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pregnancy in women with antiphospholipid syndrome n.
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Pregnancy in women with antiphospholipid syndrome

Pregnancy in women with antiphospholipid syndrome

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Pregnancy in women with antiphospholipid syndrome

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  1. Pregnancy in women with antiphospholipid syndrome Dr .FarinazFarahbod

  2. Antiphospholipid syndrome (APS) in women refers to a syndrome characterized by both: ●Arterial or venous thrombosis or specific pregnancy complications and ●Laboratory evidence of antibodies to proteins bound to anionic phospholipids

  3. The three main types of antiphospholipid antibodies • lupus anticoagulants (LA) • anticardiolipinantibodies • anti-beta-2-glycoprotein-1 antibodies

  4. Pregnancy morbidity • ≥1 unexplained fetal deaths ≥10 weeks of gestation • ≥1 preterm deliveries of a morphologically normal infant before 34 weeks of gestation due to severe preeclampsia, eclampsia, or features consistent with placental insufficiency. • ≥3 unexplained, consecutive, spontaneous pregnancy losses <10 weeks of gestation

  5. Although many women with aPL also have systemic lupus erythematosus (SLE), the risk of pregnancy loss appears to be independent, at least in part, of lupus • lupus anticoagulant is the strongest predictor of pregnancy complication

  6. the evidence described above supports an association between aPL and pregnancy morbidity, the predictive value of these antibodies is poor. The reported prevalence of aCL in women with uncomplicated pregnancies ranges from 0 to 11 percent, with a median value of about 2 percent

  7. Thromboembolic disease • Pregnancy and the puerperiumare associated with an increased risk of thromboembolic disease, and this risk is particularly high in pregnant women with APS. In prospective studies, the risk of thromboembolic disease during pregnancy or postpartum was 5 to 12 percent among women with known APS

  8. Potential mechanisms for morbidity • involve platelet and endothelial cell activation as well as procoagulant effects of aPL • aPLhave a direct effect on human placental trophoblast, decreasing trophoblast viability, syncytialization, and invasion in vitro • affect the production of hormones and signaling molecules by trophoblasts, and stimulate coagulation and complement activation

  9. Neonatal APS • presence of at least one type of aPL in serum and the occurrence of at least one clinical feature, such as venous or arterial thrombosesor thrombocytopenia • Passively-acquired aPL completely disappears by 6 to 12 months of age

  10. Women with aPL without APS • It is unclear whether asymptomatic healthy women with antiphospholipid antibodies (aPL) who do not meet criteria for antiphospholipid syndrome (APS) are at increased risk of pregnancy morbidity. The bulk of evidence suggests little or no increase in risk in this group • aPLwas not a significant risk factor for fetal loss in first pregnancies

  11. MANAGEMEN APS based on aCL and/or LAC and prior thrombosis • use of therapeutic dose LMWH for anticoagulation of these women during pregnancy • both LMWH and low-dose ASA during pregnancy

  12. APS based on aCL and/or LAC and pregnancy morbidity • LMWH plus aspirin • aspirin alone • hydroxychloroquine

  13. The study suggestes that pravastatin may improve pregnancy outcomes in women with refractory obstetric APS when taken at the onset of PE or IUGR until the end of pregnancy PMID:27454295 PMCID:PMC4966313 DOI: 10.1172/JCi86957

  14. Early or late loss • low-dose ASA (50 to 100 mg per day), beginning when conception is attempted, and prophylactic dose LMWH upon confirmation of intrauterine pregnancy; low-dose ASA and prophylactic or intermediate-dose unfractionated heparin is a reasonable alternative

  15. Preterm delivery related to uteroplacental insufficiency • low-dose ASA therapy (50 to 100 mg per day), beginning at the end of the first trimester and continuing through delivery • LMWH with low-dose ASA in cases of ASA failure or when placental examination shows extensive decidual inflammation and vasculopathyand/or thrombosis

  16. aPL without clinical criteria for APS • low-dose ASA alone for these patients • low-dose ASA enhances leukocyte-derived interleukin-3 production, which stimulates normal trophoblast growth and hormone expression

  17. In vitro fertilization in women with aPL • do not prescribe prophylactic antithrombotic therapy during in vitro fertilization (IVF)

  18. Maternal-fetal monitoring • Baseline platelet count • serum creatinineconcentration • ALT and AST • urine protein-to-creatinineratio • repeat measurement of aPL during pregnancy is unnecessary. • Screening for anti-Ro/SSA and anti-La/SSB antibodies.

  19. Ultrasound examination before 20 weeks of gestation • serial sonograms every three to four weeks beginning in the late second or early third trimester to evaluate fetal growth and amniotic fluid volume.

  20. Peripartummanagement • Heparin should be discontinued 24 hours before labor and delivery • delivery (induction or cesarean) at 39 weeks of gestation • Patients with prior thromboses should not be off anticoagulants more than 48 hours. • Low-dose ASA can be stopped any time after 36 weeks of gestation

  21. women with a past history of serious arterial thrombotic complications, such as stroke or myocardial infarction, the potential benefit of reducing this risk by continuing ASA through labor and delivery outweighs the small risk of incisional bleeding.

  22. Postpartum management • Women with laboratory criteria for aPL and a prior history of arterial or venous thrombosisare at high risk of recurrence and are generally on lifelong anticoagulation with warfarin

  23. In women receiving antepartum low-dose ASA and prophylactic-dose heparin regimens, we continue the regimen for six weeks postpartum. • women with aPL and a family history of thrombosis suggested postpartum anticoagulation for those

  24. Contraception • Women with aPL should avoid estrogen-containing hormonal contraceptives

  25. TREATMENT FAILURE • Intravenous immune globulin • (IVIG) (0.4 g/kg per day for five days each month during the next attempted pregnancy) has been administered after failure of conventional therapy • a smaller percentage of women in the IVIG-treated group developed hypertension or maternal diabetes

  26. Therapeutic plasma exchang • three to four treatments per week • Weekly plasma exchange

  27. Hydroxychloroquine • hydroxychloroquinemight be beneficial in women with APS-related recurrent pregnancy loss • reverse platelet activation induced by human IgGantiphospholipid antibodies • depress aPL levels in humans

  28. Glucocorticoids • an increased risk of adverse obstetrical and maternal consequences of steroid therapy, including premature rupture of membranes, preterm delivery, fetal growth restriction, infection, preeclampsia, gestational diabetes, maternal osteopenia (especially when used with heparin), and avascular necrosis, have been demonstrated consistentlyand have led to abandonment of this approach

  29. باتشکر