Immune Thrombocytopenia and Pregnancy 

Updated: Sep 21, 2020
Author: Shamudheen Rafiyath, MD; Chief Editor: Srikanth Nagalla, MD, MS, FACP 


Practice Essentials

Thrombocytopenia is common in mothers and newborns and usually is caused by an increased rate of platelet destruction. The reference range of a normal platelet count in nonpregnant women and newborns is 150,000-400,000/µL; however, mean platelet counts in pregnant women generally are lower.

Thrombocytopenia in pregnancy has many common causes, including gestational thrombocytopenia, viral and bacterial infections, and preeclampsia complicated by hemolysis, elevated liver enzymes, and low platelet (HELLP) syndrome.[1]  This article focuses on immune thrombocytopenia (ITP) and neonatal alloimmune thrombocytopenia (NAIT). Although relatively rare, these immunologic causes of thrombocytopenia are important, as neonatal outcomes can be significantly impaired and subsequent pregnancies can be affected (See images below.)

Immune thrombocytopenia. An infant born with neona Immune thrombocytopenia. An infant born with neonatal lupus syndrome and severe thrombocytopenia. Note extensive bruising and petechiae.
Immune thrombocytopenia. An infant born with a cep Immune thrombocytopenia. An infant born with a cephalohematoma.

Immune thrombocytopenia occurs in approximately 1 to 3 in 10,000 pregnancies; this rate is 10-fold greater than the incidence of ITP in the general population. The increased frequency in pregnancy could be due to frequent blood testing and unmasking of asymptomatic mild thrombocytopenia in pregnancy.[2]  ITP can occur during any trimester, or the diagnosis may be known prior to the pregnancy. Compared with ITP in the general population, ITP in pregnant women is associated with greater risk of bleeding at platelet counts < 20,000 to 30,000/μL.[3]


Immune thrombocytopenia is a rare autoimmune disease due to an abnormal T cell response, notably supported by splenic T follicular helper cells, that stimulates the proliferation and differentiation of autoreactive B cells. The antiplatelet autoantibodies they produce facilitate platelet phagocytosis by macrophages, essentially in the spleen. These autoantibodies can cross the placenta; thus, both mother and newborn can be affected. Macrophages contribute to the perpetuation of the autoimmune response as the main antigen-presenting cell during ITP. CD8+ T cells also contribute to thrombocytopenia by increasing platelet apoptosis.[4]

Besides this peripheral platelet destruction, inappropriate bone marrow production also exacerbates thrombocytopenia, due to an immune response against megakaryocytes. Moreover, the level of circulating thrombopoietin, the main growth factor of megakaryocytes, is low.[4]  

NAIT is caused by maternal immunization against fetal paternally derived platelet-specific antigens (similar to rhesus [Rh] disease). The mother has a normal platelet count, while the fetus can be severely thrombocytopenic. The foreign antigens promote the production of immunoglobulin by the mother. This is initially immunoglobulin M, whose large size prevents transplacental passage. Subsequently, the mother produces immunoglobulin G. The smaller size of this molecule permits passage across the placenta, resulting in the destruction of fetal platelets and neonatal thrombocytopenia.


ITP occurs in 1 to 2 of every 1,000 pregnancies, which in the United States represents about 3,000 to 6,000 cases of ITP in pregnancy per year.[5]  Although ITP accounts for less than 3% of all cases of thrombocytopenia during pregnancy, it is the most common cause of a platelet count below 50 × 109/L detected in the first and second trimesters.[6]  The frequency of NAIT is estimated at 1-2 cases per thousand deliveries.

In Helsinki, Finland, the frequency of ITP is 1.8 cases per 1,000 deliveries.[7]  The frequency of NAIT was reported as 0.5 cases per 1,000 and 1.5 cases per 1,000 liveborn neonates in England[8] and France,[9] respectively. In Japan, the frequency of NAIT was 0.3 cases per 1,000 liveborn neonates, and incompatibility for human platelet antigen (HPA)-4 was the cause of 80% of these cases.[10]

The recurrence risk for NAIT is extremely high (nearly 100% of subsequent pregnancies are affected if the sibling carries the significant paternally derived antigen).[11] In general, siblings with the platelet antigen will be as severely affected or more severely affected than the preceding affected child.[11]

ITP occurs in all races. However, more than 50% of all cases of NAIT have been reported in whites. Most cases of alloimmune thrombocytopenia (and the most severe cases) occur in white mothers homozygous for the P1A2 allele (HPA-1b).[12]  The prevalence of homozygous HPA-1b in whites is estimated at 2.5%.[13]  Multiple other platelet-specific antigens exist that can cause alloimmune thrombocytopenia; the prevalence of these varies in different ethnic groups.

ITP is diagnosed more commonly in females than males (ratio 3:1).[14]  NAIT occurs in newborns of both sexes. ITP commonly is diagnosed in the second or third decade of life. NAIT develops in fetal life, with 25-50% of fetal intracranial hemorrhages detectable on prenatal ultrasound prior to the onset of labor.[15]


Women with ITP generally do well in pregnancy. ITP is an autoimmune disease, and exacerbations and remissions are common. Pregnancy does not appear to affect the course of the disease. ITP is not an absolute contraindication to pregnancy but in unusually severe or refractory cases or for women taking potentially teratogenic medications, deferring pregnancy may be indicated.[6]  Duration of maternal ITP is a risk factor for preterm birth and women with chronic ITP experience more adverse outcomes than those with a pregnancy-related diagnosis of ITP.[5]  

Fetuses and newborns with NAIT can experience permanent neurologic sequelae, organ damage, and death from intracranial and intra-abdominal bleeds due to severe thrombocytopenia. However, after birth, maternal antibodies are fairly rapidly degraded and the thrombocytopenia resolves.

Women and newborns with severe thrombocytopenia can experience intracranial and intra-abdominal bleeding. This can result in significant morbidity, including neurologic damage and/or death. Women requiring long-term steroid therapy can develop complications from the medication exposure.

Transfusion of blood products can result in transfusion reactions in the recipient. With current blood bank crossmatching, significant transfusion reactions are rare. Additionally, transfusions pose the rare risk of transmission of viral infections, especially hepatitis and human immunodeficiency virus. Monteith et al reported that pregnant women infected with hepatitis C virus had a significantly higher frequency of thrombocytopenia and significantly lower platelet counts compared with controls.[16]

Maternal hemorrhage at time of birth is a risk in women with ITP, particularly if the platelet count falls below 20,000/µL. However, a 1997 review found that no maternal deaths had been reported in the previous 20 years,[11]  and maternal morbidity is minimal if appropriate therapy is administered during pregnancy and childbirth.

