-title>Garcia Del Rio E, Rodriguez C, Rodriguez-Martorell J, Serrano A. Antiphospholipid syndrome and asymptomatic carriers of antiphospholipid antibody: prospective analysis of 404 individuals</article-title>
. <source>J Rheumatol</source> 
               <year>2004</year>
; <volume>31</volume>
: <fpage>1560</fpage>
—<lpage>1567</lpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>McClain MT</surname>
</name>
, <name name-style="western"><surname>Arbuckle MR</surname>
</name>
, <name name-style="western"><surname>Heinlen LD</surname>
</name>
 et al. <article-title>The prevalence, onset, and clinical significance of antiphospholipid antibodies prior to diagnosis of systemic lupus erythematosus</article-title>
. <source>Arthritis Rheum</source> 
               <year>2004</year>
; <volume>50</volume>
: <fpage>1226</fpage>
—<lpage>1232</lpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Love PE</surname>
</name>
, <name name-style="western"><surname>Santoro SA</surname>
</name> 
               <article-title>Antiphospholipid antibodies, anticardiolipin and the lupus anticoagulant in systemic lupus erythematosus (SLE) and in non-SLE disorders</article-title>
. <source>Ann Intern Med</source> 
               <year>1990</year>
; <volume>112</volume>
: <fpage>682</fpage>
—<lpage>689</lpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Papadopolous E.</surname>
</name>
, <name name-style="western"><surname>Magder L.</surname>
</name>
, <name name-style="western"><surname>Petri M.</surname>
</name> 
               <article-title>Antiphospholipid antibodies and venous thrombosis (VT) in SLE</article-title>
. <source>Arthritis Rheum</source> 
               <year>1999</year>
; <volume>42</volume>
: <fpage>S369</fpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Shah NM</surname>
</name>
, <name name-style="western"><surname>Khamashta MA</surname>
</name>
, <name name-style="western"><surname>Atsumi T.</surname>
</name>
, <name name-style="western"><surname>Hughes Grv.</surname>
</name> 
               <article-title>Outcome of patients with anticardiolipin antibodies: a 10 year follow-up of 52 patients</article-title>
. <source>Lupus</source> 
               <year>1998</year>
; <volume>7</volume>
: <fpage>3</fpage>
—<lpage>6</lpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>de Bandt M.</surname>
</name>
 , <name name-style="western"><surname>Benali K.</surname>
</name>
, <name name-style="western"><surname>Guillevin L.</surname>
</name>
 et al. <article-title>Longitudinal determination of antiphospholipid antibodies in lupus patients without previous manifestations of antiphospholipid syndrome: a prospective study</article-title>
. <source>J Rheumatol</source> 
               <year>1999</year>
; <volume>26</volume>
: <fpage>91</fpage>
—<lpage>96</lpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Wahl DG</surname>
</name>
, <name name-style="western"><surname>Bounameaux H.</surname>
</name>
, <name name-style="western"><surname>de Moerloose P.</surname>
</name>
, <name name-style="western"><surname>Sarasin FP</surname>
</name> 
               <article-title>Prophylactic antithrombotic therapy for patients with systemic lupus erythematosus with or without antiphospholipid antibodies: do the benefits outweigh the risks? A decision analysis</article-title>
. <source>Arch Intern Med</source> 
               <year>2000</year>
; <volume>160</volume>
: <fpage>2042</fpage>
—<lpage>2048</lpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Erkan D.</surname>
</name>
, <name name-style="western"><surname>Yazici Y.</surname>
</name>
, <name name-style="western"><surname>Peterson MG</surname>
</name>
, <name name-style="western"><surname>Sammaritano L.</surname>
</name>
, <name name-style="western"><surname>Lockshin MD</surname>
</name> 
               <article-title>A cross-sectional study of clinical thrombotic risk factors and preventive treatments in antiphospholipid syndrome</article-title>
. <source>Rheumatology</source> 
               <year>2002</year>
; <volume>41</volume>
: <fpage>924</fpage>
—<lpage>929</lpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Bruce IN</surname>
</name>
 `<article-title>Not only...but also': factors that contribute to accelerated atherosclerosis and premature coronary heart disease in systemic lupus erythematosus</article-title>
. <source>Rheumatology</source> 
               <year>2005</year>
; <volume>44</volume>
: <fpage>1492</fpage>
—<lpage>1502</lpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Ho KT</surname>
</name>
, <name name-style="western"><surname>Ahn CW</surname>
</name>
, <name name-style="western"><surname>Alarcón GS</surname>
</name>
 et al. <article-title>Systemic lupus erythematosus in a multiethnic cohort (LUMINA): XXVIII. Factors predictive of thrombotic events</article-title>
