anti phospholipid syndrome
DESCRIPTION
Immunology, HematologyTRANSCRIPT
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Anti Phospho-Lipid Antibody (APLA) Syndrome (APS)
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Other namesMultiple terms for APS exist. Some confusing.
•Hughes syndrome
•Anticardiolipin Syndrome (ACL)
•Anti- Phospho Lipid Antibody (APLA) syndrome
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Other namesMultiple terms for APS exist. Some confusing.
• Lupus anticoagulant (LA) syndrome: Misleading term because – patients with APS may not have SLE, and – LA is associated with thrombotic rather than
hemorrhagic complications.
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Other namesMultiple terms for APS exist. Some confusing.
• Lupus anticoagulant (LA) syndrome: Misleading term because – Patients with APS may not have SLE, and – LA is associated with thrombotic rather than
hemorrhagic complications.
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Anti-phospholipid syndrome (APS)Is a disorder that manifests as- • Recurrent venous or arterial thrombosis and/or
• Complications of pregnancy (fetal losses) +
• Characteristic lab abnormalities.
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Anti-phospholipid syndrome (APS)APS is currently the preferred term.
Previous Classification-• Primary - no associated disease, • Secondary- in association with SLE /other
rheumatic (AI) disorders
Current classification - 1. APS with, or 2. APS without associated rheumatic disease.
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Anti-phospholipid syndrome (APS)APS is currently the preferred term.
Previous Classification-• Primary - no associated disease, • Secondary- in association with SLE /other
rheumatic (AI) disorders
Current classification - 1. APS with, or 2. APS without associated rheumatic disease.
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Antiphospholipid syndrome (APS)
Although antiphospholipid (aPL) abs are linked to APS, their role in pathogenesis (cause or an epiphenomenon) is unclear.
Up to 5% of healthy people have aPL abs.
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APS• It is a heterogenous disorder in terms of
clinical manifestations and range of autoantibodies.
• In 2006, revised criteria for the diagnosis of APS were published in an international consensus statement.
• At least one clinical criterion and one laboratory criterion must be present for a patient to be classified as having APS.
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Antiphospholipid Syndrome Criteria Sydney revision of Sapporo criteria 2006
CLINICAL CRITERIA
1. Vascular Thrombosis
2. Pregnancy Morbidity: a) death of normal fetus
at > 10 wks b) premature birth at < 34
wks due to preeclampsia c) >3 consecutive abortions at <10wks d) placental insufficiency at < 34 wks
LAB CRITERA
1. anti-Cardiolipin IgG / IgM
2. anti–beta-2 glycoprotein I (GP1)
3. Lupus anticoagulant (LAC)
- medium to - high titer - at least X 2 times - 12 wks apart
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Antiphospholipid Syndrome Criteria Sydney revision of Sapporo criteria 2006
CLINICAL CRITERIA
1. Vascular Thrombosis
2. Pregnancy Morbidity: a) death of normal fetus
at > 10 wks b) premature birth at < 34
wks due to preeclampsia c) >3 consecutive abortions at <10wks d) placental insufficiency at < 34 wks
LAB CRITERA
1. anti-Cardiolipin IgG / IgM
2. anti–beta-2 glycoprotein I (GP1)
3. Lupus anticoagulant (LAC)
- medium to - high titer - at least X 2 times - 12 wks apartDefinite APS: 1 Clinical + 1 Lab criteria
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APS: The clinical criteria are-1. Vascular thrombosis –One or more clinical episodes of arterial,
venous, or small-vessel thrombosis – In any tissue or organ – Thrombosis may involve (cerebral, coronary,
pulmonary, limb, hepatic, renal, ocular or adrenal) any circulation. –Confirmed by imaging, doppler, or histopath
studies
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APS: The clinical criteria are-1. Vascular thrombosis
Inv is warranted if DVT/ PE/ acute ischemia/ MI/ CVA (esp. recurrent) is present
in a young individual in the absence of other risk factors.