Neonatal thrombocytopenia due to the active transport of antiplatelet antibodies through the placenta is a clinically more significant problem, and it occurred in 9 of 66 (13.6%) pregnancies complicated by ITP in a review by Yamada et al.[17]  Of those infants, 5 of 66 (7.5%) had severe thrombocytopenia, with platelet counts less than 50,000/µL. Splenectomy prior to pregnancy was the only risk factor associated with the development of neonatal thrombocytopenia by logistic regression analysis.

Severe neonatal thrombocytopenia places the infant at risk for intracranial or visceral hemorrhage. None of the 9 thrombocytopenic infants in the Yamada trial had intracranial hemorrhage documented on clinical neurological examination or ultrasound. Neonatal intracranial hemorrhage previously has been reported to have a very low incidence (0-2.3%) in newborns of mothers with ITP.[18]

Neonatal morbidity is far more common in NAIT, with 10% of affected newborns dying and 20% experiencing neurological sequelae secondary to intracranial hemorrhage.[13]  Affected infants can have generalized petechiae, hemorrhage into abdominal viscera, and excessive bleeding after venipuncture or circumcision.




A detailed history is necessary to identify the cause of thrombocytopenia. The history should elucidate the following:

  • Any personal or family history of bleeding
  • Concomitant medical disorders including thrombosis
  • Drug and vaccine history
  • History of alcohol use
  • Signs and symptoms consistent with autoimmune disorders
  • History of fever
  • Previous obstetric history, including preeclampsia, thrombocytopenia in pregnancy, and neonatal thrombocytopenia

Pregnant women with immune thrombocytopenia (ITP) can be asymptomatic or can present with a history of easy bruisability, bleeding into the mucous membranes (epistaxis or gingival bleeding), or petechiae. They may have a history of menorrhagia or menometrorrhagia prior to pregnancy.

A maternal history of delivering a term newborn with thrombocytopenia, visceral or intracranial hemorrhage, or spontaneous or prolonged bleeding after venipuncture or circumcision raises suspicion for neonatal alloimmune thrombocytopenia (NAIT). However, about 50% of neonates with NAIT are first-born children, and thus are delivered to women whose risk for the disorder is previously unrecognized and unknown.[19, 20]

Case history

A  24-year-old part Hawaiian and part Samoan woman has been pregnant four times and given birth once (G4 P1). She has had no spontaneous abortions (SAB0) and two elective abortions (EAB2). She was referred for twice-weekly antepartum testing due to a prior stillbirth at 31 weeks' estimated gestational age. A specific cause of the fetal demise was never determined; chromosome analysis revealed a normal male (46, XY) pattern, placental pathology was normal, and an autopsy was not performed.

Her pregnancy and antepartum testing results are normal until 35 and 5/7 weeks' estimated gestational age. She is admitted for prolonged fetal monitoring; the findings are completely normal (see images below) and she is discharged home later that day.

Immune thrombocytopenia. Nonstress test 1 week bef Immune thrombocytopenia. Nonstress test 1 week before delivery showing a normal reactive fetal heart rate pattern.
Immune thrombocytopenia. Nonstress test 4 days bef Immune thrombocytopenia. Nonstress test 4 days before delivery showing a reactive fetal heart rate with an unusual pseudosinusoidal pattern that lasted 9 minutes.

She presents 4 days later with 2 days of decreased fetal movement. Fetal heart tones cannot be auscultated, and an ultrasound confirms intrauterine fetal demise. Labor is induced, and she delivers a 2729 g male fetus. Autopsy demonstrates a large subdural hemorrhage (54 g) surrounding the brain and spinal cord (see images below).

Immune thrombocytopenia. Neonatal brain at autopsy Immune thrombocytopenia. Neonatal brain at autopsy showing extensive subdural hemorrhage.
Immune thrombocytopenia. Neonatal spine at autopsy Immune thrombocytopenia. Neonatal spine at autopsy showing extensive hemorrhage at base of spine.

The woman's blood is sent for platelet antigen typing. Her platelet-associated immunoglobulin titers are high, at 7.5 (reference range 0-4.3). She tests positive for HPA-1a; this distinguishes her case from most of those in whites, which involve alloimmunization in an HPA-1a–negative mother exposed to paternal HPA-1a antigen. However, many different platelet antigens exist, and platelet antigens other than HPA-1a may be significant in nonwhite ethnic groups; for example, HPA-4 has been shown to be involved in 80% of NAIT cases in Japanese patients.[65]  Because the baby's father declines to have his blood drawn, his platelets cannot be tested with the mother's serum, so the present studies neither support nor exclude a diagnosis of NAIT.

Two years later, the woman presents pregnant with a new partner. The new father's platelets are tested against the mother's serum to verify that no antibodies in the maternal serum will react to paternal platelets, and no antiplatelet antibodies are present. She has an uncomplicated pregnancy and delivers a full-term healthy infant.


A thorough clinical examination is important to look for the following:

  • Mucocutaneous bleeding
  • Petechiae
  • Skeletal abnormalities
  • Hepatosplenomegaly
  • Lymphadenopathy,
  • Features of preeclampsia and other signs of thrombotic microangiopathy

Most women with ITP have normal findings on physical examination (splenomegaly is absent). Petechiae may be identified in patients with severe thrombocytopenia.

Newborns with NAIT may have normal findings on physical examinations, or they may have a cephalohematoma, ecchymoses over the presenting part, and generalized petechiae (see images below).

Immune thrombocytopenia. An infant born with neona Immune thrombocytopenia. An infant born with neonatal lupus syndrome and severe thrombocytopenia. Note extensive bruising and petechiae.
Immune thrombocytopenia. An infant born with a cep Immune thrombocytopenia. An infant born with a cephalohematoma.