. <source>Rheumatology</source> 
               <year>2005</year>
; <volume>44</volume>
: <fpage>1303</fpage>
—<lpage>1307</lpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Diz-Kucukkaya R.</surname>
</name>
, <name name-style="western"><surname>Hacihanefioglu A.</surname>
</name>
, <name name-style="western"><surname>Yenerel M.</surname>
</name>
 et al. <article-title>Antiphospholipid antibodies and antiphospholipid syndrome in patients presenting with immune thrombocytopenic purpura: a prospective cohort study</article-title>
. <source>Blood</source> 
               <year>2001</year>
; <volume>98</volume>
: <fpage>1760</fpage>
—<lpage>1764</lpage>
.</citation> 
         </ref> 
         <ref> 
            <citation citation-type="journal" xlink:type="simple"> 
               <name name-style="western"><surname>Atsumi T.</surname>
</name>
, <name name-style="western"><surname>Furukawa S.</surname>
</name>
, <name name-style="western"><surname>Amengual O.</surname>
</name>
, <name name-style="western"><surname>Koike T.</surname>
</name> 
               <article-title>Antiphospholipid antibody associated thrombocytopenia and the paradoxical risk of thrombosis</article-title>
. <source>Lupus</source> 
               <year>2005</year>
; <volume>14</volume>
: <fpage>499</fpage>
—<lpage>504</lpage>
.</citation> 
         </ref> 
      </ref-list>
</back>
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<namePart type="family">Hereng</namePart>
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<affiliation>Department of Internal Medicine,</affiliation>
<affiliation>E-mail: m-lambert@chru-lille.fr</affiliation>
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<name type="personal"><namePart type="given">E.</namePart>
<namePart type="family">Hachulla</namePart>
<affiliation>Department of Internal Medicine</affiliation>
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<affiliation>Department of Internal Medicine</affiliation>
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<namePart type="family">Dubucquoi</namePart>
<affiliation>Immunology Laboratory</affiliation>
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<name type="personal"><namePart type="given">C.</namePart>
<namePart type="family">Caron</namePart>
<affiliation>Hemostasis Laboratory, University Hospital of Lille, Faculty of Medicine and Lille University, 59035 Lille Cedex, France</affiliation>
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<name type="personal"><namePart type="given">D.</namePart>
<namePart type="family">Launay</namePart>
<affiliation>Department of Internal Medicine</affiliation>
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<name type="personal"><namePart type="given">S.</namePart>
<namePart type="family">Morell-Dubois</namePart>
<affiliation>Department of Internal Medicine</affiliation>
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<name type="personal"><namePart type="given">V.</namePart>
<namePart type="family">Queyrel</namePart>
<affiliation>Department of Internal Medicine</affiliation>
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<abstract lang="en">One hundred and three consecutive asymptomatic anti-phospholipid (aPL) antibody-positive carriers, taking aspirin (n = 75) or not (n = 28), were studied retrospectively to determine whether aspirin could provide primary prevention of anti-phospholipid syndrome (APS) symptoms. All patients positive for anti-cardiolipin antibodies (aCL; >25 UGPL or UMPL) and/or lupus anti-coagulant were followed for a mean of 64 ± 24.7 months. Among aPL-positive patients, 37 had systemic lupus erythematosus (SLE), 20 had prolonged activated partial thromboplastin times, 19 had other connective tissue diseases, 16 had autoimmune thrombocytopenia (AIT), 11 had diverse diseases. Nineteen patients experienced thrombotic event(s) during follow-up. Clinical features, biological parameters and hydroxychloroquine use were comparable for the two groups, but thrombotic events differed (log-rank test; P = 0.02). Four of the 10 SLE patients not taking aspirin developed thrombosis compared with 3/27 SLE patients taking aspirin (log-rank test; P = 0.03). Anti-phospholipid -positive patients with AIT developed fewer thromboses while taking aspirin (log-rank test; P = 0.01). In conclusion, aPL-positive SLE and AIT patients should take aspirin to prevent APS manifestations. Prospective therapeutic trials are needed to confirm aspirin's prophylactic role in such patients. Lupus (2008) 17, 11—15.</abstract>
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Influence of aspirin on the clinical outcomes of 103 anti-phospholipid antibodies-positive patients

Influence of aspirin on the clinical outcomes of 103 anti-phospholipid antibodies-positive patients

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