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The clinical criteria are-2. Pregnancy morbidity –One or more late-term (>10 wks) spontaneous
abortions–One or more premature births of a
morphologically healthy neonate at /before 34 wks due to pre/eclampsia or severe placental insufficiency – Three or more unexplained, consecutive,
spontaneous abortions before 10 wks gestation
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Laboratory criteria:Patients must have raised1. IgG or IgM anticardiolipin (aCL), or 2. anti–beta-2 glycoprotein I (GP1), or 3. Lupus anticoagulant (LA)
On • at least 2 occasions • at least 12 weeks apart
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Additionally..• Other antiphospholipid (aPL)–associated clinical
features recognized by the 2006 consensus statement but not included in the criteria are-
• Cardiac valve disease • Livedo reticularis • Thrombocytopenia • Nephropathy, and • Neurologic manifestations
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Suspect APLA syndrome if…
• Thrombosis• Miscarriage• Heart murmur or cardiac valvular vegetations• Hematologic abnormalities (TCP or HA)• Nephropathy• Non-thrombotic neurologic symptoms • Unexplained adrenal insufficiency• Avascular necrosis of bone• Pulmonary hypertension
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Suspect APLA syndrome if…
• Thrombosis• Miscarriage• heart murmur or cardiac valvular vegetations• hematologic abnormalities (TCP or HA)• nephropathy• Non-thrombotic neurologic symptoms, • Unexplained adrenal insufficiency• Avascular necrosis of bone• Pulmonary hypertension - in the absence of other risk factors
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APLA Syndrome - Etiology
APS is an autoimmune disorder of unknown cause.
Possible triggers are- • Associated autoimmune or rheumatic diseases • Infections and • Drugs associated with the LA or aCL antibodies.
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APLA Syndrome -EtiologyAsso diseases Infections Drugs Others
SLE Syphilis Cardiac- Procainamide, quinidine, propranolol, hydralazine
Familial association
Sjogrens HCV Neuroleptic /psychiatric - Phenytoin, chlorpromazine
HLA associations: between aCL ab and indivs with certain HLA genes
RA HIV Other - Interferon alfa, quinine, amoxicillinAI TCP HTLV I
AI HA MalariaPsoriatic arthropathy
Bacterial septicemia
PSSMCTDPMR/ GCABehcet’s
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Differential Diagnosis
• DIC• IE• TTP
• Acquired prothrombotic disorders
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Acquired prothrombotic disorders
• Conditions associated with a hypercoagulable state: - Pregnancy and postpartum - major surgery - Obesity and immobility - malignancy - Congestive heart failure - Nephrotic syndrome
• Estrogen treatment
• Antiphospholipid syndrome
-
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APS: Laboratory Studies
The hallmark that defines antiphospholipid syndrome (APS) is
• The presence of antiphospholipid (APL) antibodies or
• Abnormalities in phospholipid-dependent tests of coagulation.
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APS: Laboratory Studies
The hallmark that defines antiphospholipid syndrome (APS) is
• The presence of antiphospholipid (APL) antibodies or
• Abnormalities in phospholipid-dependent tests of coagulation.
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APS: Laboratory Studies
The hallmark that defines antiphospholipid syndrome (APS) is
• The presence of antiphospholipid (APL) antibodies or
• Abnormalities in phospholipid-dependent tests of coagulation.
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APS: Laboratory Studies
• In addition to the clinical criteria listed, at least one of the following laboratory criteria is necessary for the classification of APS:
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APS: Laboratory Studies• Presence of LA in plasma on 2 or more occasions
at least 12 weeks apart
• Presence of moderate to high levels of anticardiolipin (aCL) (IgG or IgM) in serum/ plasma (ie, >40 IgG phospholipid units (GPL)/mL or IgM phospholipid units (MPL)/mL or >99th percentile) on 2 or more occasions at least 12 weeks apart
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APS: Laboratory Studies• Presence of moderate to high levels of anti–beta-2 glycoprotein I antibodies (IgG or
IgM) in serum or plasma (>99th percentile) on 2 or more occasions at least 12 weeks apart
• Presence of LA in plasma on 2 or more occasions at least 12 weeks apart
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APS: Laboratory StudiesLA is directed against plasma coagulation molecules.• Results in the paradoxical prolongation of clotting assays,
such as aPTT, kaolin clotting time, and dilute Russell viper venom time (DRVVT).