Diagnostic Considerations

Thrombocytopenia is extremely common in mothers and newborns, affecting 7-8% of all women during pregnancy[12] and 15-20% of newborns admitted to neonatal intensive care units (NICUs).[21] Particular attention must be paid to the peripheral smear to rule out macrothrombocytopenia, which may occasionally occur in the absence of other disorders associated with the MYH9 gene (deafness, cataracts, and nephritis).[22] Immune thrombocytopenias are relatively rare causes of thrombocytopenia, but they always must be considered in the differential diagnosis because neonatal outcomes can be impaired significantly, and subsequent pregnancies can be affected.

Immune thrombocytopenia (ITP)

Other problems to consider in the differential diagnosis of ITP include the following:

  • Gestational thrombocytopenia
  • Preeclampsia
  • Systemic lupus erythematosus
  • Hemolytic-uremic syndrome
  • Thrombotic microangiopathy (TMA)
  • Antiphospholipid syndrome
  • Disseminated intravascular coagulation (DIC)
  • Hereditary thrombocytopenias (eg, May Hegglin anomaly, von Willebrand disease)
  • Thrombocytopenia secondary to drug exposure (eg, heparin, sulfonamides)
  • Other miscellaneous medical conditions that can cause thrombocytopenia (eg, leukemia, viral infection)
  • Acute fatty liver of pregnancy
  • Deficiency of vitamin B12, copper, and rarely folate.

Gestational thrombocytopenia occurs in the last half of pregnancy and accounts for three quarters of all cases of thrombocytopenia in pregnancy. A platelet count of less than 50,000/µL makes this diagnosis very unlikely. These women typically do not have a history of ITP, except during previous pregnancies, which usually resolves 4-8 weeks after delivery. The neonates of these women are not thrombocytopenic.[23] ​

Neonatal alloimmune thrombocytopenia (NAIT)

Other problems to consider in the differential diagnosis of NAIT include the following:

  • Sepsis
  • Congenital infections (eg, cytomegalovirus or HIV)
  • Stress (in premature newborns in the NICU)
  • Hypoxia secondary to perinatal asphyxia or aspiration
  • Congenital genetic syndrome
  • Congenital leukemia
  • Cyanotic congenital heart disease
  • Maternal preeclampsia (particularly if infant is growth restricted)
  • Maternal drug ingestion
  • Intracranial vascular abnormality

Differential Diagnoses



Approach Considerations




Laboratory Studies

A baseline investigation of thrombocytopenia in pregnancy include the following:

  • Complete blood cell count (CBC)
  • Reticulocyte count
  • Peripheral smear examination
  • Coagulation screen
  • Liver function tests
  • Autoimmune disease screening
  • Virology screen
  • Vitamin B12, zinc, and folate levels

Spurious thrombocytopenia or pseudo-thrombocytopenia need to be ruled out by testing the platelet count in a citrate sample.

There is no diagnostic test to differentiate gestational thrombocytopenia and immune-mediated thrombocytopenia. Therefore, the diagnosis of immune thrombocytopenia (ITP) is based on a personal history of bleeding, a low platelet count prior to pregnancy, and/or a family history that excludes hereditary thrombocytopenia (HT).[6]  Platelet counts of less than 70,000/µL are suspicious for the disorder if no other etiology for thrombocytopenia is identified.[24]  Other testing, based on patient history and clinical findings, helps to rule out other possible etiologies for thrombocytopenia in pregnancy

The variation in the platelet count may be due to peripheral destruction of platelets or congenital platelet disorders. The appearance of schistocytes in the peripheral smear along with an increase in the lactate dehydrogenase l, elevated renal function, and anemia are evidence of thrombotic microangiopathy. The presence of abnormal white cell morphology, immature cells, and teardrop erythrocytes is suggestive of concomitant bone marrow pathology.

Bone marrow biopsy is needed in selected patients with signs and symptoms pointing to a lymphoproliferative disorder (fever, night sweats, weight loss, splenomegaly, and lymphadenopathy).

Antiplatelet antibodies can be detected in the serum of women with ITP. The direct assay for the measurement of platelet-bound autoantibodies has an estimated sensitivity of 49-66% and an estimated specificity of 78-92%. A negative test does not exclude the diagnosis.[25] Additionally, many women with gestational thrombocytopenia have high levels of circulating platelet-associated immunoglobulin. Therefore, current antiplatelet antibody assays cannot be used to differentiate between ITP and gestational thrombocytopenia.

In newborns, a platelet count less than 150,000/µL is consistent with thrombocytopenia. Consider neonatal alloimmune thrombocytopenia (NAIT) in the differential diagnosis of any significantly thrombocytopenic newborn (platelet count > 50,000/µL) or in newborns with intracranial hemorrhages (platelet count < 100,000/µL) in whom other illnesses commonly associated with thrombocytopenia have been excluded, as follows[21] :

  • Platelet antigen typing can determine the genotype of the mother and father of the baby to determine if they are discordant.

  • Test the maternal sera for the presence of a platelet antibody that binds paternal, but not maternal, platelets.

  • A lack of antiplatelet antibody does not exclude the diagnosis of NAIT because, in a number of cases, no antiplatelet antibody could be detected when fetuses were profoundly thrombocytopenic due to NAIT.[11]




Approach Considerations

Women who have been diagnosed with immune thrombocytopenia (ITP) prior to pregnancy should be offered preconception counseling. For the counseling session, it is necessary to obtain details of her case, including the presentation of ITP, prior medical treatment, whether splenectomy was performed, and response to treatment. In addition, an obstetric history should be obtained; in women who have previously given birth, this should include the neonatal platelet count.

The patient should be educated about the need for additional blood tests and followup during pregnancy and the potential need to consider treatment for ITP, which is the case in one-third of pregnant women with ITP. The small risk of maternal and fetal complications should be discussed. However, most of these women can safely proceed with pregnancy, as the risk of complications is low if they receive appropriate care, so they should not be discouraged from pregnancy.[26]  A history of ITP in a mother or ITP in a previous pregnancy is not a contraindication to future pregnancies.[27]

Pregnant women at risk to deliver a newborn with severe thrombocytopenia should deliver at an institution capable of caring for the newborn. In general, a hospital with a level III neonatal intensive care unit (NICU) is necessary to provide an appropriate level of care.

Immune thrombocytopenia

Treatment for ITP in pregnancy is well established and effective.[28, 29, 30, 1]  Medical therapy is initiated if the maternal platelet count decreases to less than 20,000/µL, if spontaneous bleeding occurs and the platelet count is less than 50,000/µL, or if surgery or delivery is anticipated and the platelet count is less than 50,000/µL.

