The Laboratory Diagnosis of the Antiphospholipid Syndrome

Ahluwalia, Jasmina; Sreedharanunni, Sreejesh

doi:10.1007/s12288-016-0739-y

Cited by 15 publications

(17 citation statements)

References 36 publications

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Section: Discussionmentioning

confidence: 99%

“…The diagnosis of APS is primarily based on the detection of antiphospholipid antibodies in a patient’s serum and evidence of thrombosis [ 7 ]. Triple positivity of lupus anticoagulant, anticardiolipin antibodies, and beta-2 glycoprotein 1 antibodies create the highest risk of thromboembolic events [ 7 ]. Deficiencies in protein C, protein S, and antithrombin should be explored, as well as mutations, including factor V Leiden, prothrombin, and plasminogen inhibitor genes [ 6 ].…”

Section: Discussionmentioning

confidence: 99%

“…Deficiencies in protein C, protein S, and antithrombin should be explored, as well as mutations, including factor V Leiden, prothrombin, and plasminogen inhibitor genes [ 6 ]. Antibodies directed against phosphatidylserine should also be considered when initial APS studies are negative [ 7 ]. Recent studies have demonstrated a significant association between aPS and APS, and seronegative APS patients have been found to be positive for aPS [ 8 , 9 ].…”

Section: Discussionmentioning

confidence: 99%

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Antiphosphatidylserine Antibody as a Cause of Multiple Dural Venous Sinus Thromboses and ST-Elevation Myocardial Infarction

2018

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Patient: Male, 48Final Diagnosis: Antiphospholipid syndromeSymptoms: Chest pain • confusion • seizure-like activityMedication: —Clinical Procedure: Endovascular venous suction thrombectomySpecialty: HematologyObjective:Rare diseaseBackground:Antiphospholipid syndrome (APS) is an autoimmune disease characterized by antibodies directed against phospholipids on plasma membranes. Through unclear mechanisms, APS confers hypercoagulability. APS may cause recurrent thromboses in the arterial and venous vasculature. We report a case of primary APS resulting in cerebral venous thrombosis and ST-elevation myocardial infarction (STEMI) for which only antiphosphatidylserine (aPS) IgM antibody was positive after extensive investigation.Case Report:A 48-year-old male was admitted after a witnessed generalized seizure with subsequent confusion. Imaging demonstrated thrombosis of multiple central nervous system (CNS) sinuses, including the superior sagittal sinus and bilateral transverse sinuses. The patient was heparinized with aggressive hydration, which proved inadequate, prompting endovascular thrombectomy. Three months later, despite anticoagulation therapy, the patient developed a STEMI when International Normalized Ratio (INR) was 1.8. Echocardiogram (ECHO) and PAN CT scan were normal. Initial coagulation studies demonstrated normal anticardiolipin antibody, prothrombin time, partial thromboplastin time, and platelet count. Outpatient coagulation studies revealed normal antithrombin III, protein C/S, hemoglobin electrophoresis, homocysteine, anti-β2 glycoprotein 1 antibodies, and D-Dimer. Factor V Leiden, JAK 2 mutation, prothrombin gene mutation, and tests for paroxysmal nocturnal hemoglobinuria (PNH) were negative. A positive phosphatidylserine IgM was detected. The patient was continued on warfarin (10 mg daily) with a target INR of 3.0–3.5 and clopidogrel (75 mg daily).Conclusions:Despite extensive investigation, this patient only showed evidence of elevated aPS IgM antibodies, likely contributing to his CNS venous sinus thromboses and STEMI. It is important to screen for antiphosphatidylserine antibodies in cases of unprovoked thrombosis when standard thrombophilia analysis is unrevealing. This will assist in identifying pathogenicity and help prevent recurrence of subsequent thromboses.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Antiphosphatidylserine Antibody as a Cause of Multiple Dural Venous Sinus Thromboses and ST-Elevation Myocardial Infarction

2018

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“…Antiphospholipid antibody syndrome (APS) is defined by the development of (often multiple) venous or arterial thromboses or by the occurrence of maternal morbidity, primarily recurrent fetal losses, in the presence of antiphospholipid antibodies (aPLs). These aPLs include lupus anticoagulant (LA), anticardiolipin antibodies (aCLs), or antibodies against β 2 glycopro-tein-1 (β 2 GPI) [1][2][3][4][5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

