Antiphospholipid syndrome: five year follow up.

Asherson, Ronald A.; Baguley, Elaine; Pal, Chaitanya

doi:10.1136/ard.50.11.805

Cited by 95 publications

(34 citation statements)

References 22 publications

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“…It has also been confirmed that the use of immunosuppressive drugs and/or corticosteroids has no role in the treatment of Hughes syndrome [30]. The present consensus on the management of recurrent fetal wastage is to give lowdose aspirin (75-150 mg/day) before pregnancy.…”

Section: Discussionmentioning

confidence: 99%

‘Secondary’ Hughes (Antiphospholipid) Syndrome in Unusual Clinical Settings

et al. 1998

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Objectives and Importance: Hughes (antiphospholipid) syndrome is mainly seen among patients with systemic lupus erythematosus (SLE). This has been called ‘secondary’ in contrast to ‘primary’ where no obvious underlying disease is detectable. The objective of this report is to highlight the fact that Hughes syndrome can, however, also occur in association with other underlying diseases or, as a result of certain therapies. The importance of this report is in emphasizing the fact that secondary Hughes syndrome can occur in several settings other than SLE or SLE-like illness. Clinical Presentation: Here we describe 3 patients with clinical features of arterial or venous thromboses associated with significant levels of anticardiolipin antibodies. Their underlying diseases were, however, neither SLE nor ‘SLE-like’ illness. One of them had been on oral contraceptive pills, the 2nd patient had Behçet’s disease and the 3rd patient had liver carcinoma associated with hepatitis C infection. Thus, these patients could be classified under the category of ‘secondary’ Hughes (antiphospholipid) syndrome. Conclusion: The 1st patient recovered and remained well during a 12-month follow-up after the discontinuation of oral contraceptive pills combined with long-term low-dose aspirin therapy. The last patient remained normal in the 12-month follow-up period on long-term warfarin treatment at a dose adequate to keep the international normalized ratio above 3. The 2nd patient died of uncontrollable hypercoagulability associated with advanced extensive malignancy and related complications. It is, therefore, recommended that the possibility of Hughes syndrome be considered in any clinical situation characterized with hypercoagulable state. If proven, long-term anticoagulation may benefit the patient.

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Section: Discussionmentioning

confidence: 99%

‘Secondary’ Hughes (Antiphospholipid) Syndrome in Unusual Clinical Settings

et al. 1998

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“…As previous high titres of aCL/aPL may decrease coin cidentally with the thrombotic occlusive event, in that these antibodies might be consumed at the site or at the time of thrombosis [17,39], only other prospective serial evaluations will provide further elements to clarify this point which is crucial mainly with respect to the under standing of the causal relationships between antiphos pholipids and thrombosis. The results are still conflicting, but this fact might also depend on the too little number of clinical studies report ing these data, thus underscoring the need for more exten sive investigations.…”

Section: (5) Look At the Time O F Appearance O F La/acl/apl With Respmentioning

confidence: 99%

“…On the contrary, persistent LA/aCL/ aPL-positive results, beyond the phases of activity of dis ease, do need attention [15,39],…”

Section: Some Guidelinesmentioning

confidence: 99%

“…LA/aCL/aPL being often disclosed in the context of an autoimmune disease (mainly SLE), many conventional immunosuppressive schedules had been employed with the goal of negativing both the LA phenomenon and the antiphospholipid production. However, though LA levels may decrease or even disappear after administration of steroids (paralleling a reduction in the clinical activity of the underlying disease) in 50% of the SLE patients [3,29], aCL/aPL are much more resistant to suppression despite aggressive schedules including plasma exchange and pulse intravenous cyclophosphamide [1,39,43,[63][64][65][66]. Fur thermore, recurrent thrombosis in SLE patients with per sistent LA/aCL/aPL-positive results frequently occurs over phases of quiescence of the underlying disease [15,22,29], Lastly, it is intriguing that consistent amounts of antiphospholipid antibodies have been detected in differ ent commercial kits of intravenous immunoglobulin which are successfully employed in the clinical context of LA/aCL/aPL-related pregnancy loss [67].…”

Section: (5) Look At the Time O F Appearance O F La/acl/apl With Respmentioning

confidence: 99%

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Guidelines for Looking at the Antiphospholipid Antibodies in Systemic Lupus Erythematosus

Stratta

Canavese²,

Ferrero³

et al. 1997

Nephron

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Lupus anticoagulant (LA), anticardiolipin (aCL), and/or antiphospholipid (aPL) antibodies are the hallmarks of the antiphospholipid syndrome, characterized by widespread thrombosis. The syndrome has been described as primary or secondary when aCL/aPL are the only classes of detectable autoantibodies or occur in the context of systemic lupus erythematosus (SLE) or SLE-like disease. However, since LA/aCL/aPL have been extensively looked for, it has become evident that they may also be detected in the absence of any clinical correlation with thrombosis. In particular, among SLE patients, these antibodies mean a high risk of thrombosis only in a small subset, sharing clinical features with primary antiphospholipid syndrome. As laboratory examination is still unable to distinguish between high-risk and non-high-risk antiphospholipid antibodies, it is crucial to have some reasonable criteria able to guide the day-to-day clinical practice. We attempt to trace the following guidelines: (1) distinguish between transient and persistent LA/aCL/aPL results; (2) do not forget the LA phenomenon in the era of aCL/aPL; (3) maintain a strict communication with the laboratory; (4) exclude other causes of primary coagulation abnormalities; (5) look at the time of appearance of LA/aCL/aPL with respect to thrombosis; (6) analyze any possible laboratory clue putatively useful to distinguish between ‘rouge’ and ‘non-rouge’ LA/aCL/aPL; (7) look for signs of widespread noninflammatory vasculopathy; (8) do not engage a war to the knife against LA/aCL/aPL by immunosuppressive therapies.

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“…Тогда же были определены основные признаки синд рома, включающие рецидивирующие венозные и/или артери альные тромбозы, спонтанные аборты, тромбоцитопению и се рологические маркеры -антифосфолипидные антитела (аФЛ): волчаночный антикоагулянт (ВА) и антикардиолипиновые ан титела (аКЛ) [2]. Позднее стало ясно, что антифосфолипидный синдром (АФС) может быть самостоятельной нозологической единицей, называемой в этом случае "первичным АФС", или наблюдаться у пациентов с каким-либо аутоиммунным заболе ванием, чаще с системной красной волчанкой (СКВ), и расце ниваться соответственно как "вторичный" АФС [3].…”

unclassified

Aspirin in antiphospholipid syndrome

Kondratjeva¹,

Решетняк²

2005

rsp

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Antiphospholipid syndrome: five year follow up.

Cited by 95 publications

References 22 publications

‘Secondary’ Hughes (Antiphospholipid) Syndrome in Unusual Clinical Settings

‘Secondary’ Hughes (Antiphospholipid) Syndrome in Unusual Clinical Settings

Guidelines for Looking at the Antiphospholipid Antibodies in Systemic Lupus Erythematosus

Aspirin in antiphospholipid syndrome

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