Patients with ITP and platelet counts greater than 50,000/µL with active bleeding need to be evaluated for other causes of hemorrhage. If no other etiology of bleeding can be identified, the patient should be treated medically for ITP until her platelet count increases to greater than 100,000/µL.

When therapy is indicated, most hematologists use a glucocorticoid as initial therapy. High-dose dexamethasone, 40 mg daily for 4 days without taper, or prednisone 1- 2 mg/kg/day are both effective. A meta-analysis showed better overall response with high-dose dexamethasone compared with prednisone (79% versus 59%) and better complete response (64% versus 36%) at 2 weeks and fewer bleeding events (12% versus 24%) at 10 days, as well as fewer adverse effects. However, there was no difference in overall response or complete response at 6 months. These researchers concluded that high-dose dexamethasone might be preferable to prednisone for patients with severe ITP who require a rapid rise in platelet count.[31]

 Steroids are not entirely benign during pregnancy and orofacial fetal abnormalities such as cleft palate occur 3-fold more commonly in infants exposed in the first trimester.[32]  Maternal hyperglycemia and hypertension may also result.                                                                                    

Opinions vary concerning the minimal platelet count required for epidural anesthesia; however, many anesthesiologists are hesitant to utilize epidural anesthesia for labor with a patient whose platelet count is less than 100,000/µL. Thus, patients with platelet counts below this level often are treated with prednisone at 36-37 weeks' gestation.

Intravenous immunoglobulin (IVIG) can be used in women who do not respond to prednisone. Because patients respond more quickly to IVIG than prednisone (a response can be observed as quickly as 6 h), IVIG is a good choice for first-line therapy in women with platelet counts less than 10,000/µL or in association with perioperative or postpartum bleeding. IVIG (usual prescription 0.4 mg/kg/d for 3-5 d) is costly and of limited availability, so it should be used judiciously.[33]  A retrospective study of 67 neonates with thrombocytopenia born to mothers with ITP suggested a benefit of starting IVIG when the platelet count is below 50 × 109/L after the first platelet transfusion, to avoid multiple transfusions.[34]

Intravenous (IV) anti-D (WinRho, WinRho SD) has been utilized in both children and adults to treat ITP. Children have a better response than adults; overall, approximately 70% of treated individuals respond to IV anti-D with increasing platelet counts.[35]  Doses utilized have ranged from 25-200 mcg/kg/d. In some studies, IV anti-D was administered daily for 5 days; in others, it was given as a single dose. Toxicity was minimal, and infusions were completed in less than 5 minutes.[35, 36]  Anti-D is effective in Rh-positive individuals only and may be associated with immune hemolysis.[37]

Experience with IV anti-D in pregnancy to treat ITP has been limited. This is likely because of concerns of possible fetal hemolysis from transplacental passage of the IgG molecules. Significant fetal hemolysis from maternal antepartum prophylaxis has not been reported[38] ; however, doses of IV anti-D used for prophylaxis to prevent Rh disease are much lower than those used to treat ITP. Thus, IVIG tends to be used more commonly in pregnancy.

Timing of response with the various agents is as follows[39] :

  • IVIG: 1-3 days for initial reponse and 2-7 days for peak response
  • Dexamethasone:  2-14 days for initial response and 4-28 days for peak response
  • Prednisone: -  4 -14 days for initial response and 7-28 days for peak response

Platelet transfusions should be used sparingly because maternal antiplatelet antibodies result in rapid destruction of transfused platelets.[40]  Administer platelet transfusions to women with hemorrhage or platelet counts less than 10,000/µL. 

The platelet count threshold for a non-bleeding pregnant woman nearing delivery or a procedure depends on the expected mode of delivery or type of procedure. In the absence of bleeding, transfuse to a platelet counts of 30,000/µL for vaginal delivery and transfuse to 50,000/µL if plan for cesarean delivery.

The safety and efficacy of thrombopoietin mimetics are not established in pregnant women with ITP. In one case report, in which romiplostim was used during pregnancy in addition to steroids and IVIG, the newborns still experienced intraventricular hemorrhage, although there was no developmental delay at 10 months.[41]

Rituximab crosses the placenta, and data are insufficient to recommend use in ITP during pregnancy.[42]

Cyclophosphamide, mycophenolate, vincristine, and danazol are contraindicated during pregnancy.

Neonatal alloimmune thrombocytopenia (NAIT)

The goal of treatment in NAIT is to prevent intracranial or visceral bleeds in the fetus and newborn. Prenatal diagnosis and treatment is important because 25-50% of NAIT-related intracranial hemorrhages occur while the fetus is in utero.[15]  The only reliable method of determining the fetal platelet count is to perform cordocentesis and check the fetal blood directly, because fetal platelet counts do not correlate with maternal antibody levels. Cordocentesis is associated with a 1-2% chance of emergent cesarean delivery for fetal indications.[12]  Thus, a risk for fetal loss exists with each cordocentesis procedure performed.

Platelet membrane specific antigens are present in the fetus at 18 weeks' gestation; therefore, cordocentesis commonly is initiated in mothers with human platelet antigen–1b (HPA-1b) with platelet alloantibodies at 20 weeks' gestation. Continued monitoring and treatment for NAIT is quite controversial. Controversy exists because NAIT is rare and only small numbers of successfully treated patients are reported in the literature.

European authors have advocated weekly platelet transfusions and have demonstrated that this therapy is effective in increasing the fetal platelet count.[43, 44, 45]  Brussel et al have advocated a less invasive management and treatment plan, reporting on a total of 73 patients with NAIT.[46, 47]  Mothers of fetuses found to be thrombocytopenic at initial cordocentesis were treated with IVIG 1 g/kg/wk. A repeat cordocentesis was performed after 4-6 weeks to assess efficacy of treatment.

In their randomized controlled trial, some mothers were treated with IVIG, others with IVIG and dexamethasone.[47]  The addition of dexamethasone did not enhance the effect of IVIG. At least 62% of patients responded to IVIG alone. Patients failing to respond either were delivered early or were continued on IVIG plus prednisone (60 mg/d). This salvage therapy was effective in 50% of cases that failed to respond to IVIG alone. None of the mothers treated according to this management plan had a fetus with an intracranial hemorrhage. These authors advocate administering platelet transfusions if the fetal platelet count is less than 20,000/µL at the time of cordocentesis because they noted an increased rate of fetal exsanguination secondary to cordocentesis when the platelet count was in this range.

