Rituximab for Management of Refractory Pregnancy-Associated Immune Thrombocytopenic Purpura

Gall, Brent; Yee, Adrian; Berry, Brian; Bircham, Deborah; Hayashi, Allen; Dansereau, Jerome; Hart, Janace

doi:10.1016/s1701-2163(16)34741-7

Cited by 35 publications

(22 citation statements)

References 28 publications

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“…Belimumab was detected in umbilical cord blood and amniotic fluid in a study on cynomolgus monkeys treated with belimumab throughout pregnancy, confirming that transplacental transfer resulted in fetal exposure (65). Case reports on rituximab given during the second and third quarter showed cord blood levels similar to or higher than maternal levels at delivery (16)(17)(18)(19).…”

Section: N Biological Therapies In the Pregnant Patientmentioning

confidence: 90%

“…In this respect the London Position Statement of the World Congress of Gastroenterology on the Biological Therapy for IBD stated that vaccination of infants exposed to biological therapy in utero should be given according standard schedules, except for live-virus vaccines, which are not recommended if biological agents are detectable in the infant bloodstream (71). Table III summaries the reports of maternal exposure to rituximab either prior to or during pregnancy (16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34). Rituximab has various indications.…”

Section: Anti-tnfαmentioning

confidence: 99%

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Are biological drugs safe in pregnancy?

et al. 2015

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The introduction of biological therapies has significantly improved the outcome of inflammatory rheumatic diseases. As most of these diseases affect women and men in childbearing age, some concerns have been voiced as to the safety of these drugs in relation to reproduction and pregnancy. Data from many hundreds of pregnancies in patients affected by inflammatory bowel disease and inflammatory arthritis have suggested that exposure to anti-TNF therapies at conception and/or during pregnancy is not associated with adverse pregnancy outcomes or any increase in congenital abnormalities. However, the exposure to anti-TNFα agents, particularly to monoclonal antibodies, in late pregnancy is associated with high drug levels in the newborn and their long-term effects on children remain unknown. Therefore, limiting the use of anti-TNFα to the first 30 weeks of pregnancy is recommended to reduce fetal exposure. Live-virus vaccines should be given only when levels of anti-TNFα drugs are undetectable in the serum of infants. Studies suggest that many of these drugs do enter breast milk in small amounts, but the extent to which the infant absorbs them is less clear. Limited reports have not suggested adverse pregnancy outcomes in women whose partners were exposed to anti-TNF therapies at the time of conception. Pregnancy data for rituximab, abatacept, anakinra, tocilizumab and belimumab are limited and their use in pregnancy cannot currently be recommended.

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Section: N Biological Therapies In the Pregnant Patientmentioning

confidence: 90%

Section: Anti-tnfαmentioning

confidence: 99%

Are biological drugs safe in pregnancy?

et al. 2015

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“…[102] However, potential fetal toxicity associated with rituximab is of concern. [126127] Treatment of aHUS also includes plasma infusion and plasma exchange to restore the missing mediators (factor H and I) and remove anti-factor H.[95128] In approximately 50% of patients, renal function does not improve during their first episode of aHUS with plasma exchange therapy. [102] The criteria use to define aHUS resistant to plasma exchange therapy include (i) the absence of platelet count increase, (ii) absence of LDH level decrease, and (iii) absence of significant decrease (>25%) of serum creatinine, despite 3–5 plasma exchange.…”