• The presence of LA is confirmed by mixing normal aCL antibodies react primarily to membrane phospholipids• platelet-poor plasma with the patient's plasma.• If a clotting factor is deficient, the addition of normal
plasma corrects the prolonged clotting time. • If the clotting time does not normalize during mixing
studies, an inhibitor is present; the absence of a specific clotting factor inhibitor confirms that a LA is present.
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APS: Laboratory StudiesLA is directed against plasma coagulation
molecules.• Results in the paradoxical prolongation of clotting
assays, (such as aPTT, kaolin clotting time, and dilute Russell viper venom time (DRVVT)).
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APS: Laboratory StudiesLA is directed against plasma coagulation
molecules.• Results in the paradoxical prolongation of clotting
assays, such as aPTT, kaolin clotting time, and dilute Russell viper venom time (DRVVT).
• The presence of LA is confirmed by mixing normal platelet-poor plasma with the patient's plasma.
If
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APS: Laboratory Studies• If a clotting factor is deficient, the addition of
normal platelet poor plasma corrects the prolonged clotting time.
• If the clotting time does not normalize during mixing studies, an inhibitor is present; the absence of a specific clotting factor inhibitor confirms that a LA is present.
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APS: Laboratory Studies
• aCL antibodies react primarily to membrane phospholipids
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APS: Summary of Laboratory StudiesFollowing laboratory tests should be done:• aCL antibodies (IgG, IgM)• Anti–beta-2 glycoprotein I antibodies (IgG, IgM)• Activated partial thromboplastin time (aPTT)• LA tests such as DRVVT• Serologic test for syphilis (false-positive result)• CBC count (thrombocytopenia, hemolytic
anemia) • A low ANA level may be present and does not
necessarily imply coexisting SLE.
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False Positives• Infections:
- Syphilis, TB, Q-fever, Spotted Fever, Klebsiella, HCV,
Leprosy, HIV. - The abs are usually transient, not b2 GPI
dependent
• Malignancy: Lymphoma, paraproteinemia
• Drug induced: phenothiazines, procainamide, quinidine,
phenytoin, hydralazine
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APS Treatment: Thrombosis• Full anticoagulation with IV/ SC heparin followed
by warfarin therapy.• Based on the most recent evidence, a reasonable
target for the INR is –Venous thrombosis -2.0-3.0–Arterial thrombosis 3.0– Recurrent thrombotic events -may require 3.0-4.0 – Severe or refractory cases- combination of warfarin+
aspirin maybe used. • Treatment is generally lifelong.
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APS Treatment: Thrombosis• Full anticoagulation with IV/ SC heparin followed
by warfarin therapy.• Based on the most recent evidence, a reasonable
target for the INR is – Venous thrombosis -2.0-3.0– Arterial thrombosis 3.0– Recurrent thrombotic events -may require 3.0-4.0
• Severe or refractory cases- combination of warfarin+ aspirin maybe used.
• Treatment is generally lifelong.
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APS Treatment: Thrombosis• Full anticoagulation with IV/ SC heparin followed
by warfarin therapy.• Based on the most recent evidence, a reasonable
target for the INR is – Venous thrombosis -2.0-3.0– Arterial thrombosis 3.0– Recurrent thrombotic events -may require 3.0-4.0
• Severe or refractory cases- combination of warfarin+ aspirin maybe used.
• Treatment is generally lifelong.
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APS Treatment: Thrombosis• Full anticoagulation with IV/ SC heparin followed
by warfarin therapy.• Based on the most recent evidence, a reasonable
target for the INR is –Venous thrombosis -2.0-3.0–Arterial thrombosis 3.0– Recurrent thrombotic events -may require 3.0-4.0
• Severe or refractory cases- combination of warfarin+ aspirin maybe used.
• Treatment is generally lifelong.