Other authors have advocated using IVIG as a primary treatment, particularly in patients who are at risk for NAIT and have no history of a previous child affected with intracranial hemorrhage.[48]  Fetuses that fail to respond to IVIG receive weekly platelet transfusions for the duration of the pregnancy.[24]

A meta-analysis of 26 studies found comparable outcomes regarding the occurrence of intracranial hemorrhage, regardless of the antenatal management strategy: serial fetal blood sampling (FBS), intrauterine platelet transfusions (IUPT), or weekly IVIG, with or without corticosteroids. There was no consistent evidence for benefit for the addition of steroids to IVIG.[49]

In a retrospective study, Giers et al concluded that in the treatment of fetal NAIT, the intrauterine transfusion of either maternal platelets or HPA-matched donor platelets had equal clinical efficacy.[50]  No procedure-related fetal or neonatal loss resulted from the use of either maternal (15 fetuses) or donor (42 fetuses) platelets, and both types of treatment reliably increased fetal platelet counts.

Management of the newborn with NAIT is fairly straightforward. Because of the significant risk of intracranial hemorrhage, an immediate cranial ultrasound should be performed. Severely thrombocytopenic newborns (< 10,000/µL) or newborns with intracranial or visceral hemorrhages should receive a matched platelet transfusion (maternal or homozygous HPA-1b donor) as soon as possible. If maternal platelets are utilized, they must be processed to remove platelet alloantibodies. Reserve random platelets for life-threatening hemorrhage when matched platelets are not immediately available, because reports exist of worsening thrombocytopenia and disseminated intravascular coagulation (DIC) following random platelet transfusion in cases of NAIT.[11]

IVIG (1 g/kg/d) has been demonstrated to increase newborn platelet counts in most cases of NAIT. A substantial increase is observed in 24-72 hours, which is adequate for newborns who are stable and without evidence of bleeding.

Exchange transfusions can be performed to remove antiplatelet antibody and shorten the course of neonatal disease.[11]  Approximately 30% of available immunoglobulin G antiplatelet antibodies are estimated to be removed per double volume procedure.

Medical Care

Management of maternal ITP

Clinical management of pregnancy-associated ITP is a complex task requiring close collaboration by the obstetrician, hematologist, and anesthetist. Pregnant women with ITP should be seen monthly in the first and second trimester, every 2 weeks after 28 weeks, and weekly after 36 weeks. Visits should involve routine obstetric care with emphasis on blood pressure, urine dipstick analysis for protein, weight, and serial platelet counts.[51]  However, the need for additional care will vary depending on the patient's platelet count and clinical condition.

The goal is to treat when required to maintain an adequate platelet count to avoid maternal hemorrhagic complications in the antenatal, intrapartum, and postnatal period. The current International Consensus Report considers that in the absence of symptoms or any planned intervention, a platelet count of 20 - 30 × 109/L is safe during most of pregnancy and patients can often be managed by observation only.[52]

Preparation for delivery

At week 34 to 36, there should be a review of whether or not treatment needs to be commenced to minimize the risk of hemorrhage around the time of delivery. The review should take into account individual clinical features, obstetric factors, the trend in platelet count, and the patient's personal wishes. Considerations include the following:

  • If the patient is asymptomatic and platelet counts are stable and greater than 50 ×10 9/L, no treatment is generally required.
  • If the platelet counts are less than 50 × 10 9/L, treatment should be considered.
  • If the platelet count is between 50 and 70 × 10 9/L, treatment should be considered if neuraxial anesthesia is desired for delivery or cesarean delivery is planned because of an obstetric indication.

The platelet threshold deemed safe for administering spinal or epidural anesthesia remains controversial due to the theoretical risk of epidural hematoma formation and neurological damage. There is a paucity of data for a specific platelet count predictive of neuraxial anesthetic complication. A systematic review of neuraxial techniques for anesthesia included 14 papers reporting 326 neuraxial techniques in 325 patients diagnosed with ITP. All but one were obstetric patients, of which nine had a platelet count < 50 × 109/L  and 19 had a platelet count of 50 - 70 × 109/L. There were no hemorrhagic complications associated with neuraxial techniques.

Archived British Committee for Standards in Haematology (BCSH)  ITP guidance from 2003 recommended a  platelet count of > 80 ×109/L if epidural anesthesia is to be used for cesarean delivery.[53] The 2019 International Consensus Report suggests that regional axial anesthesia can be safely performed/L at a platelet count ≥70 × 109/L, if no other hemostatic abnormalities are present.[52] This assumes the absence of bruising, bleeding, and history of anticoagulation and the presence of a normal international normalized ratio, activated partial thromboplastin time, and fibrinogen level.

In these cases, an anesthetist should counsel the patient regarding the risk and benefit of regional anesthesia versus general anesthesia.  

In addition to the known prothrombotic state of pregnancy, some women may have risk factors (eg, anti-cardiolipin antibody syndrome) requiring venous thromboembolism prophylaxis. A platelet count > 50 × 109/L is generally recommended for such patients receiving anticoagulation.[52]

Management of neonate born to women with ITP

One trial evaluated the safety of breastfeeding in women with ITP and did not document thrombocytopenia developing in any breastfed infants.[21] IgG antiplatelet antibodies are transmitted through the breast milk, so consider monitoring the platelet counts in breastfed newborns of mothers with ITP.

The major neonatal concern in ITP is the risk of fetal or newborn intracranial or visceral hemorrhage due to severe thrombocytopenia. Newborn thrombocytopenia is difficult to predict because newborn platelet counts do not always correlate with maternal platelet counts or antiplatelet antibody titers.[7, 18]  The newborn platelet count does correlate with the platelet count of previous first and second siblings at birth.[54]

Maternal platelet counts that fall within the reference range after pre-pregnancy splenectomy or corticosteroid treatment do not guarantee a fetal platelet count within the reference range. In fact, splenectomy prior to pregnancy has been reported as a risk factor for the development of newborn thrombocytopenia.[55] Splenectomy possibly increases the amount of free antiplatelet antibody in the maternal sera due to the removal of the platelet/antibody destruction site.[56]

Fetal platelet counts can be obtained by fetal scalp sampling during labor or cordocentesis at 38-39 weeks' estimated gestational age; however, neither is reliable at predicting thrombocytopenia at birth. Fetal scalp sampling is technically difficult and often unreliable.[57] Owing to the risk of hemorrhage in the fetus and possible inaccuracy of the fetal platelet count, it is best avoided.[58] In a clinical trial, platelet counts were obtained by cordocentesis in 42 women with ITP. Two of the 42 newborns had severe thrombocytopenia at birth; neither case was detected with cordocentesis.[59] At present, no reliable method of determining which newborns are at risk for severe thrombocytopenia exists.