“…Increasing evidence shows that binding of aPLs to membrane receptors on endothelial cells results in an increased risk of thrombosis, accelerated atherosclerosis, acute myocardial infarction (AMI), and cerebrovascular accidents in APS patients. In addition, APS has been associated not only with adverse cardiovascular events but also with subclinical markers associated with endothelial dysfunction, such as increased intima-media thickness of the carotid arteries and changes in the ankle-brachial index [1][2][3][4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

The Issue of the Antiphospholipid Antibody Syndrome

2020

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Antiphospholipid antibody syndrome (APS) is a state of hypercoagulability secondary to an autoimmune disorder. It is associated with thrombotic events in venous and arterial vessels, obstetric complications characterized by recurrent fetal losses, and increased perinatal morbidity. APS is classified as primary, when not associated with other pathologies; or secondary, when associated with an underlying autoimmune disease with, solid tumor, or hematological disorder. Clinical findings include livedo reticularis, thrombocytopenia or hemolytic anemia, maternal morbidity, and recurrent thrombotic episodes and others. Laboratory tests show circulating antiphospholipid antibodies (aPLs); however, even in the presence of these antibodies, patients can be asymptomatic. Estimates predict that about 5% of the populations have circulating aPLs, but the incidence of APS is only five cases per 100,000 people, as diagnosis of this syndrome requires clinical and laboratory findings to be simultaneously present. In cases of secondary APS, or in acute cases with imminent risk of death (as in catastrophic APS), it may be necessary to reduce aPL serum levels using immunomodulators, immunosuppressants, or plasmapheresis, in order to treat the associated pathologies. In other situations, the use of immunotherapy is not indicated. In other patients heparin, aspirin or anticoagulants either alone or associated should be administered depending on each specific case.

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Predictors and Interrelationship of Patient‐Reported Outcomes in Antiphospholipid Syndrome: A Cross‐Sectional Study

Weiner

Smith

Hoy

et al. 2022

ACR Open Rheumatology

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Objective. This study assessed patient-reported outcomes (PROs) in individuals with persistently positive antiphospholipid antibodies (aPL) to better understand how living with aPL may affect their quality of life.Methods. Patients completed Patient-Reported Outcomes Measurement Information System Physical Function (PF) and Cognitive Function (CF) Short Forms as well as the pain intensity (PI) rating (scale of 1-10). Patients were characterized for demographics, clinical manifestations of antiphospholipid syndrome (APS), cardiovascular risk factors, laboratory test results, and medication usage. Multivariate modeling was done via linear regression.Results. Of 139 patients, 89 had primary APS, 21 had secondary APS, and 29 had persistent aPL without meeting clinical criteria for APS. The average T scores (±SD) for PF and CF were 45.4 ± 9.2 and 48.6 ± 11.6, respectively; the average for PI was 3.0 ± 2.6. Approximately half of the patients (47%) endorsed at least mild impairment in PF (T score < 45). Mean PF, CF, and PI did not differ between diagnostic groups. Individuals who endorsed more impairment on one measure also tended to endorse more impairment on another (Pearson r = 0.43-0.59). In the multivariate models, age, smoking, pain medications, and serotonergic medications were associated with impairment in at least one PRO domain. The Damage Index for APS was significantly correlated with both PF and CF.Conclusion. Individuals living with APS endorsed more impairment in PF (and potentially CF) than expected for the general population. The relationship between certain medications and PROs warrants further study, as does the longitudinal trajectory of these and other PROs.

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The Laboratory Diagnosis of the Antiphospholipid Syndrome

Cited by 15 publications

References 36 publications

Antiphosphatidylserine Antibody as a Cause of Multiple Dural Venous Sinus Thromboses and ST-Elevation Myocardial Infarction

Antiphosphatidylserine Antibody as a Cause of Multiple Dural Venous Sinus Thromboses and ST-Elevation Myocardial Infarction

The Issue of the Antiphospholipid Antibody Syndrome

Predictors and Interrelationship of Patient‐Reported Outcomes in Antiphospholipid Syndrome: A Cross‐Sectional Study

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