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APS Treatment: Obstetric considerations Guidelines available- • Heparin safe in pregnancy, preferred LMWH. • Warfarin contraindicated in pregnancy. • Heparin and warfarin safe in breast feeding.• No history of thrombosis -Prophylaxis• History of thrombosis -Full anticoagulation
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APS Treatment: Obstetric considerations Guidelines available- • History of thrombosis -Full anticoagulation– Prophylactic SC heparin (LMWH) + low-dose
aspirin during pregnancy. – Rx withheld at delivery. Restarted after, continued
for 6-12 wks postpartum. – Long-term anticoagulation then continued
postpartum.
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APS Treatment: Obstetric considerations Guidelines available- • History of thrombosis -Full anticoagulation
• Corticosteroids -not been proven effective. Increase maternal morbidity and fetal prematurity rates.
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Prophylactic therapy• Eliminate other risk factors, such as oral
contraceptives, smoking, hypertension, or hyperlipidemia.
• Low-dose aspirin; the effectiveness as primary prevention for APS remains unproven.
• Clopidogrel anecdotal reports (aspirin allergy). • In SLE, consider hydroxychloroquine, for intrinsic
antithrombotic properties.• Statins, esp for hyperlipidemia.
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Catastrophic Antiphospholipid Syndrome (CAPS)
• Catastrophic antiphospholipid syndrome is rare, affecting < 1% of those with antiphospholipid syndrome.
• Also called Asherson's syndrome after the researcher who described it in 1990s.
• These patients are generally very ill, often with active SLE.
• There is widespread thrombosis in several vascular beds
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Catastrophic Antiphospholipid Syndrome (CAPS)
Treatment • Intensive anticoagulation • Plasma exchange • Corticosteroids appears beneficial No controlled trials have been performed. • IV Ig -some benefit• Cyclophosphamide in selected cases (SLE-
associated CAPS).
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Take Home Messages: Anti- Phospholipid Syndrome
• Due to the wide spectrum of manifestations any clinician may encounter patients with APS
• This is a potentially treatable condition
• The best treatment, at present to prevent recurrent thrombosis is anticoagulation.
• The optimal duration and intensity is controversial.
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THM: Venous or Arterial thrombosis
1. Initial treatment with Heparin
2. Start Warfarin
3. Stop Heparin when therapeutic INR achieved
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Current Recommendations• Asymptomatic aPL no treatment (Aspirin?)• Venous thrombosis Warfarin INR 2.0-3.0• Arterial thrombosis Warfarin INR 3.0• Recurrent thrombosis Warfarin INR 3.0-4.0 + Aspirin
• CAPS Anticoagulation + CS + IVIg or plasmapheresis
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Potentially usable
• Non-aspirin antiplatelet agents• Hydroxychloroquine• Statins
• Thrombin inhibitors• Rituximab• Recombinant activated protein C• Prostaglandin and prostacyclin• Anti-cytokine
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Thrombocytopenia
• Mild to moderate- Platelets > 50,000: No treatment
• Severe- <50,000: corticosteroids
• Corticosteroid resistant cases: HCQ IVIG, Immunosuppressive drugs, Splenectomy
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Current Recommendations
Pregnancy Fetal protection• Asymptomatic aPL no treatment• Single loss <10wks no treatment• Recurrent loss* <10wks prophylactic heparin +ASA up to 6-12 wks postpartum, ASA
after(?)
• Recurrent loss < 10 wks therapeutic heparin + ASA, + thrombosis warfarin postpartum
• Prior thrombosis therapeutic heparin + ASA warfarin postpartum
* Late fetal loss IUGR severe pre-eclampsia
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Other Rx for APL Ass pregnancy loss• Corticosteroids : - associated with significant maternal and
fetal morbidity - ineffective
• Immunosuppression: azathioprine, plasmapheresis: numbers treated too small for conclusion
• IVIG: may be salvage therapy in women who fail on Heparin + Aspirin
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Take Home Messages: Anti- Phospholipid Syndrome
• Due to the wide spectrum of manifestations any clinician may encounter patients with APS
• This is a potentially treatable condition
• The best treatment, at present to prevent recurrent thrombosis is anticoagulation.
• The optimal duration and intensity is controversial.