Procedures during labor that may be associated with increased hemorrhagic risk to the fetus should be avoided, specifically the use of fetal scalp electrodes, fetal scalp blood sampling, vacuum extraction, and rotational forceps[52]

A platelet count at birth is recommended. Peripheral blood is preferred over heel sticks or cord samples because of better accuracy. A cranial ultrasound should be considered if the platelet count is less than 50,000/µL, even in the absence of symptoms. Intramuscular injections such as vitamin K are best avoided.[23]

Some investigators have recommended performing a cesarean delivery in all women with ITP to minimize the trauma to the newborn during the birth process. However, cesarean delivery has not been demonstrated to prevent bleeding complications in thrombocytopenic newborns. In a review of 474 newborns born to mothers with ITP, 29% of newborns born vaginally experienced a bleeding complication, compared with 30% of newborns born via cesarean delivery.[60] Reviews published to date comparing vaginal birth with cesarean delivery in women with ITP are retrospective studies; none are randomized controlled trials. In the absence of any clear benefit to the neonate (given the low rate of intracranial hemorrhage in infants born to mothers with ITP), cesarean delivery should be reserved for the usual obstetric indications.

In women with a history of delivering a significantly thrombocytopenic newborn (platelet count < 50,000/µL) or a newborn with an intracranial hemorrhage (platelet count < 100,000/µL) in whom other illnesses commonly associated with thrombocytopenia have been excluded,[61] test for neonatal alloimmune thrombocytopenia (NAIT), also referred to as fetal and neonatal alloimmune thrombocytopenia (FNAIT). Perform maternal platelet antigen typing and confirm the presence of maternal antiplatelet antibodies with specificity for paternal platelets. Perform antigen typing and zygosity testing on the father of the baby to determine if platelet antigen incompatibility between the parents exists and if all potential offspring will be at risk for NAIT. If the father is a heterozygote, each subsequent fetus has only a 50% chance of being affected. Fetal platelet typing can be performed on a chorionic villous sample, amniocytes, or fetal blood to determine if the fetus carries the significant paternally derived antigen.

Prospective screening programs have demonstrated that NAIT usually develops in babies born to women with detectable antiplatelet antibody.[13] Some investigators have suggested that all pregnant women presenting for prenatal care be typed for platelet alloantigen to determine if they are at risk for NAIT. Women at risk can be tested for the presence of platelet alloantibodies twice during gestation (similar to current screening programs for Rh disease). A comparison of the effectiveness of this type of screening program estimated a cost of $45,000 per case of alloimmunization diagnosed in whites.[13] The cost would be higher if testing were initiated in women of other ethnic groups because the rate of NAIT is lower in nonwhite women. At present, universal prenatal screening is not recommended because a clear clinical benefit has not been demonstrated.[12, 62]

Surgical Care

Splenectomy is an appropriate treatment for women with ITP who have severe thrombocytopenia that is refractory to medical therapy. Approximately two thirds of patients have a positive response to splenectomy, generally within a few days. Splenectomy is seldom performed during pregnancy because most patients can be managed medically.

If splenectomy is indicated, it should be performed in the second trimester. Surgical interventions requiring general anesthesia are avoided in the first trimester if possible to prevent fetal medication exposure during embryogenesis. Splenectomy is technically difficult in the third trimester because the enlarging uterus limits exposure to the spleen. Successful splenectomy has been reported during cesarean delivery.[63]

Women with splenectomies should be immunized against pneumococcus, meningococcus, and Haemophilus influenzae.[12]


Consulting a surgeon may be appropriate if splenectomy is indicated in a pregnant woman with ITP. A hematologist should  be consulted if a patient with ITP or NAIT is not responding to standard therapies or requires transfusions.



Guidelines Summary

The following organizations have issued guidelines for the management of immune thrombocytopenia (ITP) during pregnancy:

  • International Consensus Report
  • American College of Obstetricians and Gynecologists (ACOG)
  • American Society of Hematology (ASH)


In 2019, an international group of experts published an International Consensus Report update to their previous consensus report, including up-to-date evidence, expert opinion from around the world, and the incorporation of a new focus on the patient's perspective.[52] Recommendations (except where noted, all of them grade C—ie, absence of directly applicable clinical studies of good quality) include the following:

  • Patients with a history suggestive of ITP or those with a platelet count < 80 × 10 9/L should be investigated for possible ITP.
  • As in nonpregnant patients, the diagnosis of ITP is one of exclusion, using the patient’s history, physical examination, blood counts, and blood smear examination.
  • Laboratory evaluation is similar to the nonpregnant patient, but special consideration should be given to rule out hypertensive, microangiopathic, coagulopathic, and hepatic disorders associated with pregnancy.

Tests recommended for all patients include the following: 

  • Complete blood cell count (CBC) and peripheral blood smear review - May reveal macrothrombocytopenia or signs of other inherited thrombocytopenias; depending on family history and smear, consider genetic testing, platelet function testing, and testing for type 2b von Willebrand disease and platelet-type von Willebrand disease. Schistocytes may suggest microangiopathy in hemolysis and hypertensive disorders
  • Reticulocyte count - Elevated in hemolysis and hypertensive disorders
  • Coagulation screening (prothrombin time [PT], partial thromboplastin time (PTT) fibrinogen) - PTT may be prolonged in patients with a history of thrombosis or pregnancy loss. Consider testing for antiphospholipid antibodies, anti-cardiolipin antibodies, and lupus anticoagulant.
  • Liver function studies - If levels are elevated, consider viral infection or HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets  
  • Thyroid function studies
  • Viral serologies (HIV, hepatitis C virus)
  • Kidney function studies - Hemolytic-uremic syndrome/thrombotic thrombocytopenic purpura (HUS/TTP) may manifest for the first time in pregnancy. Consider testing for  ADAMTS-13, alternative complement pathway. Consider atypical HUS due to autoantibodies against complement components