Section: Treatment Of the Underlying Pregnancy-specific Diseasesmentioning

confidence: 99%

Acute kidney injury in pregnancy-specific disorders

Prakash

Ganiger

2017

Indian J Nephrol

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The incidence of acute kidney injury in pregnancy (P-AKI) has declined significantly over the last three decades in developing countries. However, it is still associated with significant fetomaternal mortality and morbidity. The diagnosis of P-AKI is based on the serum creatinine increase. The usual formulas for estimating glomerular filtration rate (GFR) are not validated in this population. The incidence of P-AKI with respect to total AKI cases has decreased in the last three decades from 25% in 1980s to 9% in 2000s at our centre. During the first trimester of gestation, AKI develops most often due to septic abortion or hyperemesis gravidarum. Septic abortion related AKI with respect to total AKI decreased from 9% to 5% in our study. Prevention of unwanted pregnancy and avoidance of septic abortion are keys to eliminate abortion associated AKI in early pregnancy. However, we have not seen AKI on account of hyperemesis gravidarum over a period of 33 years at our center. In the third trimester, the differential diagnosis of AKI in association with pregnancy specific conditions namely preeclampsia/HELLP syndrome, acute fatty liver of pregnancy and thrombotic microangiopathies of pregnancy (P-TMA) is more challenging, because these 3 conditions share several clinical features of thrombotic microangiopathy which makes the diagnosis very difficult on clinical grounds. It is imperative to distinguish these conditions to make appropriate therapeutic decisions. Typically, AFLP and HELLP syndrome improve after delivery of the fetus, whereas plasma exchange is the first-line treatment for pregnancy associated thrombotic microangioathies (P-TMA). We observed that preclampsia/eclampsia is the most common cause of AKI in late third trimester and postpartum periods followed by puerperal sepsis and postpartum hemorrhage. Pregnancy-associated thrombotic microangiopathies (aHUS/TTP) and AFLP are rare causes of AKI during pregnancy in developing countries.

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“…Like all IgG1 antibodies, rituximab undergoes an active transplancental transport through Fc receptors mainly during the third trimester of pregnancy, leading to the drug accumulation in the fetus. Rituximab is usually cleared from the newborn circulation within 3-4 months postpartum (44). In a recent review of 153 pregnancies in women with malignant hemopathies or severe systemic disorders treated with rituximab during gestation (45), 60% live births, 21% first-trimester abortions, and 2.2% congenital abnormalities were reported.…”

Section: Tma In Pregnancy: the Great Paradigm Shiftmentioning

confidence: 99%

Obstetric Nephrology

Fakhouri

Vercel

Frémeaux‐Bacchi

2012

Clinical Journal of the American Society of Nephrology

148

121

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Summary AKI in pregnancy remains a cause of significant fetomaternal mortality and morbidity, particularly in developing countries. Hypertensive complications of pregnancy (preeclampsia/eclampsia or hemolysis, elevated liver enzymes, and low platelets count syndrome) are the leading cause of AKI in pregnancy worldwide. Thrombotic microangiopathy is another peculiar and devastating cause of AKI in pregnancy. During the last decade, our understanding, and in some cases, our management, of these causes of AKI in pregnancy has dramatically improved. For instance, convincing data have linked pre-eclampsia/eclampsia to an increase in circulating antiangiogenic factors soluble Flt 1 and endoglin, which induce endothelial cell dysfunction, hypertension, and proteinuria. Several distinct pathogenic mechanisms underlying thrombotic microangiopathy, including thrombotic microangiopathy occurring during pregnancy, have been established. Thrombotic microangiopathy, which can present as hemolytic uremic syndrome or thrombotic thrombocytopenic purpura, can be reclassified in four potentially overlapping subtypes: disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 deficiency-related thrombotic microangiopathy, complement alternative pathway dysregulation-related thrombotic microangiopathy, secondary thrombotic microangiopathy (verotoxin and antiangiogenic drugs), and thrombotic microangiopathy of undetermined mechanism. In most cases, pregnancy is only a precipitating factor for thrombotic microangiopathy. Treatment of thrombotic microangiopathy occurring during pregnancy should be tailored to the underlying pathogenic mechanism: (1) restoration of a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 serum activity in the setting of thrombotic thrombocytopenic purpura through plasma exchanges and in some cases, B cell-depleting therapy and (2) inhibition of complement alternative pathway activation in atypical hemolytic uremic syndrome using antiC5 blocking antibody (eculizumab).

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Rituximab for Management of Refractory Pregnancy-Associated Immune Thrombocytopenic Purpura

Cited by 35 publications

References 28 publications

Are biological drugs safe in pregnancy?

Are biological drugs safe in pregnancy?

Acute kidney injury in pregnancy-specific disorders

Obstetric Nephrology

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