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• W1567622570 abstract "Thrombotic thrombocytopenic purpura (TTP) associated with pregnancy accounts for 12–31% (George, 2000; Ridolfi & Bell, 1981; Wurzei, 1979) of TTP cases and is associated with high rates of obstetric complications (Scully et al, 2006; Vesely et al, 2004; Wurzei, 1979). Given that reported rates of recurrent TTP in future pregnancies varies widely (12–61%) (Vesely et al, 2004) and prophylactic plasma exchange (PE) may be associated with complications, identifying pregnant patients at the greatest risk for relapse would be of considerable interest. We report five pregnancies in three patients with a history of TTP (identified from a cohort of TTP patients enrolled in prospective studies at the Ohio State University and followed longitudinally over a median of 48 months) in the context of serial measurement of ADAMTS13 activity. Enrollment criteria for all studies included a microangiopathic haemolytic anaemia and thrombocytopenia (<100 × 109/l) without an alternative explanation. ADAMTS13 biomarker studies were obtained every 3 months using a methodology reported previously (Jin et al, 2006) (Tables I and II). Patient 1, a 22-year-old female, presented acutely ill at 22 weeks of gestation with intrauterine fetal death, thrombocytopenia (3 × 109/l), elevated lactate dehydrogenase (LDH; 2545 u/l, normal 0–190 u/l) and microangiopathic haemolytic anaemia. She was enrolled on a therapeutic study of PE and corticosteroids, but eventually required cyclosporine (CSA) at a dose of 100 mg BID to be successfully weaned from PE. Within 4 weeks of stopping her planned 6-month course of CSA she became pregnant and presented with a platelet count of 21 × 109/l and LDH of 1428 u/l in her 22nd week of gestation. PE was initiated but secondary to her deteriorating clinical status, labour was induced and the baby died soon after birth. Following remission she was discharged on CSA but lost to follow up. After 11 months she re-presented 17 weeks pregnant on CSA and chose to continue it despite the risks. In her 24th week she developed pre-eclampsia (without any signs of TTP) requiring a cesarean section, delivering a premature but healthy baby. She continued CSA until 4 weeks postpartum. ADAMTS13 activity dropped to <2·5% following discontinuation of CSA, but she has remained in clinical remission for 4 years since this last episode. Patient 2, a 22-year-old Caucasian female, presented with a platelet count of 6 × 109/l, LDH of 1156 u/l and microangiopathic features. She was enrolled in a therapeutic study and was randomized to concurrent CSA and PE. After being successfully tapered from PE she continued CSA for what was a planned 6-month course of therapy. However, after four additional weeks of therapy she became pregnant and CSA was discontinued. As noted in Table II, her ADAMTS13 activity remained severely deficient throughout pregnancy and during her 37th week of gestation she was diagnosed with a recurrence of TTP (platelet count 9 × 109/l, LDH 706 u/l). Her course was complicated by renal failure, eventually requiring the addition of rituximab to PE to achieve remission. Patient 3 was a 28-year-old Caucasian female with a history of three uneventful pregnancies who presented with a platelet count of 9 × 109/l, LDH of 921 u/l and microangiopathic findings consistent with a diagnosis of TTP. She was enrolled on the same therapeutic study as the previous two patients and randomized to corticosteroids with PE. She achieved remission and throughout serial follow-up demonstrated ADAMTS13 activity >10% (Table II). She presented at 6 weeks of gestation (9 months since her acute episode of TTP) and serial measurements of ADAMTS13 activity, complete blood count and LDH performed every trimester remained normal. She underwent an uneventful pregnancy and delivery. We report five pregnancies in three patients with at least one previous episode of TTP in which the risk of relapse in pregnancy appeared to be greatest in those with severely deficient ADAMTS13 activity pre-pregnancy, during pregnancy and postpartum (Table II). Previous literature on ADAMTS13 data measured during pregnancy is limited. Scully et al (2006) reported five pregnancies in five patients in whom ADAMTS13 data were obtained before, during and after the pregnancies. Four of the five subjects who had previous pregnancy losses due to TTP were started on prophylactic PE beginning at 6–12 weeks gestation based on a pre-pregnancy ADAMTS13 activity level of <5%. While this report provides important insight into the utility of pre-pregnancy ADAMTS13 biomarker data in assessing the risk of TTP relapse in association with pregnancy, the activity levels measured during pregnancy cannot be utilized as they were obtained while the patients were on regular PE. There are no clear evidence-based guidelines for prophylactic treatment of TTP in pregnancy. Experience with the addition of Rituximab to PE (Scully et al, 2006) is limited but promising. Adverse effects including neonatal cytopenias, perinatal infections and pregnancy losses have been reported but these rates are not significantly different from pregnant patients not on Rituximab (Chakravarty et al, 2010). Our experience with the use of CSA in Patient 1 was also encouraging. However, unlike Rituximab, pregnancies whilst receiving treatment with CSA may have higher rates of premature birth (Bar Oz et al, 2001). Neither drug has shown significant teratogenicity to date (Chakravarty et al, 2010; Bar Oz et al, 2001). In conclusion, identifying pregnant patients at risk for TTP relapse remains challenging. Some reports have noted that women who initially present with idiopathic TTP are more likely to relapse during a pregnancy compared to those who presented initially with TTP in association with a pregnancy (25% vs. 12%)(Vesely et al, 2004) while deficient pre-pregnancy ADAMTS13 activity has been utilized to determine this risk by others (Scully et al, 2006). Our experience supports the hypothesis that severely deficient (<2·5%) ADAMTS13 activity during pregnancy predicts a high risk of relapse and identifies patients in which the risk/benefit ratio justifies prophylactic therapy. Such a correlation may exist irrespective of the circumstances of the initial TTP episode (idiopathic versus pregnancy-associated). Pregnant patients with a previous TTP episode should have ADAMTS13 activity assessed pre- and throughout pregnancy to identify those at greatest risk of relapse. None." @default.
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• W1567622570 title "ADAMTS13 activity and the risk of thrombotic thrombocytopenic purpura relapse in pregnancy" @default.
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