Other recommended tests should be based on the clinical features. The following may be considered:

  • Antinuclear antibody (ANA)
  • Helicobacter pylori testing -  H pylori stool or antigen test should be performed in patients with history of thrombocytopenia prior to pregnancy
  • Immunoglobulin levels - Quantitative immunoglobulin testing should be performed in patients with a history of thrombosis or pregnancy loss

The following tests are not recommended:

  • Bone marrow examination - Not recommended unless there are atypical features
  • Anti-platelet antibody testing  - Does not predict the course of maternal or neonatal thrombocytopenia or distinguish ITP from gestational thrombocytopenia
  • Fetal blood sampling
  • Thrombopoietin (TPO) levels - Not recommended, although it may be of value in the future

American Society of Hematology

ASH recommends the following tests for diagnosis of thrombocytopenia in pregnant patients[64] :

  • CBC
  • Reticulocyte count
  • Peripheral blood smear
  • Liver function tests
  • Viral screening (HIV, HCV, HBV)

Tests to consider if clinically indicated include the following[64] :

  • Antiphospholipid antibodies
  • ANA
  • Thyroid function tests
  • H pylori testing
  • Disseminated intravascular coagulation testing—PT, PTT, fibrinogen, fibrin split products
  • Von Willebrand disease type IIB testing
  • Direct antiglobulin (Coombs) test
  • Quantitative immunoglobulin levels

The following studies are not recommended[64] :

  • Antiplatelet antibody testing
  • Bone marrow biopsy
  • TPO levels


International Consensus Report recommendations for the treatment of maternal ITP are as follows[52] :

  • Counseling for women with ITP wishing to become pregnant is recommended.
  • A platelet count between 20 and 30 × 10 9/L in a nonbleeding patient is safe for most of pregnancy. A platelet count ≥50 × 10 9/L (see separate anesthesia recommendation below) is preferred for delivery.
  • Initial treatment is with oral steroids or IVIg.
  • IV anti-D in Rh(D)-positive nonsplenectomized women appears to be well tolerated and effective based on results from a small pilot study (grade B recommendation); however, this may potentially cause maternal or fetal hemolysis.
  • IVIg can provide a rapid, but often very transient, increase in platelet count and can be used to urgently increase platelet counts during bleeding or for delivery (grade B recommendation).
  • Combining therapies (prednisone with IVIg and/or IV anti-D) may elicit a response in patients refractory to single agents alone. High-dose methylprednisolone, in combination with IVIg and/or azathioprine, is suggested for patients refractory to oral corticosteroids or IVIg alone.
  • Rituximab can be considered in pregnancy for very severe cases, but perinatal and neonatal immunosuppression and subsequent infection are potential complications and require monitoring.
  • Thrombopoietin receptor antagonists (TPO-RAs) may be considered in late pregnancy when other treatments have failed, but published information is limited.
  • In the rare instances when splenectomy is required, it should be performed in the second trimester. Women who had a splenectomy may have a thrombocytopenic newborn, even if their platelet count is normal.
  • Vinca alkaloids, danazol, and immunosuppressive drugs not listed in these recommendations should be avoided in pregnancy.

Recommendations for obstetric analgesia and anesthesia are as follows[52] :

  • At a platelet count ≥ 70 × 10 9/L, in the absence of other hemostatic abnormalities, regional axial anesthesia can be safely performed.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) should be avoided for postpartum or postoperative analgesia in women with platelet counts < 70 × 10 9/L because of increased hemorrhagic risk.
  • A platelet count ≥50 × 10 9/L should be obtained for delivery.
  • All women, despite having ITP, who are at an increased risk for thromboembolism should receive appropriate prophylaxis for venous thromboembolism.
  • The mother with a rapidly falling platelet count should be observed more closely than those with low, but stable, levels (grade B recommendation).

Recommendations for management of delivery and newborn infants are as follows[52] :

  • Cordocentesis and fetal scalp blood sampling should be avoided in the management of the fetus/neonate of a mother with ITP in pregnancy.
  • Neonatal alloimmune thrombocytopenia should be excluded by parental testing if the neonate presents with severe thrombocytopenia.
  • The mode of delivery should be determined by obstetric indications, not by anticipation of the neonatal platelet count (grade B recommendation).
  • Procedures during labor that may be associated with increased hemorrhagic risk to the fetus should be avoided, specifically the use of fetal scalp electrodes, fetal blood sampling, ventouse delivery, and rotational forceps.
  • Previous splenectomy has been associated with worsening of maternal ITP in pregnancy and a higher risk for neonatal thrombocytopenia (grade B recommendation).
  • A mother with a previous newborn, thrombocytopenic or not, is likely to have a second baby with a similar platelet count.

American College of Obstetricians and Gynecologists

In 2016, the American College of Obstetricians and Gynecologists (ACOG) published a practice bulletin on thrombocytopenia in pregnant women, which included the following key recommendations.[12] :

  • Given the very low risk of serious neonatal hemorrhage, the mode of delivery in pregnancies complicated with ITP should be determined based upon obstetric considerations alone.
  • In pregnancies with high risk of intracranial hemorrhage (fetal platelet counts by umbilical cord blood sampling at 20 weeks of gestation of    < 20 x 10 9/L or a sibling with a perinatal intracranial hemorrhage), maternal intravenous immunoglobulin (IVIG) combined with prednisone is more effective than IVIG alone in eliciting a satisfactory fetal platelet response.
  • In pregnancies at standard risk (no history of intracranial hemorrhage in a previously affected sibling and initial fetal platelet counts > 20 × 10 9/L at 20 weeks of gestation), IVIG or prednisone therapy is beneficial, with no significant advantage of one therapy over another.
  • Epidural or spinal anesthesia is considered acceptable in patients with platelet counts ≥ 80 × 10 9/L, provided that the platelet level is stable, the patient has no other acquired or congenital coagulopathy, her platelet function is normal, and she is not on any antiplatelet or anticoagulant therapy.
  • Fetal–neonatal alloimmune thrombocytopenia should be suspected in cases of otherwise unexplained fetal or neonatal thrombocytopenia, hemorrhage, or ultrasonographic findings consistent with intracranial bleeding.

