Drug-Induced Lupus Anticoagulants and Antiphospholipid Antibodies

Dlott, Jeffrey S.; Roubey, Robert

doi:10.1007/s11926-011-0227-1

Cited by 52 publications

(31 citation statements)

References 81 publications

(140 reference statements)

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“…Anti-β2-GPI consist in a heterogeneous group of antibodies, only a few of which are responsible for tissue damage. When associated with infections or drug exposure, these antibodies may have no pathogenic role (Shoenfeld et al, 2003; Sène et al, 2008; Dlott and Roubey, 2012). As a functional test, LAC is the most powerful predictor of pathology in APS (Galli et al, 2003).…”

Section: Diagnosismentioning

confidence: 99%

“…The hepatitis C virus, human immunodeficiency virus (HIV), human herpes virus, adenovirus, and parvovirus B19 are the most common viral infections related to aPL detection; aPL can be also detected in bacterial diseases, such as leprosy and syphilis (Sène et al, 2008). Procainamide, phenothiazines, quinine, oral contraceptives, and anti-TNF agents are the drugs that may induce generation of aPL (Ramos-Casals et al, 2008; Dlott and Roubey, 2012). …”

Section: Introductionmentioning

confidence: 99%

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Antiphospholipid-Related Chorea

Peluso¹,

Antenora²,

Rosa³

et al. 2012

Front. Neur.

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Chorea is a movement disorder which may be associated with immunologic diseases, in particular in the presence of antiphospholipid antibodies (aPL). Choreic movements have been linked to the isolated presence of plasmatic aPL, or to primary, or secondary antiphospholipid syndrome. The highest incidence of aPL-related chorea is detected in children and females. The presentation of chorea is usually subacute and the course monophasic. Choreic movements can be focal, unilateral, or generalized. High plasmatic titers of aPL in a choreic patient can suggest the diagnosis of aPL-related chorea; neuroimaging investigation does not provide much additional diagnostic information. The most relevant target of aPL is β2-glycoprotein I, probably responsible for the thrombotic manifestations of antiphospholipid syndrome. Etiology of the movement disorder is not well understood but a neurotoxic effect of aPL has been hypothesized, leading to impaired basal ganglia cell function and development of neuroinflammation. Patients affected by aPL-related chorea have an increased risk of thrombosis and should receive antiplatelet or anticoagulant treatment.

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Section: Diagnosismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Antiphospholipid-Related Chorea

Peluso¹,

Antenora²,

Rosa³

et al. 2012

Front. Neur.

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“…It has been suggested that platelet aggregation is enhanced via 5HT2A antagonism by SGAs, or due to hyperhomocysteinemia [13]. Moreover, typical antipsychotics, especially phenothiazines, and clozapine, have been implicated in the induction of antiphospholipid antibodies [23]. Hyperprolactinemia has been recently found to cause Adenosine-Diphosphate-(ADP-) stimulated platelet activation [16].…”

Section: Discussionmentioning

confidence: 99%

Pulmonary Embolism Related to Amisulpride Treatment: A Case Report

Σκώκου

Gourzis

2013

Case Reports in Psychiatry

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Venous thromboembolism has been associated with antipsychotic drugs, but the underlying mechanisms are largely unknown. Hypotheses that have been made include body weight gain, sedation, enhanced platelet aggregation, increased levels of antiphospholipid antibodies, hyperhomocysteinemia, whereas hyperprolactinemia has recently attracted attention as a potential contributing factor. The highest risk has been demonstrated for clozapine, olanzapine, and low-potency first-generation antipsychotics; however, presently there is no data for amisulpride. In the present paper we describe a case of pulmonary embolism in a female bipolar patient, receiving treatment with amisulpride, aripiprazole, and paroxetine. Although a contribution of aripiprazole and paroxetine cannot completely be ruled out, the most probable factor underlying the thromboembolic event seems to be hyperprolactinemia, which was caused by amisulpride treatment. Increased plasma levels of prolactin should probably be taken into account during the monitoring of antipsychotic treatment as well as in future research concerning venous thromboembolism in psychiatric settings.

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“…35 The opsonization of dying cells that express negatively charged phospholipids on their surface has been suggested as a third circumstance that can induce autoantibodies against β2-GPI. 36 Many drugs have been linked to the generation of antiphospholipid antibodies, 37 of which procainamide-induced autoantibodies account for the highest association with thrombotic complications. 38 It is known that procainamide perturbs cellular membranes, which might result in binding of β 2 -GPI and expression of neoepitopes.…”

Section: Antiphospholipid Antibody Development After Infectionmentioning

confidence: 99%

Antiphospholipid Syndrome–Not a Noninflammatory Disease

Groot

Urbanus

2015

Semin Thromb Hemost

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The autoimmune disease antiphospholipid syndrome (APS) is characterized by thrombosis or pregnancy morbidity in patients with persistent antiphospholipid antibodies (aPLs). Although inflammation is not a key feature of the clinical presentation of the syndrome, there are indications that the inflammatory response plays an important role in APS. The major antigen of aPLs, the plasma protein β2-glycoprotein I, is involved in clearance of microparticles and in the innate immune response. In light of these physiological functions, the formation of antibodies against the protein is easily understood, as antibodies might augment the clearance reaction. In addition, inflammatory mediators are thought to play a role in the activation of leukocytes and the induction of endothelial dysfunction in APS. Moreover, evidence for a role of complement activation in the pathogenesis of the syndrome is accumulating. This review will provide an overview of current knowledge on the physiological function of β2-glycoprotein I, the formation of autoantibodies against β2-glycoprotein I and will explore the contribution of inflammation to the clinical manifestations of APS.

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Drug-Induced Lupus Anticoagulants and Antiphospholipid Antibodies

Cited by 52 publications

References 81 publications

Antiphospholipid-Related Chorea

Antiphospholipid-Related Chorea

Pulmonary Embolism Related to Amisulpride Treatment: A Case Report

Antiphospholipid Syndrome–Not a Noninflammatory Disease

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