American Society of Hematology

ASH treatment considerations include the following[64] :

  • Women with no bleeding manifestations and platelet counts ≥30 x 10 9/L do not require any treatment until 36 weeks’ gestation (sooner if delivery is imminent)
  • If platelet counts are < 30 × 10 9/L or clinically relevant bleeding is present, first-line therapy is oral corticosteroids or intravenous immunoglobulin (IVIg)
  • The recommended starting dose of IVIg is 1 g/kg
  • Prednisone and prednisolone are preferred to dexamethasone, which crosses the placenta more readily.
  • Recommended starting doses of prednisone by different experts vary from 0.25 to 0.5 to 1 mg/kg daily; no evidence exists that a higher starting dose is better.
  • Medications are adjusted to maintain a safe platelet count

Expected responses to first-line therapy are as follows[64] :

  • Oral corticosteroids—initial response 2-14 days, peak response 4-28 days
  • IVIg—initial response 1-3 days, peak response 2-7 days

Second-line therapy for refractory ITP is with combined corticosteroids and IVIg or, in the second trimester, splenectomy.  For third-line therapy, anti-D immunoglobulin and azathioprine are relatively contraindicated. Agents that are not recommended, but whose use in pregnancy has been described, include the following[64] :

  • Cyclosporine
  • Dapsone
  • Thrombopoietin receptor agonists
  • Alemtuzumab
  • Rituximab

Contraindicated agents include the following[64] :

  • Mycophenolate mofetil
  • Cyclophosphamide
  • Vinca alkaloids
  • Danazol

ASH recommendations for management at the time of delivery are as follows[64] :

  • Because of the possible need for cesarean delivery, the recommended target platelet count prior to labor and delivery is ≥50 x 10 9/L
  • A woman whose platelet count is < 80 × 10 9/L but who has not required therapy during pregnancy can be started on oral prednisone (or prednisolone) 10 days prior to anticipated delivery at a dose of 10-20 mg daily and titrated as necessary
  • The mode of delivery should be determined by obstetric indications
  • Although the minimum platelet count for the placement of regional anesthesia is unknown and local practices may differ, many anesthesiologists will place a regional anesthetic if the platelet count is ≥80 × 10 9/L
  • While platelet transfusion alone is generally not effective in ITP, its use in conjunction with IVIg can be considered if an adequate platelet count has not been achieved and delivery is emergent
  • Percutaneous umbilical blood sampling (PUBS) or fetal scalp blood sampling is not recommended, as it is not helpful in predicting neonatal thrombocytopenia and is potentially harmful
  • In the newborn, the platelet count reaches its nadir 2-5 days after delivery and rises spontaneously by day 7
  • Postpartum thromboprophylaxis should be considered, as women with ITP are at increased risk of venous thromboembolism

Neonatal care

International Consensus Report recommendations for management of neonates born to women with ITP are as follows[52] :

  • Umbilical cord platelet count should be obtained at the time of delivery or as soon as possible.
  • Repeat the platelet count as needed depending on platelet levels, trends in the count, and response to treatment (if any). If cord platelet count is < 100 × 10 9/L, repeat the platelet count daily until stable. The incidence of pseudothrombocytopenia is high in neonates because of the difficulties encountered in obtaining unclotted blood with blood draws.
  • If the platelet count is < 50 × 10 9/L at birth, perform a cranial ultrasound. A magnetic resonance imaging for confirmation or clarification can be performed without anesthesia using the sleep and swaddle approach 30 to 60 minutes prior.
  • In the case of intracranial hemorrhage, give IVIg and limited steroids to maintain platelet count > 100 × 10 9/L for 1 week if possible and > 50 × 10 9/L for another week. Platelet transfusions may increase neonatal risk.
  • If there is symptomatic bleeding or if platelet count is < 30 × 10 9/L, with or without platelet transfusion, give IVIg.
  • If severe thrombocytopenia continues for > 1 week in a breast-fed infant, consider pausing breastfeeding for a few days to see whether the platelet count increases.


Medication Summary

Medications to increase the platelet count in pregnant women with immune thrombocytopenia (ITP) and newborns with neonatal alloimmune thrombocytopenia (NAIT) include steroids and intravenous immunoglobulins. 




Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli.

Prednisone (Sterapred)

Inhibits phagocytosis of antibody-covered platelets. Used to increase platelet count.

Blood products

Class Summary

Used to increase platelet count.

Intravenous immune globulin (Gammagard S/D, Gammar-P, Gamunex, Carimune, Polygam S/D)

Has rapid onset of action and is DOC (used in conjunction with platelet transfusion) when severe thrombocytopenia or life-threatening hemorrhage occurs.


Dexamethasone (Baycadron, Decadron DSC, Dexamethasone Intensol)


Questions & Answers


What causes immune thrombocytopenia in pregnancy?

What is the pathophysiology of immune thrombocytopenia in pregnancy?

What is the US prevalence of immune thrombocytopenia in pregnancy?

What is the global prevalence of immune thrombocytopenia in pregnancy?

What are the racial predilections of immune thrombocytopenia in pregnancy?

At what age is immune thrombocytopenia typically diagnosed?

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Which clinical history findings are characteristic of immune thrombocytopenia in pregnancy?

What is a case history of immune thrombocytopenia in pregnancy?

Which physical findings are characteristic of immune thrombocytopenia in pregnancy?


Which disorders are included in the differential diagnoses of immune thrombocytopenic purpura (ITP)?

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How common is immune thrombocytopenia in pregnancy?

What are the differential diagnoses for Immune Thrombocytopenia and Pregnancy?


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When is patient transfer required for the treatment of immune thrombocytopenia in pregnancy?

How is immune thrombocytopenia in pregnancy treated?

What is the role of surgery in the treatment of immune thrombocytopenia in pregnancy?

Which specialist consultations are beneficial to patients with immune thrombocytopenia in pregnancy?

How is immune thrombocytopenia in pregnancy prevented?


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What are the ACOG treatment guidelines for immune thrombocytopenia in pregnancy?

What are the ASH treatment guidelines for immune thrombocytopenia in pregnancy?


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Which medications in the drug class Blood products are used in the treatment of Immune Thrombocytopenia and Pregnancy?

Which medications in the drug class Glucocorticoids are used in the treatment of Immune Thrombocytopenia and Pregnancy?